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Journal articles on the topic 'Cellular Proliferation'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Yao, Guang. "Modelling mammalian cellular quiescence." Interface Focus 4, no. 3 (June 6, 2014): 20130074. http://dx.doi.org/10.1098/rsfs.2013.0074.

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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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2

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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3

Zhang, Jian Chun, Howard E. Savage, Peter G. Sacks, Thomas Delohery, R. R. Alfano, A. Katz, and Stimson P. Schantz. "Innate cellular fluorescence reflects alterations in cellular proliferation." Lasers in Surgery and Medicine 20, no. 3 (1997): 319–31. http://dx.doi.org/10.1002/(sici)1096-9101(1997)20:3<319::aid-lsm11>3.0.co;2-8.

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4

CLARKE, CHRISTINE L., and ROBERT L. SUTHERLAND. "Progestin Regulation of Cellular Proliferation*." Endocrine Reviews 11, no. 2 (May 1990): 266–301. http://dx.doi.org/10.1210/edrv-11-2-266.

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5

Lenkala, Divya, Eric R. Gamazon, Bonnie LaCroix, Hae Kyung Im, and R. Stephanie Huang. "MicroRNA biogenesis and cellular proliferation." Translational Research 166, no. 2 (August 2015): 145–51. http://dx.doi.org/10.1016/j.trsl.2015.01.012.

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6

Mankoff, David A., Anthony F. Shields, and Kenneth A. Krohn. "PET imaging of cellular proliferation." Radiologic Clinics of North America 43, no. 1 (January 2005): 153–67. http://dx.doi.org/10.1016/j.rcl.2004.09.005.

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7

VINCENT, P. C. "Leukemic Cellular Proliferation: A Perspective." Annals of the New York Academy of Sciences 459, no. 1 Hematopoietic (December 1985): 308–27. http://dx.doi.org/10.1111/j.1749-6632.1985.tb20839.x.

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8

Zlotorynski, Eitan, and Reuven Agami. "A PASport to Cellular Proliferation." Cell 134, no. 2 (July 2008): 208–10. http://dx.doi.org/10.1016/j.cell.2008.07.003.

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9

Verdoorn, Cornelis. "Cellular Migration, Proliferation, and Contraction." Archives of Ophthalmology 104, no. 8 (August 1, 1986): 1216. http://dx.doi.org/10.1001/archopht.1986.01050200122064.

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10

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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11

Virgilio, Maria C., and Kathleen L. Collins. "The Impact of Cellular Proliferation on the HIV-1 Reservoir." Viruses 12, no. 2 (January 21, 2020): 127. http://dx.doi.org/10.3390/v12020127.

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Human immunodeficiency virus (HIV) is a chronic infection that destroys the immune system in infected individuals. Although antiretroviral therapy is effective at preventing infection of new cells, it is not curative. The inability to clear infection is due to the presence of a rare, but long-lasting latent cellular reservoir. These cells harboring silent integrated proviral genomes have the potential to become activated at any moment, making therapy necessary for life. Latently-infected cells can also proliferate and expand the viral reservoir through several methods including homeostatic proliferation and differentiation. The chromosomal location of HIV proviruses within cells influences the survival and proliferative potential of host cells. Proliferating, latently-infected cells can harbor proviruses that are both replication-competent and defective. Replication-competent proviral genomes contribute to viral rebound in an infected individual. The majority of available techniques can only assess the integration site or the proviral genome, but not both, preventing reliable evaluation of HIV reservoirs.

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12

Yang, Chung-May, Karl R. Olsen, Eleut Hernandez, and Scott W. Cousins. "Measurement of cellular proliferation within the vitreous during experimental proliferative vitreoretinopathy." Graefe's Archive for Clinical and Experimental Ophthalmology 230, no. 1 (January 1992): 66–71. http://dx.doi.org/10.1007/bf00166765.

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13

Lopez-Rodriguez, Maria, Alma Viso, Silvia Ortega-Gutierrez, and Ines Diaz-Laviadac. "Involvement of Cannabinoids in Cellular Proliferation." Mini-Reviews in Medicinal Chemistry 5, no. 1 (January 1, 2005): 97–106. http://dx.doi.org/10.2174/1389557053402819.

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14

Radhika, M., Mary Babu, and P. K. Sehgal. "Cellular proliferation on desamidated collagen matrices." Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology 124, no. 2 (October 1999): 131–39. http://dx.doi.org/10.1016/s0742-8413(99)00042-0.

