Journal articles on the topic 'Proliferation'
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Fraser, Hamish M., Helen Wilson, Audrey Silvestri, Keith D. Morris, and Stanley J. Wiegand. "The Role of Vascular Endothelial Growth Factor and Estradiol in the Regulation of Endometrial Angiogenesis and Cell Proliferation in the Marmoset." Endocrinology 149, no. 9 (May 22, 2008): 4413–20. http://dx.doi.org/10.1210/en.2008-0325.
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The present studies explore the roles of vascular endothelial growth factor (VEGF) and estradiol on angiogenesis and stromal and epithelial cell proliferation in the marmoset endometrium during the proliferative phase of the ovulatory cycle. At the start of the proliferative phase, marmosets were 1) treated with vehicle, 2) treated with a VEGF inhibitor (VEGF Trap, aflibercept), 3) ovariectomized, 4) ovariectomized and given replacement estradiol, or 5) treated with VEGF Trap and given replacement estradiol. The uterus was examined 10 d later in the late proliferative phase. Changes in endothelial and epithelial cell proliferation were quantified using a volumetric density method after immunohistochemistry for bromodeoxyuridine to localize proliferating cells, CD31 to visualize endothelial cells, and dual staining to distinguish endothelial cell proliferation. Endothelial proliferation was elevated in late proliferative controls but virtually absent after VEGF Trap. Ovariectomy had a similar inhibitory effect, whereas angiogenesis was restored by estrogen replacement. Estradiol replacement in VEGF Trap-treated marmosets resulted in only a small increase in endothelial cell proliferation that remained significantly below control values. VEGF Trap treatment and ovariectomy also markedly reduced stromal cell proliferation but resulted in increased stromal cell density associated with a reduction in overall endometrial volume. Estrogen replacement in both ovariectomized and VEGF Trap-treated animals restored stromal proliferation rates and cell density. These results show that endometrial angiogenesis and stromal proliferation during the proliferative phase are driven by estradiol and that the effect of estrogen on angiogenesis is mediated largely by VEGF.
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Nishimura, R., and N. Arima. "Clinical significance of proliferative activity evaluated by MIB-1 in the treatment and postoperative follow-up of early breast cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 21054. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21054.
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21054 Background: To evaluate a clinical significance of proliferative activity in breast cancer, we studied relationships between proliferative activity and recurrence rate, the time of recurrence or adjuvant therapy. Methods: We analyzed 2448 patients with primary breast cancer between 1987 and 2004 in the Kumamoto City Hospital, and 437 cases out of the patients developed recurrence. Furthermore, the rate of recurrence before and after 1999 when postoperative adjuvant therapy (such as CEF or Taxanes) was started as standard treatment was investigated. Proliferative activity was judged by immunostaining for MIB-1. The fraction of proliferating cells was classified into 3 degrees (=19%, 20–49%, 50%=). Median observation period was 70 months. Results: 1) Distribution of patients by proliferation was as follows; =19%:1215 cases(50%), 20–49%: 870 cases(35%), or 50%=: 363 cases(15%). There was a significant relationship between proliferative activity and tumor size, nodal status, ER, PgR, p53 or HER2 status. 2) Multivariate analysis for disease-free survival revealed that a proliferative activity was one of significant factors in node-negative and positive cases. Recurrence rate was 11.6% in cases with low proliferation and 31.0% in high proliferation. The mean period from operation to recurrence in cases with low proliferation was 50.2 months, whereas 19.9 months in high proliferation (p<0.0001). Moreover, 74% of recurrent cases with high proliferation recurred within 2 years after operation, and there were few recurrences from the fifth year. 3) Patients with low proliferation frequently developed bone metastasis. In local recurrence, diffuse skin recurrence was often seen in cases with high proliferation. 4) The prognosis of patients in the later period (standard therapy group) was significantly better than that of patients in the earlier period, especially in high proliferation group. Conclusions: Proliferative activity might reflect aggressive behavior of breast cancer and predict the time of recurrence. The standard adjuvant therapy was effective in inhibiting early recurrence with high proliferation. It is important to take proliferative activity into consideration in the treatment and follow-up of breast cancer. No significant financial relationships to disclose.
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Bocheński, Szymon. "Proliferation Security Initiative: A New Formula for WMD Counter-Proliferation Efforts?" Connections: The Quarterly Journal 06, no. 4 (2007): 64–83. http://dx.doi.org/10.11610/connections.06.4.05.
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Hernández-Núñez, Ismael, Ana Quelle-Regaldie, Laura Sánchez, Fátima Adrio, Eva Candal, and Antón Barreiro-Iglesias. "Decline in Constitutive Proliferative Activity in the Zebrafish Retina with Ageing." International Journal of Molecular Sciences 22, no. 21 (October 28, 2021): 11715. http://dx.doi.org/10.3390/ijms222111715.
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It is largely assumed that the teleost retina shows continuous and active proliferative and neurogenic activity throughout life. However, when delving into the teleost literature, one finds that assumptions about a highly active and continuous proliferation in the adult retina are based on studies in which proliferation was not quantified in a comparative way at the different life stages or was mainly studied in juveniles/young adults. Here, we performed a systematic and comparative study of the constitutive proliferative activity of the retina from early developing (2 days post-fertilisation) to aged (up to 3–4 years post-fertilisation) zebrafish. The mitotic activity and cell cycle progression were analysed by using immunofluorescence against pH3 and PCNA, respectively. We observed a decline in the cell proliferation in the retina with ageing despite the occurrence of a wave of secondary proliferation during sexual maturation. During this wave of secondary proliferation, the distribution of proliferating and mitotic cells changes from the inner to the outer nuclear layer in the central retina. Importantly, in aged zebrafish, there is a virtual disappearance of mitotic activity. Our results showing a decline in the proliferative activity of the zebrafish retina with ageing are of crucial importance since it is generally assumed that the fish retina has continuous proliferative activity throughout life.
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Lawrence, Ben, Simon Schimmack, Bernhard Svejda, Ignat Drozdov, Daniele Alaimo, Barton Kenney, Mark Kidd, and Irvin M. Modlin. "Prognostication by multigene proliferative marker panel compared with Ki-67 in small-intestinal NENs." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 242. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.242.
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242 Background: Ki-67 is the major proliferative marker in clinical use to determine neuroendocrine neoplasm (NEN) prognosis. Ki-67 is unable to predict the outcome of SI-NENs, as the majority have a low (≤2) Ki-67%. Therefore, we aimed to identify a sensitive panel of proliferative markers using qRT-PCR to more accurately define the proliferation of these slow growing tumors. Methods: We identified genes with a mechanistic function in cell cycle progression that were over-expressed in RNA microarrays of SI-NENs (n=8) compared to adjacent normal tissue (n=4) (dCHIP, annotation databases). Timing of marker gene expression (qRT-PCR) in proliferating cell-cycle phases (S, G2, M) was determined in flow-sorted SI-NEN cell lines (KRJ-1, H-STS) after propidium iodide staining. RNA expression of candidate proliferative markers was then investigated using an in vivo model and two independent tumor datasets, and transcript level compared to Ki-67% protein expression (immunohistochemical staining). Results: Twenty genes with a mechanistic role in proliferation were identified and 17 confirmed to be expressed in proliferating cell cycle phases. Each tumor expressed a unique profile of the 17 proliferative markers. Both Ki-67 protein and Ki-67 RNA transcript levels failed to differentiate in vivo SI-NEN models or patient samples despite variable proliferative capacity (e.g., WDNETs versus WDNECs). Although most tumors showed low levels of Ki-67 expression, the tumors expressed high levels of select alternative proliferative markers. Hierarchical clustering provided a novel and clinically meaningful prognostic classification. Conclusions: Proliferation of individual SI-NENs is regulated by unique combinations of multiple genes with a mechanistic role in cell-cycle progression. Regulation of proliferation in SI-NENs is therefore complex and cannot accurately be defined by Ki-67 as a single marker. A panel of proliferative RNA markers has potential to significantly improve prognostication in patients with SI-NENs.
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Marlatt, Michael W., Jan Bauer, Eleonora Aronica, Elise S. van Haastert, Jeroen J. M. Hoozemans, Marian Joels, and Paul J. Lucassen. "Proliferation in the Alzheimer Hippocampus Is due to Microglia, Not Astroglia, and Occurs at Sites of Amyloid Deposition." Neural Plasticity 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/693851.
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Microglia and astrocytes contribute to Alzheimer’s disease (AD) etiology and may mediate early neuroinflammatory responses. Despite their possible role in disease progression and despite the fact that they can respond to amyloid deposition in model systems, little is known about whether astro- or microglia can undergo proliferation in AD and whether this is related to the clinical symptoms or to local neuropathological changes. Previously, proliferation was found to be increased in glia-rich regions of the presenile hippocampus. Since their phenotype was unknown, we here used two novel triple-immunohistochemical protocols to study proliferation in astro- or microglia in relation to amyloid pathology. We selected different age-matched cohorts to study whether proliferative changes relate to clinical severity or to neuropathological changes. Proliferating cells were found across the hippocampus but never in mature neurons or astrocytes. Almost all proliferating cells were colabeled with Iba1+, indicating that particularly microglia contribute to proliferation in AD. Proliferating Iba1+ cells was specifically seen within the borders of amyloid plaques, indicative of an active involvement in, or response to, plaque accumulation. Thus, consistent with animal studies, proliferation in the AD hippocampus is due to microglia, occurs in close proximity of plaque pathology, and may contribute to the neuroinflammation common in AD.
