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Academic literature on the topic 'Preadipociti'

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Published: 10 March 2023

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Journal articles on the topic "Preadipociti"

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Shao, Jiahao, Ting Pan, Jie Wang, Tao Tang, Yanhong Li, Xianbo Jia, and Songjia Lai. "MiR-208b Regulates Rabbit Preadipocyte Proliferation and Differentiation." Genes 12, no. 6 (June 9, 2021): 890. http://dx.doi.org/10.3390/genes12060890.

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microRNAs (miRNAs) play an important role in gene regulation in animals by pairing with target gene mRNA. Many miRNAs are differentially expressed in the adipose tissue, often with conserved expression. In our study, we found that miR-208b expression was observed differently in the preadipocyte differentiation model. When miR-208b was overexpressed in the preadipocyte differentiation model, the overexpressed group displayed higher expression of PPARγ and FABP4—the markers of preadipocyte differentiation. Oil Red O staining revealed that the count of lipid droplets was increased in the overexpressed group. When the expression of miR-208b was inhibited, the above indicators showed an opposite trend. Moreover, results from both 5-ethynyl-2′-deoxyuridine (EDU) and cell counting kit (CCK) analysis showed that miR-208b promoted the proliferation of preadipocyte. Expression of gene CSNK2A2, a direct miR-208b target, was downregulated in the overexpressed group, providing a possible link to multiple signal pathways. Overall, our data indicate that miR-208b play a positive regulatory effect on the proliferation and differentiation of rabbit preadipocyte.
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Molgat, André S. D., AnneMarie Gagnon, Charlie Foster, and Alexander Sorisky. "The activation state of macrophages alters their ability to suppress preadipocyte apoptosis." Journal of Endocrinology 214, no. 1 (May 3, 2012): 21–29. http://dx.doi.org/10.1530/joe-12-0114.

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Adipose tissue contains macrophages whose state of activation is regulated as obesity develops. Macrophage-secreted factors influence critical processes involved in adipose tissue homeostasis, including preadipocyte proliferation and differentiation into adipocytes. Macrophage-conditioned medium (MacCM) from J774A.1 macrophages protects 3T3-L1 preadipocytes from apoptosis through platelet-derived growth factor (PDGF) signaling. Here, we investigated the effect of macrophage activation on MacCM-dependent preadipocyte survival. MacCM was prepared following activation of either J774A.1 macrophages with lipopolysaccharide (LPS) or human primary monocyte-derived macrophages (MD-macrophages) with LPS or interleukin 4 (IL4). 3T3-L1 and human primary preadipocytes were induced to undergo apoptosis in MacCM, and apoptosis was quantified by cell enumeration or Hoechst nuclear staining. Preadipocyte PDGF signaling was assessed by immunoblot analysis of phosphorylated PDGF receptor, Akt, and ERK1/2. Pro-inflammatory activation of J774A.1 macrophages with LPS inhibited the pro-survival activity of MacCM on 3T3-L1 preadipocytes, despite intact PDGF signaling. Upregulation of macrophage tumor necrosis factor a (TNFα) expression occurred in response to LPS, and TNFα was demonstrated to be responsible for the inability of LPS-J774A.1-MacCM to inhibit preadipocyte apoptosis. Furthermore, MacCM from human MD-macrophages (MD-MacCM) inhibited apoptosis of primary human preadipocytes. MD-MacCM from LPS-treated macrophages, but not IL4-treated anti-inflammatory macrophages, was unable to protect human preadipocytes from cell death. In both murine cell lines and human primary cells, pro-inflammatory activation of macrophages inhibits their pro-survival activity, favoring preadipocyte death. These findings may be relevant to preadipocyte fate and adipose tissue remodeling in obesity.
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Wagoner, Blair, Dorothy B. Hausman, and Ruth B. S. Harris. "Direct and indirect effects of leptin on preadipocyte proliferation and differentiation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (June 2006): R1557—R1564. http://dx.doi.org/10.1152/ajpregu.00860.2005.