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15

Castro⁎, J. P., and H. Almeida. "Actin carbonylated aggregates impair cellular proliferation." Free Radical Biology and Medicine 53 (September 2012): S207—S208. http://dx.doi.org/10.1016/j.freeradbiomed.2012.08.435.

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16

IIJIMA, MISA. "CELLULAR DIFFERENTIATION AND PROLIFERATION IN MEDULLOBLASTOMA." KITAKANTO Medical Journal 46, no. 6 (1996): 471–82. http://dx.doi.org/10.2974/kmj1951.46.471.

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17

Guiotto, Paolo. "A Statistical Model for Cellular Proliferation." Stochastic Analysis and Applications 21, no. 6 (January 11, 2003): 1283–303. http://dx.doi.org/10.1081/sap-120026107.

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18

Brasitus, T. A. "Calcium, cellular proliferation, and colon cancer." Gastroenterology 93, no. 3 (September 1987): 654–55. http://dx.doi.org/10.1016/0016-5085(87)90932-2.

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19

McDowell, Kristy L., Lesa A. Begley, Nirit Mor-Vaknin, David M. Markovitz, and Jill A. Macoska. "Leukocytic promotion of prostate cellular proliferation." Prostate 70, no. 4 (October 28, 2009): 377–89. http://dx.doi.org/10.1002/pros.21071.

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20

Jacobs, Jacqueline J. L., and Maarten van Lohuizen. "Polycomb repression: from cellular memory to cellular proliferation and cancer." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1602, no. 2 (June 2002): 151–61. http://dx.doi.org/10.1016/s0304-419x(02)00052-5.

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21

Saha, Naresh, Ashutosh K. Dubey, and Bikramjit Basu. "Cellular proliferation, cellular viability, and biocompatibility of HA-ZnO composites." Journal of Biomedical Materials Research Part B: Applied Biomaterials 100B, no. 1 (November 21, 2011): 256–64. http://dx.doi.org/10.1002/jbm.b.31948.

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22

Chevalier, Robert L., Barbara A. Thornhill, and Jennifer T. Wolstenholme. "Renal cellular response to ureteral obstruction: role of maturation and angiotensin II." American Journal of Physiology-Renal Physiology 277, no. 1 (July 1, 1999): F41—F47. http://dx.doi.org/10.1152/ajprenal.1999.277.1.f41.

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Renal angiotensin II (ANG II) is increased as a result of unilateral ureteral obstruction (UUO), and angiotensin AT2 receptors predominate over AT1 receptors in the early postnatal period. To examine the renal cellular response to 3-day UUO in the neonatal and adult rat, AT1and AT2 receptors were inhibited by losartan and PD-123319, respectively. Additional rats received exogenous ANG II, 0.5 mg ⋅ kg−1 ⋅ day−1. Renal cellular proliferation and apoptosis were quantitated by proliferating cell nuclear antigen and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling technique, respectively. In the neonate, UUO reduced proliferation and increased tubular apoptosis. Losartan had no detectable cellular effect, whereas PD-123319 increased cellular proliferation and suppressed apoptosis, and exogenous ANG II stimulated apoptosis. In the adult, UUO increased cellular proliferation as well as apoptosis, whereas losartan, PD-123319, and exogenous ANG II did not alter the cellular response. In conclusion, UUO impairs renal growth in the neonate by reducing proliferation and stimulating apoptosis, at least in part through angiotensin AT2 receptors. UUO stimulates both renal cellular proliferation and apoptosis in the adult, but these effects are independent of ANG II. We speculate that the unique early responses of the developing kidney to urinary tract obstruction are mediated by a highly activated renin-angiotensin system and preponderance of AT2 receptors.

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23

Chan, Jenq-Shyong, Yang Wang, Virgilius Cornea, Prabir Roy-Chaudhury, and Begoña Campos. "Early Adventitial Activation and Proliferation in a Mouse Model of Arteriovenous Stenosis: Opportunities for Intervention." International Journal of Molecular Sciences 22, no. 22 (November 13, 2021): 12285. http://dx.doi.org/10.3390/ijms222212285.