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Kabraji, Sheheryar Kairas, Giorgio Gaglia, Danae Argyropoulou, Yang Dai, Shu Wang, Johann Bergholz, Shannon Coy, et al. "Temporal and spatial topography of cell proliferation in cancer." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 3122. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3122.
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3122 Background: Tumors are complex ecosystems where exogenous and endogenous cues are integrated to either stimulate or inhibit cancer cell proliferation. However, the nature of these complex cell cycle states, their spatial organization, response to perturbation, and implications for clinical outcomes, are poorly characterized in tumor tissues. Methods: We used multiplexed tissue imaging to develop a robust classifier of proliferation, the multivariate proliferation index (MPI), using 513 unique tumors across five cancer types. Next, we used dimensionality reduction analysis to assess how the patterns of cell cycle protein expression in tumors were altered in response to perturbation. Results: The MPI outperforms single markers, like Ki67, when classifying proliferative index across diverse tumor types and reveals the proliferative architecture of tumors in situ. We find that proliferative and non-proliferative cancer cells are organized across microscopic (cell-to-cell) and macroscopic (tissue-level) scales. Both domains are reshaped by therapy, and local clusters of proliferative and non-proliferative tumor cells preferentially neighbor distinct tumor-infiltrating immune cells. We further phenotyped non-proliferating cancer cells using markers of quiescent cancer cells, cancer stem cells, and dormant cancer cells. We found that these types of non-proliferating cancer cells can occupy distinct regions within the same primary tumor. In high-dimensional marker space, populations of proliferative cancer cells express canonical patterns of cell cycle protein markers, a property we refer to as “cell cycle coherence”. Untreated tumors exist in a continuum of coherence states, ranging from optimal coherence, akin to freely cycling cells in culture, to reduced coherence characterized by either cell cycle polarization or non-canonical marker expression. Coherence can be stereotypically altered by induction and abrogation of mitogen signaling in a HER2-driven model of breast cancer. Cell cycle coherence is modulated by neoadjuvant therapy in patients with localized breast cancer, and coherence is associated with disease-free survival after adjuvant therapy in patients with colorectal cancer, mesothelioma and glioblastoma. Conclusions: The MPI robustly defines proliferating and non-proliferating cells in tissues, with immediate implications for clinical practice and research. The coherence metrics capture the diversity of post-treatment cell cycle states directly in clinical samples, a fundamental step in advancing precision medicine. More broadly, replacing binary metrics with multivariate traits provides a quantitative framework to study temporal processes from fixed static images and to investigate the rich spatial biology of human cancers.
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Levine, Richard, Magnus S. Agren, and Patricia M. Mertz. "Effect of Occlusion on Cell Proliferation during Epidermal Healing." Journal of Cutaneous Medicine and Surgery 2, no. 4 (April 1998): 193–98. http://dx.doi.org/10.1177/120347549800200403.
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Background: Occlusive dressings influence epithelization of superficial wounds by some unknown mechanism(s). Objective: The effects of occlusion on epidermal cell proliferation in two types of wounds were examined. Methods: Partial-thickness wounds and tape-stripped skin wounds were compared. An immunohistochemical technique, employing PC10 — a monoclonal antibody against proliferating cell nuclear antigen (PCNA) — was applied to formalin-fixed, paraffin-embedded porcine tissue sections. Results: The number of PC10-positive cells was low during the migratory phase, then increased to a peak of proliferation 2 to 3 days after resurfacing. An overall increased proliferative response (mean = 21%) was seen in occluded compared to control partial-thickness wounds (day 10 postoperatively); an opposite effect of occlusion on epidermal proliferation was seen in tape-stripped skin. Occlusion decreased the proliferative response (mean = 42%) compared to air-exposure. Conclusion: Occlusion increased epidermal cell proliferation in wounds (where the entire surface epithelium and papillary dermis was removed), whereas an opposite effect was seen in tape-stripped skin from which only the stratum corneum had been removed.
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Sambasiva Rao, M., and Janardan K. Reddy. "The Relevance of Peroxisome Proliferation and Cell Proliferation in Peroxisome Proliferator-Induced Hepatocarcinogenesis." Drug Metabolism Reviews 21, no. 1 (January 1989): 103–10. http://dx.doi.org/10.3109/03602538909029957.
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Shayan, Katayoon, Michael Ho, Vernon Edwards, Ronald Laxer, and Paul S. Thorner. "Synovial Pathology in Camptodactyly-Arthropathy-Coxa Vara-Pericarditis Syndrome." Pediatric and Developmental Pathology 8, no. 1 (January 2005): 26–33. http://dx.doi.org/10.1007/s10024-004-3035-z.
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At least 25 families with camptodactyly-arthropathy-coxa vara-pericarditis (CACP syndrome) have been reported, with descriptions of a distinctive synovial pathology based largely on light microscopy. Although described as “proliferative,” with numerous multinucleated giant cells, the natures of proliferating cells and giant cells have not been determined. To clarify the pathogenesis of this disorder, we studied 3 patients who had CACP syndrome and underwent synovial biopsy. Cells in the biopsies were studied by immunohistochemistry and electron microscopy. Giant cells were identified as macrophage in origin based on CD68 expression and electron microscopic features of macrophages. Most cells in the synovium were CD68 positive, in keeping with macrophages. The degree of proliferation in synovial biopsies was estimated by MIB1 immunostaining, which showed that up to 30% of cells were cycling compared with fewer than 10% in control synovial biopsies. None of the giant cells was cycling. By double immunostaining, proliferating cells were determined to be fibroblastic synoviocytes rather than macrophages. Thus the proliferative synovitis in this CACP syndrome can be more accurately thought of as hypercellularity by infiltrating macrophages with a contribution by proliferating fibroblastic synoviocytes. The synoviocyte proliferation is likely a response to the underlying genetic mutations involving the proteogly-can-4 (or CACP) gene. The encoded protein normally acts as a lubricant and possibly controls cell proliferation. Loss of one or another of these functions may be a possible mechanism that leads to synoviocyte proliferation in this disease, but the exact pathophysiology leading to this change requires further study.
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Yang, Wei. "The Application of Proliferated Form in Designing Product Modeling." Advanced Materials Research 490-495 (March 2012): 2834–37. http://dx.doi.org/10.4028/www.scientific.net/amr.490-495.2834.
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In the structure of the product modeling design, there is a kind of Proliferated form that is shown as form in quantity proliferation, is also proliferation in the form of all kinds. Proliferating form endowed modeling with new vitality and the urge to multiply. Proliferating form includes the structural proliferation, derivative proliferation, chaotic proliferation, heterogeneous proliferation and repetitive proliferation
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Chan, Ming Liang, Janka Petravic, Alexandra M. Ortiz, Jessica Engram, Mirko Paiardini, Deborah Cromer, Guido Silvestri, and Miles P. Davenport. "Limited CD4+ T cell proliferation leads to preservation of CD4+ T cell counts in SIV-infected sooty mangabeys." Proceedings of the Royal Society B: Biological Sciences 277, no. 1701 (June 30, 2010): 3773–81. http://dx.doi.org/10.1098/rspb.2010.0972.
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Human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections result in chronic virus replication and progressive depletion of CD4+ T cells, leading to immunodeficiency and death. In contrast, ‘natural hosts’ of SIV experience persistent infection with high virus replication but no severe CD4+ T cell depletion, and remain AIDS-free. One important difference between pathogenic and non-pathogenic infections is the level of activation and proliferation of CD4+ T cells. We analysed the relationship between CD4+ T cell number and proliferation in HIV, pathogenic SIV in macaques, and non-pathogenic SIV in sooty mangabeys (SMs) and mandrills. We found that CD4+ T cell proliferation was negatively correlated with CD4+ T cell number, suggesting that animals respond to the loss of CD4+ T cells by increasing the proliferation of remaining cells. However, the level of proliferation seen in pathogenic infections (SIV in rhesus macaques and HIV) was much greater than in non-pathogenic infections (SMs and mandrills). We then used a modelling approach to understand how the host proliferative response to CD4+ T cell depletion may impact the outcome of infection. This modelling demonstrates that the rapid proliferation of CD4+ T cells in humans and macaques associated with low CD4+ T cell levels can act to ‘fuel the fire’ of infection by providing more proliferating cells for infection. Natural host species, on the other hand, have limited proliferation of CD4+ T cells at low CD4+ T cell levels, which allows them to restrict the number of proliferating cells susceptible to infection.
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Collesi, Chiara, Lorena Zentilin, Gianfranco Sinagra, and Mauro Giacca. "Notch1 signaling stimulates proliferation of immature cardiomyocytes." Journal of Cell Biology 183, no. 1 (September 29, 2008): 117–28. http://dx.doi.org/10.1083/jcb.200806091.
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The identification of the molecular mechanisms controlling cardiomyocyte proliferation during the embryonic, fetal, and early neonatal life appears of paramount interest in regard to exploiting this information to promote cardiac regeneration. Here, we show that the proliferative potential of neonatal rat cardiomyocytes is powerfully stimulated by the sustained activation of the Notch pathway. We found that Notch1 is expressed in proliferating ventricular immature cardiac myocytes (ICMs) both in vitro and in vivo, and that the number of Notch1-positive cells in the heart declines with age. Notch1 expression in ICMs paralleled the expression of its Jagged1 ligand on non-myocyte supporting cells. The inhibition of Notch signaling in ICMs blocked their proliferation and induced apoptosis; in contrast, its activation by Jagged1 or by the constitutive expression of its activated form using an adeno-associated virus markedly stimulated proliferative signaling and promoted ICM expansion. Maintenance or reactivation of Notch signaling in cardiac myocytes might represent an interesting target for innovative regenerative therapy.