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Background: Arteriovenous fistula (AVF) stenosis remains an important cause of AVF maturation failure, for which there are currently no effective therapies. We examined the pattern and phenotype of cellular proliferation at different timepoints in a mouse model characterized by a peri-anastomotic AVF stenosis. Methods: Standard immunohistochemical analyses for cellular proliferation and macrophage infiltration were performed at 2, 7 and 14 d on our validated mouse model of AVF stenosis to study the temporal profile, geographical location and cellular phenotype of proliferating and infiltrating cells in this model. Results: Adventitial proliferation and macrophage infiltration (into the adventitia) began at 2 d, peaked at 7 d and then declined over time. Surprisingly, there was minimal macrophage infiltration or proliferation in the neointimal region at either 7 or 14 d, although endothelial cell proliferation increased rapidly between 2 d and 7 d, and peaked at 14 d. Conclusions: Early and rapid macrophage infiltration and cellular proliferation within the adventitia could play an important role in the downstream pathways of both neointimal hyperplasia and inward or outward remodelling.

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24

Aw, Tak Yee. "Cellular Redox: A Modulator of Intestinal Epithelial Cell Proliferation." Physiology 18, no. 5 (October 2003): 201–4. http://dx.doi.org/10.1152/nips.01448.2003.

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Mucosal proliferation, together with differentiation and apoptosis, are a continuous homeostatic process in the intestinal epithelium. The glutathione/glutathione disulfide redox status plays a key role in intestinal growth control wherein a reduced redox potential maintains a proliferative state. An oxidative shift in this potential elicits growth arrest and cell transition to a differentiated or apoptotic phenotype.

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25

Boerner, Brian P., Nicholas M. George, Natalie M. Targy, and Nora E. Sarvetnick. "TGF-β Superfamily Member Nodal Stimulates Human β-Cell Proliferation While Maintaining Cellular Viability." Endocrinology 154, no. 11 (November 1, 2013): 4099–112. http://dx.doi.org/10.1210/en.2013-1197.

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In an effort to expand human islets and enhance allogeneic islet transplant for the treatment of type 1 diabetes, identifying signaling pathways that stimulate human β-cell proliferation is paramount. TGF-β superfamily members, in particular activin-A, are likely involved in islet development and may contribute to β-cell proliferation. Nodal, another TGF-β member, is present in both embryonic and adult rodent islets. Nodal, along with its coreceptor, Cripto, are pro-proliferative factors in certain cell types. Although Nodal stimulates apoptosis of rat insulinoma cells (INS-1), Nodal and Cripto signaling have not been studied in the context of human islets. The current study investigated the effects of Nodal and Cripto on human β-cell proliferation, differentiation, and viability. In the human pancreas and isolated human islets, we observed Nodal mRNA and protein expression, with protein expression observed in β and α-cells. Cripto expression was absent from human islets. Furthermore, in cultured human islets, exogenous Nodal stimulated modest β-cell proliferation and inhibited α-cell proliferation with no effect on cellular viability, apoptosis, or differentiation. Nodal stimulated the phosphorylation of mothers against decapentaplegic (SMAD)-2, with no effect on AKT or MAPK signaling, suggesting phosphorylated SMAD signaling was involved in β-cell proliferation. Cripto had no effect on human islet cell proliferation, differentiation, or viability. In conclusion, Nodal stimulates human β-cell proliferation while maintaining cellular viability. Nodal signaling warrants further exploration to better understand and enhance human β-cell proliferative capacity.

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26

Gao, Y., U. Simanainen, and D. J. Handelsman. "138. REGION- AND TIME-DEPENDENT CHANGES IN STRUCTURE AND CELLULAR TURNOVER IN ANDROGEN DEPRIVED MOUSE EPIDIDYMIS." Reproduction, Fertility and Development 21, no. 9 (2009): 57. http://dx.doi.org/10.1071/srb09abs138.

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Epididymal maturation of spermatozoa including acquisition of motility and fertilizing ability depends on androgens both directly from testis and indirectly via the circulation. Androgen action via androgen receptor (AR) can cause both proliferative and anti-proliferative effects (1,2) so we have analysed changes in mouse epididymis following androgen deprivation either by orchidectomy or in prostate epithelial AR knockout (PEARKO) males with reduced androgen action also in epididymis (3). Structural changes (stereology), proliferation (PCNA) and apoptosis (TUNEL) were compared between mature intact males, orchidectomized males 3 day (3d) or 3 weeks (3w) after castration and PEARKO males (3) in the caput and cauda epididymis regions. In caput, epithelial volume decreased while stroma increased in castrates but not in PEARKO whereas lumen volume decreased only after 3 weeks of castration. Proliferating cells (per 100 tubules) were significantly increased 2.8-fold in PEARKO and 6.6-fold in 3d castrate group whereas in the 3wk castrate group proliferation was significantly decreased compared with intact controls. Apoptosis significantly increased by 3.3, 42 and 5.7-folds in PEARKO, 3d and 3wk castrate groups, respectively, compared with intact controls. In the cauda epididymis, castration significantly decreased the volume of lumen and increased stromal volume relative to intact controls. Epithelial proliferation was increased by 20-fold in 3d castrates compared with intact controls. Castration significantly increased apoptosis by 19 and 4.3-folds in 3d and 3wk castrates, respectively, compared with intact controls. We show that the androgen deprivation triggers changes in epididymis structure and cellular turnover in a region-specific and time-dependent manner. The results also reveal a role of testicular factors (presumably androgens) in suppression of epithelial proliferation in the epididymis.