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Lewis, Hilel, Janice M. Burke, Gary W. Abrams, and Thomas M. Aaberg. "Perisilicone Proliferation after Vitrectomy for Proliferative Vitreoretinopathy." Ophthalmology 95, no. 5 (May 1988): 583–91. http://dx.doi.org/10.1016/s0161-6420(88)33136-2.
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Chung, Hyunju, and Seungjoon Park. "Ghrelin regulates cell cycle-related gene expression in cultured hippocampal neural stem cells." Journal of Endocrinology 230, no. 2 (August 2016): 239–50. http://dx.doi.org/10.1530/joe-16-0126.
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We have previously demonstrated that ghrelin stimulates the cellular proliferation of cultured adult rat hippocampal neural stem cells (NSCs). However, little is known about the molecular mechanisms by which ghrelin regulates cell cycle progression. The purpose of this study was to investigate the potential effects of ghrelin on cell cycle regulatory molecules in cultured hippocampal NSCs. Ghrelin treatment increased proliferation assessed by CCK-8 proliferation assay. The expression levels of proliferating cell nuclear antigen and cell division control 2, well-known cell-proliferating markers, were also increased by ghrelin. Fluorescence-activated cell sorting analysis revealed that ghrelin promoted progression of cell cycle from G0/G1 to S phase, whereas this progression was attenuated by the pretreatment with specific inhibitors of MEK/extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/Akt, mammalian target of rapamycin, and janus kinase 2/signal transducer and activator of transcription 3. Ghrelin-induced proliferative effect was associated with increased expression of E2F1 transcription factor in the nucleus, as determined by Western blotting and immunofluorescence. We also found that ghrelin caused an increase in protein levels of positive regulators of cell cycle, such as cyclin A and cyclin-dependent kinase (CDK) 2. Moreover, p27KIP1 and p57KIP2 protein levels were reduced when cell were exposed to ghrelin, suggesting downregulation of CDK inhibitors may contribute to proliferative effect of ghrelin. Our data suggest that ghrelin targets both cell cycle positive and negative regulators to stimulate proliferation of cultured hippocampal NSCs.
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Yuko, Murase, Fesseha Meseret, Abbaspour Nazanin, and Young Hong Mee. "Watermelon Powder Supplementation Reduces Colonic Cell Proliferation by Upregulating p21Waf1/Cip1 Expression." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 340. http://dx.doi.org/10.1093/cdn/nzaa044_039.
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Abstract Objectives Watermelon is high in L-citrulline, a precursor for L-arginine, which in turn may reduce the risk of colorectal cancer (CRC). Research has shown that L-arginine inhibits the hyperproliferation of colorectal tumor cells as a marker for CRC. The objective of this study was, therefore, to examine the effects of watermelon powder supplementation on colonic cell proliferation and their gene expression. The hypothesis was that watermelon powder supplementation would reduce CRC risk by regulating colonic expression of genes related to epithelial cell proliferation. Methods Thirty-two 21-day-old, male, Sprague Dawley rats were randomly assigned to one of the following isocaloric diets: 0.5% watermelon powder, 0.36% L-arginine, and control for 9 weeks. All animals were injected with azoxymethane (15 mg/kg body weight). Colonic cell proliferation was measured using ki-67 immunohistochemistry, and colonic gene expression was determined using a quantitative real-time polymerase chain reaction (PCR). Results Both watermelon powder and L-arginine groups exhibited lower proliferating index (P = 0.041) and lower proliferative zone (P = 0.041). In addition, watermelon powder and L-arginine supplementation upregulated p21Waf1/Cip1 gene expression (P = 0.048). There were no significant differences in the expression of Cyclin D1, Cyclin-dependent kinase 2 (CDK2), Cyclin-dependent kinase 4 (CDK4), and Peroxisome proliferator-activated receptor γ (PPARγ). Conclusions These results suggest that watermelon or L-arginine supplementation may decrease the risk of CRC as they both reduced proliferation by upregulating a cyclin-dependent kinase inhibitor. Additional markers for gene expression involving cell proliferation are needed to confirm the present findings. Funding Sources National Watermelon Promotion Board (NWPB 15–16) National Cancer Institutes of Health (U54CA132384 for SDSU and U54132379 for UCSD).
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Martín-Sanz, Raquel, José María Sayagués, Pilar García-Cano, Mikel Azcue-Mayorga, María del Carmen Parra-Pérez, María Ángeles Pacios-Pacios, Enric Piqué-Durán, and Jorge Feito. "TP53 Abnormalities and MMR Preservation in 5 Cases of Proliferating Trichilemmal Tumours." Dermatopathology 8, no. 2 (May 25, 2021): 147–58. http://dx.doi.org/10.3390/dermatopathology8020021.
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Proliferating trichilemmal tumours (PTT) are defined by a benign squamous cell proliferation inside a trichilemmal cystic (TC) cavity. A possible explanation of this proliferative phenomenon within the cyst may be molecular alterations in genes associated to cell proliferation, which can be induced by ultraviolet radiation. Among other genes, alterations on TP53 and DNA mismatch repair proteins (MMR) may be involved in the cellular proliferation observed in PTT. Based on this assumption, but also taking into account the close relationship between the sebaceous ducts and the external root sheath where TC develop, a MMR, a p53 expression assessment and a TP53 study were performed in a series of 5 PTT cases, including a giant one. We failed to demonstrate a MMR disorder on studied PTT, but we agree with previous results suggesting increased p53 expression in these tumours, particularly in proliferative areas. TP53 alteration was confirmed with FISH technique, demonstrating TP53 deletion in most cells.
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Robey, H. L., P. S. Hiscott, and I. Grierson. "Cytokeratins and retinal epithelial cell behaviour." Journal of Cell Science 102, no. 2 (June 1, 1992): 329–40. http://dx.doi.org/10.1242/jcs.102.2.329.
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The expression of cytokeratins 18 and 19 by human retinal pigment epithelial cells (HRPE) has been suspected of being associated with HRPE proliferation. We have investigated the involvement of these cytokeratin subtypes in the proliferative and migratory behaviour of cultured HRPE. Cell proliferation markers (bromodeoxyuridine and proliferating cell nuclear antigen) and the cytokeratins were identified using immunohistochemical techniques. In vitro, cytokeratins 18 and 19, as detected by the monoclonal antibodies RGE 53 and K4.62, were expressed in a subset of HRPE and this subset was significantly less likely to be proliferating. Micro-chemotaxis chambers were used to study migrating cells and immunohistochemical staining for cytokeratins 18 and 19 revealed that actively migrating cells always expressed these two cytokeratins, whereas stationary cells did not label for these cytokeratin subtypes. It was apparent that cytokeratins 18 and 19 were not markers of proliferation, but were involved in the mobility of HRPE in vitro. Cytokeratins 18 and 19 may be useful indicators of simple epithelial cell migration in tissues.
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Willett, C. G., G. Warland, M. P. Hagan, W. J. Daly, J. Coen, P. C. Shellito, and C. C. Compton. "Tumor proliferation in rectal cancer following preoperative irradiation." Journal of Clinical Oncology 13, no. 6 (June 1995): 1417–24. http://dx.doi.org/10.1200/jco.1995.13.6.1417.
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PURPOSE This study examines the effect of preoperative irradiation on tumor proliferation in rectal cancer. PATIENTS AND METHODS One hundred twenty-two patients with locally advanced rectal cancer received 45 to 50 Gy of preoperative irradiation followed by surgery. Pretreatment tumor biopsies and postirradiation surgical specimens were scored for proliferative activity by assaying the extent of Ki-67 and proliferating-cell nuclear antigen (PCNA) immunostaining and the number of mitoses per 10 high-power fields (hpf). Preirradiation and postirradiation proliferative activity was determined and correlated to clinical outcome. RESULTS There was an overall reduction in the tumor proliferative activity of rectal cancer after irradiation compared with its preirradiation state. Decreases in the activity of all three markers of tumor proliferation (Ki-67 and PCNA immunostaining, and mitotic counts) were observed in irradiated tumors compared with pretreatment biopsies. Postirradiation tumor proliferative activity was associated with pathologic tumor stage. A high level of proliferative activity was observed in tumors downstaged to the rectal wall (T1-2) compared with tumors that retained transmural penetration (T3-4). Multivariate analysis indicated that postirradiation proliferative activity and stage were independently associated with survival following surgery. Patients with tumors that exhibited elevated proliferative activity postirradiation had improved survival compared with patients with tumors that showed less proliferative activity. CONCLUSION Moderate- to high-dose preoperative irradiation decreases both the tumor size and proliferative activity of rectal cancers. Elevated postirradiation tumor proliferative activity correlates strongly with improved survival. This may aid in identifying high-risk patients following preoperative irradiation and surgery.
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NEUMANN, IVER B. "The Proliferation of Proliferation." Cooperation and Conflict 37, no. 4 (December 2002): 431–36. http://dx.doi.org/10.1177/001083602762574496.
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Dakic, Vanja, Renata de Moraes Maciel, Hannah Drummond, Juliana M. Nascimento, Pablo Trindade, and Stevens K. Rehen. "Harmine stimulates proliferation of human neural progenitors." PeerJ 4 (December 6, 2016): e2727. http://dx.doi.org/10.7717/peerj.2727.
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Harmine is theβ-carboline alkaloid with the highest concentration in the psychotropic plant decoction Ayahuasca. In rodents, classical antidepressants reverse the symptoms of depression by stimulating neuronal proliferation. It has been shown that Ayahuasca presents antidepressant effects in patients with depressive disorder. In the present study, we investigated the effects of harmine in cell cultures containing human neural progenitor cells (hNPCs, 97% nestin-positive) derived from pluripotent stem cells. After 4 days of treatment, the pool of proliferating hNPCs increased by 71.5%. Harmine has been reported as a potent inhibitor of the dual specificity tyrosine-phosphorylation-regulated kinase (DYRK1A), which regulates cell proliferation and brain development. We tested the effect of analogs of harmine, an inhibitor of DYRK1A (INDY), and an irreversible selective inhibitor of monoamine oxidase (MAO) but not DYRK1A (pargyline). INDY but not pargyline induced proliferation of hNPCs similarly to harmine, suggesting that inhibition of DYRK1A is a possible mechanism to explain harmine effects upon the proliferation of hNPCs. Our findings show that harmine enhances proliferation of hNPCs and suggest that inhibition of DYRK1A may explain its effects upon proliferationin vitroand antidepressant effectsin vivo.
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Wadham, C., J. R. Gamble, M. A. Vadas, and Y. Khew-Goodall. "Translocation of protein tyrosine phosphatase Pez/PTPD2/PTP36 to the nucleus is associated with induction of cell proliferation." Journal of Cell Science 113, no. 17 (September 1, 2000): 3117–23. http://dx.doi.org/10.1242/jcs.113.17.3117.
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Pez is a non-transmembrane tyrosine phosphatase with homology to the FERM (4.1, ezrin, radixin, moesin) family of proteins. The subcellular localisation of Pez in endothelial cells was found to be regulated by cell density and serum concentration. In confluent monolayers Pez was cytoplasmic, but in cells cultured at low density Pez was nuclear, suggesting that it is a nuclear protein in proliferating cells. This notion is supported by the loss of nuclear Pez when cells are serum-starved to induce quiescence, and the rapid return of Pez to the nucleus upon refeeding with serum to induce proliferation. Vascular endothelial cells normally exist as a quiescent confluent monolayer but become proliferative during angiogenesis or upon vascular injury. Using a ‘wound’ assay to mimic these events in vitro, Pez was found to be nuclear in the cells that had migrated and were proliferative at the ‘wound’ edge. TGFbeta, which inhibits cell proliferation but not migration, inhibited the translocation of Pez to the nucleus in the cells at the ‘wound’ edge, further strengthening the argument that Pez plays a role in the nucleus during cell proliferation. Together, the data presented indicate that Pez is a nuclear tyrosine phosphatase that may play a role in cell proliferation.
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Morimoto, Y., and K. Saga. "Proliferating cells in human eccrine and apocrine sweat glands." Journal of Histochemistry & Cytochemistry 43, no. 12 (December 1995): 1217–21. http://dx.doi.org/10.1177/43.12.8537637.
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Morphological observations of sweat glands showed degenerated debris of secretory cells in the secretory lumen in both apocrine and eccrine sweat glands. This suggested that dead secretory cells of human eccrine and apocrine sweat glands were released into the lumen and replaced by other cells. However, we did not know which type of cells replaced lost secretory cells. Therefore, we studied the proliferating cells in human eccrine and apocrine sweat glands by labeling S-phase cells in vitro with 5-bromo-2'-deoxyuridine (BrdUrd) and by immunostaining proliferation-associated proliferating cell nuclear antigen (PCNA) with anti-PCNA monoclonal antibody. BrdUrd and anti-PCNA antibody labeled a few secretory cells in eccrine and apocrine sweat glands, but neither method labeled myoepithelial cells. Luminal and peripheral cells of the eccrine and apocrine coiled duct were labeled with both BrdUrd and PCNA. However, we could not find any highly proliferative germinative cells in coiled ducts. Our results suggest that lost secretory cells could be replaced by proliferation of secretory cells themselves rather than by proliferation of myoepithelial cells or duct cells.
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Frampton, Gabriel, Yoshiyuki Ueno, Matthew Quinn, Matthew McMillin, Hae Yong Pae, Cheryl Galindo, Dinorah Leyva-Illades, and Sharon DeMorrow. "The novel growth factor, progranulin, stimulates mouse cholangiocyte proliferation via sirtuin-1-mediated inactivation of FOXO1." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 11 (December 1, 2012): G1202—G1211. http://dx.doi.org/10.1152/ajpgi.00104.2012.
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Progranulin (PGRN), a secreted growth factor, regulates the proliferation of various epithelial cells. Its mechanism of action is largely unknown. Sirtuin 1 (Sirt1) is a protein deacetylase that is known to regulate the transcriptional activity of the forkhead receptor FOXO1, thereby modulating the balance between proapoptotic and cell cycle-arresting genes. We have shown that PGRN is overexpressed in cholangiocarcinoma and stimulates proliferation. However, its effects on hyperplastic cholangiocyte proliferation are unknown. In the present study, the expression of PGRN and its downstream targets was determined after bile duct ligation (BDL) in mice and in a mouse cholangiocyte cell line after stimulation with PGRN. The effects of PGRN on cholangiocyte proliferation were assessed in sham-operated (sham) and BDL mice treated with PGRN or by specifically knocking down endogenous PGRN expression using Vivo-Morpholinos or short hairpin RNA. PGRN expression and secretion were upregulated in proliferating cholangiocytes isolated after BDL. Treatment of mice with PGRN increased biliary mass and cholangiocyte proliferation in vivo and in vitro and enhanced cholangiocyte proliferation observed after BDL. PGRN treatment decreased Sirt1 expression and increased the acetylation of FOXO1, resulting in the cytoplasmic accumulation of FOXO1 in cholangiocytes. Overexpression of Sirt1 in vitro prevented the proliferative effects of PGRN. Conversely, knocking down PGRN expression in vitro or in vivo inhibited cholangiocyte proliferation. In conclusion, these data suggest that the upregulation of PGRN may be a key feature stimulating cholangiocyte proliferation. Modulating PGRN levels may be a viable technique for regulating the balance between ductal proliferation and ductopenia observed in a variety of cholangiopathies.
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Ozaltin, Fatih, Nesrin Besbas, Aysin Bakkaloglu, Safak Gucer, Rezan Topaloglu, Seza Ozen, Gulsev Kale, and Melda Caglar. "Apoptosis and proliferation in childhood acute proliferative glomerulonephritis." Pediatric Nephrology 20, no. 11 (June 18, 2005): 1572–77. http://dx.doi.org/10.1007/s00467-005-1985-7.
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Hatchell, D. L., T. McAdoo, S. Sheta, R. T. King, and J. V. Bartolome. "Quantification of Cellular Proliferation in Experimental Proliferative Vitreoretinopathy." Archives of Ophthalmology 106, no. 5 (May 1, 1988): 669–72. http://dx.doi.org/10.1001/archopht.1988.01060130731033.
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Park, Hyeon Young, Mi-Jin Kim, Seunghyeong Lee, Jonghwa Jin, Sungwoo Lee, Jung-Guk Kim, Yeon-Kyung Choi, and Keun-Gyu Park. "Inhibitory Effect of a Glutamine Antagonist on Proliferation and Migration of VSMCs via Simultaneous Attenuation of Glycolysis and Oxidative Phosphorylation." International Journal of Molecular Sciences 22, no. 11 (May 25, 2021): 5602. http://dx.doi.org/10.3390/ijms22115602.
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Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the development of atherosclerosis and restenosis. Glycolysis and glutaminolysis are increased in rapidly proliferating VSMCs to support their increased energy requirements and biomass production. Thus, it is essential to develop new pharmacological tools that regulate metabolic reprogramming in VSMCs for treatment of atherosclerosis. The effects of 6-diazo-5-oxo-L-norleucine (DON), a glutamine antagonist, have been broadly investigated in highly proliferative cells; however, it is unclear whether DON inhibits proliferation of VSMCs and neointima formation. Here, we investigated the effects of DON on neointima formation in vivo as well as proliferation and migration of VSMCs in vitro. DON simultaneously inhibited FBS- or PDGF-stimulated glycolysis and glutaminolysis as well as mammalian target of rapamycin complex I activity in growth factor-stimulated VSMCs, and thereby suppressed their proliferation and migration. Furthermore, a DON-derived prodrug, named JHU-083, significantly attenuated carotid artery ligation-induced neointima formation in mice. Our results suggest that treatment with a glutamine antagonist is a promising approach to prevent progression of atherosclerosis and restenosis.
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O'Reilly, Michael A., Richard H. Watkins, Rhonda J. Staversky, and William M. Maniscalco. "Induced p21Cip1 in premature baboons with CLD: implications for alveolar hypoplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 4 (October 2003): L964—L971. http://dx.doi.org/10.1152/ajplung.00171.2003.