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27

Zempleni, Janos, and Donald M. Mock. "Mitogen-induced proliferation increases biotin uptake into human peripheral blood mononuclear cells." American Journal of Physiology-Cell Physiology 276, no. 5 (May 1, 1999): C1079—C1084. http://dx.doi.org/10.1152/ajpcell.1999.276.5.c1079.

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We sought to determine whether the proliferation of immune cells affects the cellular uptake of the vitamin biotin. Peripheral blood mononuclear cells (PBMC) were isolated from healthy adults. The proliferation of PBMC was induced by either pokeweed lectin, concanavalin A, or phytohemagglutinin. When the medium contained a physiological concentration of [3H]biotin, nonproliferating PBMC accumulated 406 ± 201 amol [3H]biotin ⋅ 106cells−1 ⋅ 30 min−1. For proliferating PBMC, [3H]biotin uptake increased to between 330 and 722% of nonproliferating values. Maximal transport rates of [3H]biotin in proliferating PBMC were also about four times greater than those in nonproliferating PBMC, suggesting that proliferation was associated with an increase in the number of biotin transporters on the PBMC membrane. The biotin affinities and specificities of the transporter for proliferating and nonproliferating PBMC were similar, providing evidence that the same transporter mediates biotin uptake in both states. [14C]urea uptake values for proliferating and nonproliferating PBMC were similar, suggesting that the increased [3H]biotin uptake was not caused by a global upregulation of transporters during proliferation. We conclude that PBMC proliferation increases the cellular accumulation of biotin.

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28

Meng, Qingbing, Jie Zhao, Hongbing Liu, Guoyou Zhou, Wensheng Zhang, Xingli Xu, and Minqian Zheng. "HMGB1 promotes cellular proliferation and invasion, suppresses cellular apoptosis in osteosarcoma." Tumor Biology 35, no. 12 (August 29, 2014): 12265–74. http://dx.doi.org/10.1007/s13277-014-2535-3.

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29

Wang, Zheng, Evelyn E. Gurule, Timothy P. Brennan, Jeffrey M. Gerold, Kyungyoon J. Kwon, Nina N. Hosmane, Mithra R. Kumar, et al. "Expanded cellular clones carrying replication-competent HIV-1 persist, wax, and wane." Proceedings of the National Academy of Sciences 115, no. 11 (February 26, 2018): E2575—E2584. http://dx.doi.org/10.1073/pnas.1720665115.

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The latent reservoir for HIV-1 in resting CD4+ T cells is a major barrier to cure. Several lines of evidence suggest that the latent reservoir is maintained through cellular proliferation. Analysis of this proliferative process is complicated by the fact that most infected cells carry defective proviruses. Additional complications are that stimuli that drive T cell proliferation can also induce virus production from latently infected cells and productively infected cells have a short in vivo half-life. In this ex vivo study, we show that latently infected cells containing replication-competent HIV-1 can proliferate in response to T cell receptor agonists or cytokines that are known to induce homeostatic proliferation and that this can occur without virus production. Some cells that have proliferated in response to these stimuli can survive for 7 d while retaining the ability to produce virus. This finding supports the hypothesis that both antigen-driven and cytokine-induced proliferation may contribute to the stability of the latent reservoir. Sequencing of replication-competent proviruses isolated from patients at different time points confirmed the presence of expanded clones and demonstrated that while some clones harboring replication-competent virus persist longitudinally on a scale of years, others wax and wane. A similar pattern is observed in longitudinal sampling of residual viremia in patients. The observed patterns are not consistent with a continuous, cell-autonomous, proliferative process related to the HIV-1 integration site. The fact that the latent reservoir can be maintained, in part, by cellular proliferation without viral reactivation poses challenges to cure.

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30

Wikle, Thomas A. "Cellular Tower Proliferation in the United States." Geographical Review 92, no. 1 (January 2002): 45. http://dx.doi.org/10.2307/4140950.

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31

Day, Regina M., and Yuichiro J. Suzuki. "Cell Proliferation, Reactive Oxygen and Cellular Glutathione." Dose-Response 3, no. 3 (May 1, 2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.03.010.

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A variety of cellular activities, including metabolism, growth, and death, are regulated and modulated by the redox status of the environment. A biphasic effect has been demonstrated on cellular proliferation with reactive oxygen species (ROS)—especially hydrogen peroxide and superoxide—in which low levels (usually submicromolar concentrations) induce growth but higher concentrations (usually >10–30 micromolar) induce apoptosis or necrosis. This phenomenon has been demonstrated for primary, immortalized and transformed cell types. However, the mechanism of the proliferative response to low levels of ROS is not well understood. Much of the work examining the signal transduction by ROS, including H2O2, has been performed using doses in the lethal range. Although use of higher ROS doses have allowed the identification of important signal transduction pathways, these pathways may be activated by cells only in association with ROS-induced apoptosis and necrosis, and may not utilize the same pathways activated by lower doses of ROS associated with increased cell growth. Recent data has shown that low levels of exogenous H2O2 up-regulate intracellular glutathione and activate the DNA binding activity toward antioxidant response element. The modulation of the cellular redox environment, through the regulation of cellular glutathione levels, may be a part of the hormetic effect shown by ROS on cell growth.

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32

Guinee, Donald G., Sherrie L. Perkins, William D. Travis, Joseph A. Holden, Sheryl R. Tripp, and Michael N. Koss. "Proliferation and Cellular Phenotype in Lymphomatoid Granulomatosis." American Journal of Surgical Pathology 22, no. 9 (September 1998): 1093–100. http://dx.doi.org/10.1097/00000478-199809000-00008.

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33

Shigihara, Yasushi, and Ricardo V. Lloyd. "Apoptosis and Cellular Proliferation in Skin Neoplasms." Applied Immunohistochemistry 5, no. 1 (1997): 29–34. http://dx.doi.org/10.1097/00022744-199703000-00005.

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34

Sabapathy, Kanaga, and Erwin F. Wagner. "JNK2: A Negative Regulator of Cellular Proliferation." Cell Cycle 3, no. 12 (December 2004): 1520–23. http://dx.doi.org/10.4161/cc.3.12.1315.

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35

Alison, MR. "Review : Assessing cellular proliferation: what's worth measuring?" Human & Experimental Toxicology 14, no. 12 (December 1995): 935–44. http://dx.doi.org/10.1177/096032719501401201.

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36

Wikle, Thomas A. "Cellular Tower Proliferation in the United States." Geographical Review 92, no. 1 (January 1, 2002): 45–62. http://dx.doi.org/10.1111/j.1931-0846.2002.tb00133.x.

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37

Gutierrez-Herrera, E., A. E. Ortiz, A. Doukas, and W. Franco. "Fluorescence excitation photography of epidermal cellular proliferation." British Journal of Dermatology 174, no. 5 (March 18, 2016): 1086–91. http://dx.doi.org/10.1111/bjd.14400.

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38

Aranda, Fignacio, and Juan B. Laforga. "Cellular Proliferation in Breast Ductal Infiltrating Carcinoma." Pathology - Research and Practice 193, no. 10 (January 1997): 683–88. http://dx.doi.org/10.1016/s0344-0338(97)80027-1.

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39

Evans, S. M., D. P. Magarelli, S. E. Hahn, and C. J. Koch. "Hypoxia and cellular proliferation in human tumors." International Journal of Radiation Oncology*Biology*Physics 51, no. 3 (November 2001): 79–80. http://dx.doi.org/10.1016/s0360-3016(01)01970-8.

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Altman, J. D., A. Camrud, L. Camrud, M. Jorgenson, J. Allen, D. Lewis, R. S. Schwartz, V. Chorneky, and G. G. Kerslick. "Intravascular soft X-rays inhibit cellular proliferation." Cardiovascular Radiation Medicine 2, no. 1 (January 2001): 57. http://dx.doi.org/10.1016/s1522-1865(00)00064-0.

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Stacey, Dennis W., Steven R. Degudicibus, and Mark R. Smith. "Cellular ras activity and tumor cell proliferation." Experimental Cell Research 171, no. 1 (July 1987): 232–42. http://dx.doi.org/10.1016/0014-4827(87)90266-7.