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Aberrant pulmonary epithelial and mesenchymal cell proliferation occurs when newborns are treated with oxygen and ventilation to mitigate chronic lung disease. Because the cyclin-dependent kinase inhibitor p21 inhibits proliferation of oxygen-exposed cells, its expression was investigated in premature baboons delivered at 125 days (67% of term) and treated with oxygen and ventilation pro re nata (PRN) for 2, 6, 14, and 21 days. Approximately 5% of all cells expressed p21 during normal lung development of which <1% of these cells were pro-surfactant protein (SP)-B-positive epithelial cells. The percentage of cells expressing p21 increased threefold in all PRN-treated animals, but different cell populations expressed it during disease progression. Between 2 and 6 days of treatment, p21 was detected in 30-40% of pro-SP-B cells. In contrast, only 12% of pro-SP-B cells expressed p21 by 14 and 21 days of treatment, by which time p21 was also detected in mesenchymal cells. Even though increased epithelial and mesenchymal cell proliferation occurs during disease progression, those cells expressing p21 did not also express the proliferative marker Ki67. Thus two populations of epithelial and mesenchymal cells can be identified that are either expressing Ki67 and proliferating or expressing p21 and not proliferating. These data suggest that p21 may play a role in disorganized proliferation and alveolar hypoplasia seen in newborn chronic lung disease.
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Meininger, C. J., and H. J. Granger. "Mechanisms leading to adenosine-stimulated proliferation of microvascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 1 (January 1, 1990): H198—H206. http://dx.doi.org/10.1152/ajpheart.1990.258.1.h198.
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This study investigated the mechanisms by which adenosine stimulates proliferation of microvascular endothelial cells. The metabolic byproducts of adenosine, inosine and hypoxanthine were unable to stimulate proliferation. When adenosine uptake was prevented, the stimulation of proliferation was unchanged, suggesting that uptake of adenosine with subsequent incorporation into the nucleotide pool is not the mechanism for increasing proliferation. Treatment of endothelial cells with adenosine analogues, presumably selective for either the A1 or A2 receptor, stimulated proliferation equally. This suggested that adenosine 3', 5'-cyclic monophosphate (cAMP) might not mediate the proliferative response to adenosine. However, radioimmunoassay of cell extracts after treatment with either analogue showed an increase in cAMP. In addition, adenylate cyclase blockade with 2', 5'-dideoxyadenosine prevented the proliferative response brought about by these analogues. These data suggest that the proliferative response to adenosine depends on an increase in cAMP. A 2-h pulse of cholera toxin stimulated endothelial cell proliferation, further supporting a role for cAMP. Pretreatment of endothelial cells with pertussis toxin blocked the stimulation of proliferation, indicating that a Gi or similar G protein is also involved in proliferation. We conclude that the proliferative response to adenosine involves a pertussis toxin-sensitive substrate as well as an increase in cAMP.
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Nadasdy, T., Z. Laszik, K. E. Blick, L. D. Johnson, and F. G. Silva. "Proliferative activity of intrinsic cell populations in the normal human kidney." Journal of the American Society of Nephrology 4, no. 12 (June 1994): 2032–39. http://dx.doi.org/10.1681/asn.v4122032.
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The proliferative activity of various normal human renal cell populations is unknown. Recently, antibodies to cell proliferation-associated nuclear proteins, such as proliferating cell nuclear antigen (PCNA) and KI-67, which are applicable to archival paraffin sections, became available. With antibodies to PCNA and Ki-67 after microwave pretreatment of the paraffin sections, the proliferation indexes (ratio of positive nuclei with PCNA and Ki-67 antibodies/all nuclei counted x 100, i.e. percentage of positive cells) of 12 different intrinsic renal cell populations in 20 normal human kidneys have been determined. The following proliferation indexes (percentages of positive cells) were found with the PCNA and the Ki-67 antibodies, respectively: proximal tubular epithelium, 0.22, 0.24; thin limb of Henle, 0.29, 0.30; thick ascending limb of Henle, 0.32, 0.29; distal tubular epithelium (distal convoluted tubules and cortical collecting ducts, 0.33, 0.44; medullary collecting ducts, 0.32, 0.3; glomerular mesangial cells, 0.07, 0.12; glomerular visceral epithelial cells, 0.04, 0.08; glomerular parietal epithelial cells, 0.07, 0.1; glomerular capillary endothelium, 0.42, 0.47; peritubular capillary endothelial cells, 0.38, 0.43; endothelium of large intrarenal vessels (arteries and veins), 0.09, 0.12. Thus, normally capillary endothelium (glomerular and peritubular) appears to have the highest proliferation index in the human kidney by these techniques. These results indicate major variation in the proliferative activity of normal human renal cell populations, along with a significant correlation between PCNA and Ki-67 staining. Furthermore, this study provides normal values for the proliferative activity of different human renal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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Zhang, Xiuguo, Naoki Tanaka, Takero Nakajima, Yuji Kamijo, Frank J. Gonzalez, and Toshifumi Aoyama. "Peroxisome proliferator-activated receptor α-independent peroxisome proliferation." Biochemical and Biophysical Research Communications 346, no. 4 (August 2006): 1307–11. http://dx.doi.org/10.1016/j.bbrc.2006.06.042.
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Collesi, Chiara, Giulia Felician, Ilaria Secco, Maria Ines Gutierrez, Elisa Martelletti, Hashim Ali, Lorena Zentilin, Michael P. Myers, and Mauro Giacca. "Reversible Notch1 acetylation tunes proliferative signalling in cardiomyocytes." Cardiovascular Research 114, no. 1 (November 24, 2017): 103–22. http://dx.doi.org/10.1093/cvr/cvx228.
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Abstract Aims The Notch signalling pathway regulates the balance between proliferation and differentiation in several tissues, including the heart. Our previous work has demonstrated that the proliferative potential of neonatal cardiomyocytes relies on Notch1 activity. A deep investigation on the biochemical regulation of the Notch signalling in cardiomyocytes is the focus of the current research. Methods and results We show that the Notch1 intracellular domain is acetylated in proliferating neonatal rat cardiomyocytes and that acetylation tightly controls the amplitude and duration of Notch signalling. We found that acetylation extends the half-life of the protein, and enhanced its transcriptional activity, therefore counteracting apoptosis and sustaining cardiomyocyte proliferation. Sirt1 acted as a negative modulator of Notch1 signalling; its overexpression in cardiomyocytes reverted Notch acetylation and dampened its stability. A constitutively acetylated fusion protein between Notch1 and the acetyltransferase domain of p300 promoted cardiomyocyte proliferation, which was remarkably sustained over time. Viral vector-mediated expression of this protein enhanced heart regeneration after apical resection in neonatal mice. Conclusion These results identify the reversible acetylation of Notch1 as a novel mechanism to modulate its signalling in the heart and tune the proliferative potential of cardiomyocytes.
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Weerasooriya, Viraine, Michael J. Rennie, Shri Anant, David H. Alpers, Bruce W. Patterson, and Samuel Klein. "Dietary fiber decreases colonic epithelial cell proliferation and protein synthetic rates in human subjects." American Journal of Physiology-Endocrinology and Metabolism 290, no. 6 (June 2006): E1104—E1108. http://dx.doi.org/10.1152/ajpendo.00557.2005.
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Although it has been proposed that high fiber consumption can prevent proliferative diseases of the colon, the clinical data to support this hypothesis have been inconsistent. To provide a more robust measure of the effects of fiber on colonic mucosal growth than previous studies, we evaluated both cell proliferation and colonic mucosal protein synthesis in nine healthy volunteers after they consumed a typical Western diet (<20 g fiber/day) or a Western diet supplemented with wheat bran (24 g/day) in a randomized crossover design. Biopsies taken from the sigmoid colon were used to assess mucosal proliferation by determining proliferating cell nuclear antigen (PCNA) in crypt cells and to assess mucosal protein synthetic rate using stable isotopically labeled leucine infusion. Fiber supplementation produced a 12% decrease in labeling index (%crypt cells stained with PCNA) ( P < 0.001) and an 11% decrease in mucosal protein fractional synthetic rate (FSR; P < 0.05). Moreover, mucosal protein FSR correlated directly with labeling index (r2= 0.22, P < 0.05). These data demonstrate that increased wheat bran consumption decreases colonic mucosal proliferation and support the potential importance of dietary fiber in preventing proliferative diseases of the colon.
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Joseph, Robert. "Proliferation, counter‐proliferation and NATO." Survival 38, no. 1 (March 1996): 111–30. http://dx.doi.org/10.1080/00396339608442834.
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Zhu, Su-Ning, Mian Chen, Jenny Jongstra-Bilen, and Myron I. Cybulsky. "GM-CSF regulates intimal cell proliferation in nascent atherosclerotic lesions." Journal of Experimental Medicine 206, no. 10 (September 14, 2009): 2141–49. http://dx.doi.org/10.1084/jem.20090866.
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The contribution of intimal cell proliferation to the formation of early atherosclerotic lesions is poorly understood. We combined 5-bromo-2′-deoxyuridine pulse labeling with sensitive en face immunoconfocal microscopy analysis, and quantified intimal cell proliferation and Ly-6Chigh monocyte recruitment in low density lipoprotein receptor–null mice. Cell proliferation begins in nascent lesions preferentially at their periphery, and proliferating cells accumulate in lesions over time. Although intimal cell proliferation increases in parallel to monocyte recruitment as lesions grow, proliferation continues when monocyte recruitment is inhibited. The majority of proliferating intimal cells are dendritic cells expressing CD11c and major histocompatibility complex class II and 33D1, but not CD11b. Systemic injection of granulocyte/macrophage colony-stimulating factor (GM-CSF) markedly increased cell proliferation in early lesions, whereas function-blocking anti–GM-CSF antibody inhibited proliferation. These findings establish GM-CSF as a key regulator of intimal cell proliferation in lesions, and demonstrate that both proliferation and monocyte recruitment contribute to the inception of atherosclerosis.
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Wang, Yahui, Conghui Yao, Ethan Stancliffe, Ronald Fowle-Grider, Rencheng Wang, Cheng Wang, Michaela Schwaiger-Haber, Leah P. Shriver, Jason Weber, and Gary J. Patti. "Abstract 3773: Mitochondrial fusion is required to support higher rates of respiration in proliferating cancer cells." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3773. http://dx.doi.org/10.1158/1538-7445.am2022-3773.
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Abstract Proliferating cancer cells exhibit an elevated rate of glucose consumption and lactate excretion, a phenomenon described as the “Warburg effect”. Although increased glycolytic flux in proliferating cells is well established, metabolic changes associated with mitochondria still remain elusive. Here, using various inducible quiescence models and mass spectrometry-based metabolomics, we directly compared mitochondrial respiration and TCA cycle activity from the same cells in the proliferative and quiescent states. We found that mitochondrial respiration and TCA cycle flux is significantly increased during proliferation in both transformed and non-transformed cell lines. This increase was supported by mitochondrial fusion rather than mitochondrial biogenesis. Notably, as cells transitioned from a quiescent state to a proliferative state, the elongation of mitochondria occurred as quickly as 3 hours. Our results reveal that the Warburg effect, which was originally associated with dysfunctional mitochondria, does not necessitate decreased mitochondrial respiration. Rather, in many proliferating cancer cells, mitochondrial respiration is actually elevated, underscoring the importance of mitochondrial respiration during proliferation. Citation Format: Yahui Wang, Conghui Yao, Ethan Stancliffe, Ronald Fowle-Grider, Rencheng Wang, Cheng Wang, Michaela Schwaiger-Haber, Leah P. Shriver, Jason Weber, Gary J. Patti. Mitochondrial fusion is required to support higher rates of respiration in proliferating cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3773.
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Tsunoda, Mikiya, Hiroyasu Aoki, Munetomo Takahashi, Haruka Shimizu, Haru Ogiwara, Shigeyuki Shichino, Kouji Matsushima, and Satoshi Ueha. "Abstract 5180: T cell receptor repertoire analysis revealed tissue tropism of tumor-reactive T-cell clones in cell cycle reporter mice." Cancer Research 83, no. 7_Supplement (April 4, 2023): 5180. http://dx.doi.org/10.1158/1538-7445.am2023-5180.
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Abstract Tumor-reactive T cells are composed of clones with various TCRs, and each clone has different in vivo kinetics. By analyzing TCR repertoire of tumor and tumor-draining lymph node (dLN), we have demonstrated that Tumor-reactive CD8+ T cells can be classified into “dLN Major”, “Tumor Major”, and “Double Major” clones, which exhibited high frequency in the dLN, tumor, or both tissues. To investigate whether this classification was related to the tissue tropism in the proliferation of each clone, we here employed tumor-bearing Fucci transgenic mice expressing a fluorescent cell-cycle indicator to identify the proliferation of T-cell clones in each tissue. We purified proliferating- and resting-CD8+ T cells from the tumors and dLN and analyzed their TCR repertoire in an LLC subcutaneous tumor model. All Tumor Major clones were proliferated in the tumor, while nearly 0% for dLN Major, indicated their different proliferative capacity in the tumor. The percentage of proliferating clones in the dLN was 20% for Tumor Major and 15% for dLN Major, indicating that these clones had equivalent proliferative capacity in the dLN. These proliferating dLN major clones overlapped more with the tumor than the non-proliferating dLN major clones, suggesting that proliferating dLN Major clones had higher tumor migration capacity. Furthermore, these proliferating dLN major clones were more proliferative in the tumor. These results suggested that dLN Major responded to antigen presentation in the dLN but not in the tumor, whereas Tumor Major responded to those in the dLN and tumor. In addition, there are two types of dLN major, “clones that are proliferating in dLN” and “clones that are not proliferating in dLN” indicating that the former may contribute to the anti-tumor response. Immune checkpoint inhibitor (ICI) treatment not only reactivates clones in the tumor but also activates tumor-reactive clones in the dLN. In conformity with these previous studies, the percentage of proliferating clones among dLN Major increased to about 50% and 80% in the dLN in mice with anti-PD-L1 and anti-CD4 treatment, respectively. This result suggests ICI treatment enhances anti-tumor responses mainly by promoting the activation and proliferation of dLN Major clones. This study shows new findings that tumor-reactive T cells differ in the tissue tropism of their proliferation of each clone. In the future, a quantitative understanding of the contribution of each class of clones to the anti-tumor response will hopefully lead to the development of new combined immunotherapies that optimize the anti-tumor T-cell response. Citation Format: Mikiya Tsunoda, Hiroyasu Aoki, Munetomo Takahashi, Haruka Shimizu, Haru Ogiwara, Shigeyuki Shichino, Kouji Matsushima, Satoshi Ueha. T cell receptor repertoire analysis revealed tissue tropism of tumor-reactive T-cell clones in cell cycle reporter mice. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5180.
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Abrisqueta, Pau, Neus Villamor, Ana Muntañola, Carles Codony, Mireia Camós, Eva Calpe, Maria Joao Baptista, et al. "Biological Analysis and Prognostic Significance of Proliferative Cellular Compartment in Chronic Lymphocytic Leukemia (CLL)." Blood 114, no. 22 (November 20, 2009): 667. http://dx.doi.org/10.1182/blood.v114.22.667.667.
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Abstract Abstract 667 Historically CLL has been considered a non-proliferative disease characterized by accumulation of leukemic cells. However, recent clinical and biological observations are questioning this concept. From the clinical standpoint, although some patients have lymphocyte counts stable during the course of the disease, others exhibit a short lymphocyte doubling time, suggesting the existence of a significant cell proliferation. Some specific anatomic locations (bone marrow (BM) and lymph nodes) seem to be more prone to proliferation than peripheral blood (PB). The amount of cell proliferation and its prognostic significance has not been properly analyzed. Against this background, gene expression profiling of proliferation genes and the amount of cell proliferation in different tissue compartments (BM and PB) were examined in patients with CLL. In isolated CD19/CD5+ tumoral cells from 20 paired PB and BM samples, expression of genes (n=93) involved in the initiation and development of the cell cycle was analyzed by low-density TaqMan® arrays. The amount of proliferative (Ki67 positive) CLL cells was measured by flow cytometry in 50 paired samples. In addition, coexpression of molecules associated with cellular activation (CD38, CD71, CD69), adhesion (CD49d), chemokine receptors (CXCR4, CXCR3, CCR7), interaction between T and B cells (CD86), signaling (ZAP-70), and Toll-like receptors (TLR9) was compared between Ki67+ and Ki67- CLL subpopulations. Finally, the degree of proliferation was correlated with the main clinical and biological characteristics. As assessed by gene expression profile, the great majority of genes involved in the initiation and development of cell cycle were more expressed in BM than in PB. Of note, Ki67+ CLL cells were significantly higher in BM than in PB (mean: 1.13% vs 0.88%; p= 0.004). This difference on Ki67+ expression between BM and PB was particularly significant (mean: 1.6% vs 1.1%; p=0.01) in patients who progressed of their disease at any particularly time (n=20), whereas it was not observed in patients with stable disease. Proliferating (Ki67+) CLL cells had significantly increased expression of ZAP-70 (mean fluorescence intensity (MFI): 162 vs 94, p<0.001), CD38 (MFI: 75 vs 27, p<0.001), CD86 (MFI: 31 vs 11, p=0.002), CD71 (MFI: 73 vs 24, p<0.001), and TLR9 (MFI: 49 vs 25, p<0.001) in comparison to non-proliferating Ki67- cells; CXCR4 was significantly decreased in proliferating cells (MFI: 212 vs 340, p=0.006). No differences were observed in CD49d, CD69, CCR7, and CXCR3 expression between Ki67+ and Ki67- CLL cells. When Ki67 expression was analyzed at diagnosis (n=41 paired samples, median follow-up of 4.2 years), patients with Ki67+ CLL cells ≥ 1% in BM had a shorter time to progression than those with Ki67 <1% (progression at 4 years: 47% vs 12%, respectively; p=0.008) (figure). In addition, patients with lymphocyte doubling time < 12 months, ZAP-70 expression ≥ 20%, or CD38 expression ≥ 30%, but not with increased CD49d expression, exhibit a higher percentage of Ki67+ CLL cells in both BM and PB (Table). In conclusion, in CLL expression of genes related to proliferation was significantly increased in BM compared to PB. Moreover, the number of proliferating CLL cells was also increased in BM, particularly in those patients with an aggressive disease, and presented different immunophenotype characteristics in comparison to non-proliferating CLL cells. Finally, the amount of Ki67+ CLL cells correlated with a shorter time to progression. These results challenge the concept of CLL as disease more accumulative than proliferative. These new insights on the proliferation pathways in CLL not only may provide a better understanding of the pathogenesis of this disease, but also would be of prognostic relevance and can support the use of new treatments aimed at inhibiting proliferation in CLL. Lymphocyte doubling timeZAP-70CD38CD49d<12 months (n=10)>12 months (n=37)≥20% (n=15)<20% (n=35)≥30% (n=19)<30% (n=31)≥30% (n=17)<30% (n=32)Mean% Ki67+ CLL cells in PB1.20.7P=0.021.40.6P<0.0011.10.7P=0.0151.10.8P=0.08Mean% Ki67+ CLL cells in BM1.60.8P=0.03220.8P=0.0011.31P=0.191.50.9P=0.053 Disclosures: No relevant conflicts of interest to declare.