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KLEIN, NANCY A., GABRIELA M. PÉRGOLA, RAJESHWAR RAO TEKMAL, IRIS A. MONTOYA, TAMMY D. DEY, and ROBERT S. SCHENKEN. "Cytokine Regulation of Cellular Proliferation in Endometriosis." Annals of the New York Academy of Sciences 734, no. 1 The Human End (September 1994): 322–32. http://dx.doi.org/10.1111/j.1749-6632.1994.tb21762.x.

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Giannini, C., B. W. Scheithauer, P. C. Burger, M. R. Christensen, P. C. Wollan, T. J. Sebo, P. A. Forsyth, and C. J. Hayostek. "Cellular Proliferation in Pilocytic and Diffuse Astrocytomas." Journal of Neuropathology and Experimental Neurology 58, no. 1 (January 1999): 46–53. http://dx.doi.org/10.1097/00005072-199901000-00006.

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44

Orekhov, A. N., E. R. Andreeva, V. V. Tertov, and I. M. Khubulova. "Cellular lipidosis and proliferation in human aorta." Atherosclerosis 115 (June 1995): S62. http://dx.doi.org/10.1016/0021-9150(95)96488-e.

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Jampel, H. D., L. J. B. McGuigan, G. R. Dunkelberger, N. L. L'Hernault, and H. A. Quigley. "Cellular Proliferation After Experimental Glaucoma Filtration Surgery." Archives of Ophthalmology 106, no. 1 (January 1, 1988): 89–94. http://dx.doi.org/10.1001/archopht.1988.01060130095036.

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Pellen-Mussi, P., P. Fravalo, M. Guigand, and M. Bonnaure-Mallet. "Evaluation of cellular proliferation on collagenous membranes." Journal of Biomedical Materials Research 36, no. 3 (September 5, 1997): 331–36. http://dx.doi.org/10.1002/(sici)1097-4636(19970905)36:3<331::aid-jbm8>3.0.co;2-f.

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Petr, Michael J., Thomas C. Origitano, and Robert D. Wurster. "PLA2Activity Regulates Ca2+Storage-Dependent Cellular Proliferation." Experimental Cell Research 244, no. 1 (October 1998): 310–18. http://dx.doi.org/10.1006/excr.1998.4181.

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James, B. M., J. H. Gillard, N. M. Antoun, I. S. Scott, N. Coleman, E. M. Pinto, S. J. Jefferies, and N. G. Burnet. "Glioblastoma Doubling Time and Cellular Proliferation Markers." Clinical Oncology 19, no. 3 (April 2007): S33. http://dx.doi.org/10.1016/j.clon.2007.01.373.

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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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Abstract:

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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Henriques, S., E. Silva, S. Cruz, M. F. Silva, G. Ferreira-Dias, L. Lopes-da-Costa, and L. Mateus. "Oestrous cycle-dependent expression of Fas and Bcl2 family gene products in normal canine endometrium." Reproduction, Fertility and Development 28, no. 9 (2016): 1307. http://dx.doi.org/10.1071/rd14245.

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Abstract:

During the oestrous cycle canine endometrium undergoes cyclical cellular proliferation, apoptosis and differentiation. To study the regulation of endometrial apoptosis and proliferation events the expression of apoptosis-related genes was analysed by real-time polymerase chain reaction and cellular expression of their proteins was identified through immunohistochemistry. Cellular apoptosis and proliferation events were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and proliferation marker Ki67 immunostaining, respectively. The highest proliferative index was observed in the follicular phase (all endometrial cellular components) and at early dioestrus (basal glands). This was associated with a low apoptotic index and a strong expression of anti- (Bcl2) and pro-apoptotic proteins (Fas, FasL, Bax). Subsequently (Days 11–45 of dioestrus), basal glandular epithelium experienced the highest apoptotic index, coincidental with a decrease of Bcl2 expression and a low ratio of Bcl2/Bax transcription. An increase in the apoptotic index of crypts, stromal and endothelial cells was observed at late dioestrus and the beginning of anoestrus. These results indicate that pro- and anti-apoptotic proteins regulate the balance between cell proliferation and death in the canine endometrium during the oestrous cycle. High Bcl2 expression in both the follicular and early dioestrous phases stimulate glandular proliferation and prevent apoptosis but, in the non-pregnant uterus, a decrease in Bcl2 expression together with an increase in pro-apoptotic proteins induces apoptosis of basal glandular epithelium cells.

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