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Green, S. E., P. Chapman, J. Burn, A. D. Burt, M. Bennett, D. R. Appleton, J. S. Varma, and J. C. Mathers. "Colonic epithelial cell proliferation in hereditary non-polyposis colorectal cancer." Gut 43, no. 1 (July 1, 1998): 85–92. http://dx.doi.org/10.1136/gut.43.1.85.
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Background—Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa.Aims—To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC.Patients—Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls.Methods—Crypt cell proliferation was measured at five sites in the colon using two different techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed.Results—There were no significant differences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant differences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers.Conclusion—Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC.
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Yoshimura, A., K. Inui, T. Nemoto, S. Uda, Y. Sugenoya, S. Watanabe, N. Yokota, T. Taira, S. Iwasaki, and T. Ideura. "Simvastatin suppresses glomerular cell proliferation and macrophage infiltration in rats with mesangial proliferative nephritis." Journal of the American Society of Nephrology 9, no. 11 (November 1998): 2027–39. http://dx.doi.org/10.1681/asn.v9112027.
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Inhibition of 3-hydro-3-methylglutaryl coenzyme A reductase inhibits the production of mevalonate and has been shown to suppress proliferation in many cell types. Therefore, 3-hydro-3-methylglutaryl coenzyme A reductase inhibitors may have a beneficial effect in glomerular disease, because glomerular cell proliferation is a central feature in the active glomerular injury. This study examines the effect of simvastatin on glomerular pathology in a rat mesangial proliferative glomerulonephritis (GN) induced by anti-thymocyte antibody (anti-Thy 1.1 GN). There was no difference in the degree of the antibody and complement-mediated initial injuries between simvastatin-treated and control GN rats. The most pronounced feature of simvastatin-treated GN was the suppression of the early glomerular cell proliferation. The proliferative activity was maximal at day 4 after disease induction (26.5+/-7.0 of proliferating cell nuclear antigen-positive cells/glomerulus); however, approximately 70% of proliferation was suppressed by simvastatin treatment. At day 4 after disease induction, simvastatin administration also decreased alpha-smooth muscle actin expression in the glomerulus, which is a marker for mesangial cell activation. Inhibition of monocyte/macrophage recruitment into glomeruli by simvastatin was also a prominent feature. There was a 30% decrease in the number of glomerular ED-1+ cells by simvastatin treatment at day 2 after disease induction. Furthermore, simvastatin remarkably suppressed subsequent mesangial matrix expansion and type IV collagen accumulation in glomeruli. We also found that the platelet-derived growth factor expression was reduced in simvastatin-treated nephritic rats, which might simply reflect the reduction in mesangial cell proliferation and mesangial cellularity. There was no significant difference in plasma cholesterol or triglyceride levels between simvastatin- and vehicle-treated nephritic rats at day 2 and day 4, which corresponded to the times when simvastatin treatment resulted in a reduction in mesangial cell proliferation. In conclusion, this is the first report to find that mesangial cell proliferation and matrix expansion have been blocked by simvastatin in vivo. The protective effect of simvastatin in the matrix expansion in anti-Thy1.1 GN was partly by inhibition of mesangial cell proliferation and monocyte/ macrophage recruitment into glomeruli, which were independent of a change in circulating lipids.
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Selzman, Craig H., Stephanie A. Miller, Michael A. Zimmerman, Fabia Gamboni-Robertson, Alden H. Harken, and Anirban Banerjee. "Monocyte chemotactic protein-1 directly induces human vascular smooth muscle proliferation." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (October 1, 2002): H1455—H1461. http://dx.doi.org/10.1152/ajpheart.00188.2002.
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Although monocyte chemotactic protein-1 (MCP-1) is best known for its ability to recruit mononuclear cells, few studies have examined the effects of this chemokine on other events in the vascular response to injury. The purpose of the present study was to determine the influence of MCP-1 on human vascular smooth muscle (VSMC) proliferation. MCP-1 induced concentration-dependent VSMC proliferation as measured by bromodeoxyuridine (BrdU) uptake. Direct cell counting demonstrated a twofold increase in VSMC after stimulation with MCP-1. This mitogenic effect was similar to that observed with the prototypical atherogenic cytokine platelet-derived growth factor. Immunohistochemistry and Western blot analysis revealed that MCP-1 increased both proliferating nuclear cell antigen and cyclin A expression. Whereas MCP-1 did not promote nuclear factor-κB activation, MCP-1-induced VSMC proliferation appeared to be dependent on phosphotidylinositol 3-kinase activation. In conclusion, MCP-1 directly induces VSMC growth, which is associated with activation of cell cycle proteins and intracellular proliferative signals. Within the inflammatory paradigm of vascular remodeling, these data suggest that MCP-1 is more than simply a chemokine but also a potent mitogen for VSMC proliferation.
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Jiang, Zhisheng, Serena F. Generoso, Marta Badia, Bernhard Payer, and Lucas B. Carey. "A conserved expression signature predicts growth rate and reveals cell & lineage-specific differences." PLOS Computational Biology 17, no. 11 (November 11, 2021): e1009582. http://dx.doi.org/10.1371/journal.pcbi.1009582.
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Isogenic cells cultured together show heterogeneity in their proliferation rate. To determine the differences between fast and slow-proliferating cells, we developed a method to sort cells by proliferation rate, and performed RNA-seq on slow and fast proliferating subpopulations of pluripotent mouse embryonic stem cells (mESCs) and mouse fibroblasts. We found that slowly proliferating mESCs have a more naïve pluripotent character. We identified an evolutionarily conserved proliferation-correlated transcriptomic signature that is common to all eukaryotes: fast cells have higher expression of genes for protein synthesis and protein degradation. This signature accurately predicted growth rate in yeast and cancer cells, and identified lineage-specific proliferation dynamics during development, using C. elegans scRNA-seq data. In contrast, sorting by mitochondria membrane potential revealed a highly cell-type specific mitochondria-state related transcriptome. mESCs with hyperpolarized mitochondria are fast proliferating, while the opposite is true for fibroblasts. The mitochondrial electron transport chain inhibitor antimycin affected slow and fast subpopulations differently. While a major transcriptional-signature associated with cell-to-cell heterogeneity in proliferation is conserved, the metabolic and energetic dependency of cell proliferation is cell-type specific.
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Quan, Yadan, Xinchun Zhang, Siying Xu, Kang Li, Feng Zhu, Qian Li, Xianxian Cai, and Rong Lu. "Tcf7l2 localization of putative stem/progenitor cells in mouse conjunctiva." American Journal of Physiology-Cell Physiology 311, no. 2 (August 1, 2016): C246—C254. http://dx.doi.org/10.1152/ajpcell.00014.2016.
Full textAbstract:
Conjunctival integrity and preservation is indispensable for vision. The self-renewing capacity of conjunctival cells controls conjunctival homeostasis and regeneration; however, the source of conjunctival self-renewal and the underlying mechanism is currently unclear. Here, we characterize the biochemical phenotype and proliferative potential of conjunctival epithelial cells in adult mouse by detecting proliferation-related signatures and conducting clonal analysis. Further, we show that transcription factor 7-like 2 (T-cell-specific transcription factor 4), a DNA binding protein expressed in multiple types of adult stem cells, is highly correlated with proliferative signatures in basal conjunctival epithelia. Clonal studies demonstrated that Transcription factor 7-like 2 (Tcf7l2) was coexpressed with p63α and proliferating cell nuclear antigen (PCNA) in propagative colonies. Furthermore, Tcf7l2 was actively transcribed concurrently with conjunctival epithelial proliferation in vitro. Collectively, we suggest that Tcf7l2 may be involved in maintenance of stem/progenitor cells properties of conjunctival epithelial stem/progenitor cells, and with the fornix as the optimal site to isolate highly proliferative conjunctival epithelial cells in adult mice.
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Stoeber, Kai, Thea D. Tlsty, Lisa Happerfield, Geraldine A. Thomas, Sergei Romanov, Lynda Bobrow, E. Dillwyn Williams, and Gareth H. Williams. "DNA replication licensing and human cell proliferation." Journal of Cell Science 114, no. 11 (June 1, 2001): 2027–41. http://dx.doi.org/10.1242/jcs.114.11.2027.
Full textAbstract:
The convergence point of growth regulatory pathways that control cell proliferation is the initiation of genome replication, the core of which is the assembly of pre-replicative complexes resulting in chromatin being ‘licensed’ for DNA replication in the subsequent S phase. We have analysed regulation of the pre-replicative complex proteins ORC, Cdc6, and MCM in cycling and non-proliferating quiescent, differentiated and replicative senescent human cells. Moreover, a human cell-free DNA replication system has been exploited to study the replicative capacity of nuclei and cytosolic extracts prepared from these cells. These studies demonstrate that downregulation of the Cdc6 and MCM constituents of the replication initiation pathway is a common downstream mechanism for loss of proliferative capacity in human cells. Furthermore, analysis of MCM protein expression in self-renewing, stable and permanent human tissues shows that the three classes of tissue have developed very different growth control strategies with respect to replication licensing. Notably, in breast tissue we found striking differences between the proportion of mammary acinar cells that express MCM proteins and those labelled with conventional proliferation markers, raising the intriguing possibility that progenitor cells of some tissues are held in a prolonged G1 phase or ‘in-cycle arrest’. We conclude that biomarkers for replication-licensed cells detect, in addition to actively proliferating cells, cells with growth potential, a concept that has major implications for developmental and cancer biology.
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Scoggins, Charles R., Ingrid M. Meszoely, Michihiko Wada, Anna L. Means, Liying Yang, and Steven D. Leach. "p53-Dependent acinar cell apoptosis triggers epithelial proliferation in duct-ligated murine pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 4 (October 1, 2000): G827—G836. http://dx.doi.org/10.1152/ajpgi.2000.279.4.g827.
Full textAbstract:
The mechanisms linking acinar cell apoptosis and ductal epithelial proliferation remain unknown. To determine the relationship between these events, pancreatic duct ligation (PDL) was performed on p53(+/+) and p53(−/−) mice. In mice bearing a wild-type p53 allele, PDL resulted in upregulation of p53 protein in both acinar cells and proliferating duct-like epithelium. In contrast, upregulation of Bcl-2 occurred only in duct-like epithelium. Both p21WAF1/CIP1 and Bax were also upregulated in duct-ligated lobes. After PDL in p53(+/+) mice, acinar cells underwent widespread apoptosis, while duct-like epithelium underwent proliferative expansion. In the absence of p53, upregulation of p53 target genes and acinar cell apoptosis did not occur. The absence of acinar cell apoptosis in p53(−/−) mice also eliminated the proliferative response to duct ligation. These data demonstrate that PDL-induced acinar cell apoptosis is a p53-dependent event and suggest a direct link between acinar cell apoptosis and proliferation of duct-like epithelium in duct-ligated pancreas.
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Yao, Guang. "Modelling mammalian cellular quiescence." Interface Focus 4, no. 3 (June 6, 2014): 20130074. http://dx.doi.org/10.1098/rsfs.2013.0074.
Full textAbstract:
Cellular quiescence is a reversible non-proliferating state. The reactivation of ‘sleep-like’ quiescent cells (e.g. fibroblasts, lymphocytes and stem cells) into proliferation is crucial for tissue repair and regeneration and a key to the growth, development and health of higher multicellular organisms, such as mammals. Quiescence has been a primarily phenotypic description (i.e. non-permanent cell cycle arrest) and poorly studied. However, contrary to the earlier thinking that quiescence is simply a passive and dormant state lacking proliferating activities, recent studies have revealed that cellular quiescence is actively maintained in the cell and that it corresponds to a collection of heterogeneous states. Recent modelling and experimental work have suggested that an Rb-E2F bistable switch plays a pivotal role in controlling the quiescence–proliferation balance and the heterogeneous quiescent states. Other quiescence regulatory activities may crosstalk with and impinge upon the Rb-E2F bistable switch, forming a gene network that controls the cells’ quiescent states and their dynamic transitions to proliferation in response to noisy environmental signals. Elucidating the dynamic control mechanisms underlying quiescence may lead to novel therapeutic strategies that re-establish normal quiescent states, in a variety of hyper- and hypo-proliferative diseases, including cancer and ageing.
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Hultsch, T., R. Martin, and R. J. Hohman. "The effect of the immunophilin ligands rapamycin and FK506 on proliferation of mast cells and other hematopoietic cell lines." Molecular Biology of the Cell 3, no. 9 (September 1992): 981–87. http://dx.doi.org/10.1091/mbc.3.9.981.
Full textAbstract:
The immunosuppressive drugs FK506 and cyclosporin A have an identical spectrum of activities with respect to IgE receptor (Fc epsilon RI)-mediated exocytosis from mast cells and T cell receptor-mediated transcription of IL-2. These findings suggest a common step in receptor-mediated signal transduction leading to exocytosis and transcription and imply that immunosuppressive drugs target specific signal transduction pathways, rather than specific cell types. This hypothesis is supported by studies on the effect of rapamycin on IL-3 dependent proliferation of the rodent mast cell line PT18. Rapamycin inhibits proliferation of PT18 cells, achieving a plateau of 80% inhibition at 1 nM. This inhibition is prevented in a competitive manner by FK506, a structural analogue of rapamycin. Proliferation of rat basophilic leukemia cells and WEHI-3 cells was also inhibited, at doses comparable to those shown previously to inhibit IL-2-dependent proliferation of cytotoxic T lymphocyte line (CTLL) cells. In contrast, proliferation of A-431 cells, a epidermoid cell line, was not affected by rapamycin. DNA histograms indicate that complexes formed between the rapamycin-FK506-binding protein (FKBP) and rapamycin arrest-proliferating PT18 cells in the G0/G1-phase. It is concluded that FKBP-rapamycin complexes may inhibit proliferative signals emanating from IL-3 receptors, resulting in growth arrest of cytokine-dependent, hematopoietic cells.
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Aiken, S. G., L. P. Lefkovitch, S. J. Darbyshire, and K. C. Armstrong. "Vegetative proliferation in inflorescences of red fescue (Festuca rubra s.l, Poaceae)." Canadian Journal of Botany 66, no. 1 (January 1, 1988): 1–10. http://dx.doi.org/10.1139/b88-001.
Full textAbstract:
A continuous range of variation in vegetative proliferation among members of the red fescue complex is documented in (ii) the number of spikelets proliferating in the inflorescence, (ii) the position where initiation of proliferation occurs, (iii) the rachilla, where abnormal elongation may result in internodes 3–10 mm long, and (iv) the position of proliferation, which may be either lateral or terminal on the rachilla. Both facultative and obligatory vegetative proliferation occur. Recorded chromosome counts of 2n = 49, 50, 63, and 70; low pollen stainability; absence of seed; and occurrence of proliferation in spikelets of known hybrids suggest that at least some specimens are the products of hybridization. In North America, the name Festuca prolifera has been applied to vegetatively proliferating specimens of F. richardsonii, F. rubra s.l,, and some specimens that may be hybrids. Although proliferating spikelets are conspicuous, they do not justify taxonomic rank.
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Emerson, S. G., and J. H. Antin. "Bone marrow progenitor cells induce a regulatory autologous proliferative T lymphocyte response." Journal of Immunology 142, no. 3 (February 1, 1989): 766–72. http://dx.doi.org/10.4049/jimmunol.142.3.766.
Full textAbstract:
Abstract The proliferative response of human T lymphocytes to autologous bone marrow progenitor cells was studied by in vitro coculture in autologous serum. Irradiated enriched bone marrow progenitor cells induced the proliferation of cocultured peripheral blood T cells, with maximal proliferation at 8 days and stimulator:proliferator ratios of 1/1. This autologous proliferative T lymphocyte response was completely abrogated by the inclusion of anti-HLA-DR, anti-CD2, or anti LFA-3 antibodies into the coculture, and partially inhibited by anti-CD4. Repetitive stimulation with autologous progenitors at days 14 and 28 expanded and further enriched the autoreactive T cells, which proliferated specifically in the presence of autologous progenitors. When incubated for 12 h with bone marrow before short term hematopoietic culture, these autoreactive T cells inhibited hematopoiesis 60 to 100%. These data indicate that a subset of T lymphocytes recognize proliferating hematopoietic progenitors and regulate the growth and differentiation of normal bone marrow cells.
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Molochkova, Yu V., A. N. Khlebnikova, V. A. Molochkov, L. E. Gurevich, and A. V. Molochkov. "Comparative study of Ki67 protein expression in oral lichen planus and leukoplakia." Vestnik dermatologii i venerologii 94, no. 4 (December 7, 2018): 15–20. http://dx.doi.org/10.25208/0042-4609-2018-94-4-15-20.
Full textAbstract:
Oral lichen planus (OLP) is included in the category of potentially malignant diseases. Benign processes are differentiated from malignant ones by the nature of cell proliferative activity. The aim of the present study was the comparative study of proliferative activity in OLP and leuk oplakia cells, as well as the cells of oral squamous cell carcinoma.Materials and methods. Biopsy specimens from 16 patients with OPL, 13 with leukoplakia, and 7 with oral squamous cell carcinoma were investigated. Immunohistochemical studies were performed using Ki67 monoclonal antibodies.Results. The average Ki67 index in OPL cells was 9.3 ± 2.3 %. Proliferating cells were located exclusively in the basal epidermis layer. In leukoplakia cells, the average Ki67 index was 20.5 ± 6.1 %; the proliferating cells were located in the basal layer and lower parts of the spinous (suprabasal) layer of the epidermis. In squamous cell carcinoma, the average Ki67 index was 57.4 ± 2.04 %. Proliferating cells were located diffusely over all cell complexes from the lower to the highest layers of the epidermis. Differences in the proliferation level were significant for the leukoplakia/OPL pair (p = 0.003) and squamous cell carcinoma/OPL pair (p < 0.001), while for squamous cell carcinoma/leukoplakia pair the difference was not significant (p = 0.211).Conclusion. The differences in the proliferation level and in the nature of the proliferating cell distributionin through the epidermis can be applied in the differential diagnosis of OPL and leuk oplakia.