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Leptin has been shown to reduce body fat in vivo. Adipocytes express the leptin receptor; therefore, it is realistic to expect a direct effect of leptin on adipocyte growth and metabolism. In vitro studies examining the effect of leptin on adipocyte metabolism require supraphysiological doses of the protein to see a decrease in lipogenesis or stimulation of lipolysis, implying an indirect action of leptin. It also is possible that leptin reduces adipose mass by inhibiting preadipocyte proliferation (increase in cell number) and/or differentiation (lipid filling). Thus we determined direct and indirect effects of leptin on preadipocyte proliferation and differentiation in vitro. We tested the effect of leptin (0–500 ng/ml), serum from leptin-infused rats (0.25% by volume), and adipose tissue-conditioned medium from leptin-infused rats (0–30% by volume) on preadipocyte proliferation and differentiation in a primary culture of cells from male Sprague-Dawley rat adipose tissue. Leptin (50 ng/ml) stimulated proliferation of preadipocytes ( P < 0.05), but 250 and 500 ng leptin/ml inhibited proliferation of both preadipocyte and stromal vascular cell fractions ( P < 0.01), as measured by [3H]thymidine incorporation. Serum from leptin-infused rats inhibited proliferation of the adipose and stromal vascular fractions ( P = 0.01), but adipose tissue-conditioned medium had no effect on proliferation of either cell fraction. None of the treatments changed preadipocyte differentiation as measured by sn-glycerophosphate dehydrogenase activity. These results suggest that leptin could inhibit preadipocyte proliferation by modifying release of a factor from tissue other than adipose tissue.
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Tchkonia, Tamara, Yourka D. Tchoukalova, Nino Giorgadze, Tamar Pirtskhalava, Iordanes Karagiannides, R. Armour Forse, Ada Koo, et al. "Abundance of two human preadipocyte subtypes with distinct capacities for replication, adipogenesis, and apoptosis varies among fat depots." American Journal of Physiology-Endocrinology and Metabolism 288, no. 1 (January 2005): E267—E277. http://dx.doi.org/10.1152/ajpendo.00265.2004.

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Fat depots vary in function and size. The preadipocytes that fat cells develop from exhibit distinct regional characteristics that persist in culture. Human abdominal subcutaneous cultured preadipocytes undergo more extensive lipid accumulation, higher adipogenic transcription factor expression, and less TNF-α-induced apoptosis than omental preadipocytes. We found higher replicative potential in subcutaneous and mesenteric than in omental preadipocytes. In studies of colonies arising from single preadipocytes, two preadipocyte subtypes were found, one capable of more extensive replication, differentiation, and adipogenic transcription factor expression and less apoptosis in response to TNF-α than the other. The former was more abundant in subcutaneous and mesenteric than in omental preadipocyte populations, potentially contributing to regional variation in replication, differentiation, and apoptosis. Both subtypes were found in strains derived from single human preadipocytes stably expressing telomerase, confirming that both subtypes are of preadipocyte lineage. After subcloning of cells of either subtype, both subtypes were found, indicating that switching can occur between subtypes. Thus proportions of preadipocyte subtypes with distinct cell-dynamic properties vary among depots, potentially permitting tissue plasticity through subtype selection during development. Furthermore, mesenteric preadipocyte cell-dynamic characteristics are distinct from omental cells, indicating that visceral fat depots are not functionally uniform.
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Kwon, Hyo-Shin, and Byeong-Churl Jang. "Anti-adipogenic Effect and Mechanism in 3T3-L1 Preadipocyte Differentiation by Salvianolic Acid B." Keimyung Medical Journal 41, no. 2 (December 15, 2022): 67–75. http://dx.doi.org/10.46308/kmj.2022.00213.

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Salvianolic acid B (Sal B) is one of the most active hydrophilic compounds extracted from Salvia miltiorrhiza root. Previous in vitro and in vivo studies demonstrate the ability of Sal B to modulate adipocyte differentiation. However, the lipid-modulating effect and mechanism of Sal B in adipocytes remain controversial. Here we investigated the regulatory effect and mode of action of Sal B on lipid accumulation in 3T3-L1 preadipocyte differentiation. Lipid droplet (LD) accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation were measured by Oil Red O staining and AdipoRed assay. The growth inhibition during 3T3-L1 preadipocyte differentiation was measured by cell count analysis. Western blotting and real-time qPCR analysis were utilized to determine the protein and mRNA expression in the preadipocyte differentiation. Notably, in 3T3-L1 preadipocyte differentiation, treatment with Sal B at 100 M led to a marked decrease in LD accumulation and TG content without influencing cell growth. Sal B treatment (100 M) further reduced the expression and phosphorylation levels of adipogenic transcription factors, including CCAAT/enhancer-binding protein- (C/EBP-), peroxisome proliferator-activated receptor-gamma (PPAR)-, and signal transducer and activator of transcription (STAT)-3/5. Treatment with Sal B (100 M) also reduced the expression and phosphorylation levels of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), two lipogenic enzymes and perilipin A, an LD-binding and stabilizing protein. These results collectively demonstrate that Sal B at 100 M strongly inhibits lipid accumulation in 3T3-L1 preadipocyte differentiation, mediated through regulation of the expression and phosphorylation levels of C/EBP-, PPAR-, STAT-3/5, FAS, ACC, and perilipin.
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Charrière, Guillaume, Béatrice Cousin, Emmanuelle Arnaud, Mireille André, Francis Bacou, Luc Pénicaud, and Louis Casteilla. "Preadipocyte Conversion to Macrophage." Journal of Biological Chemistry 278, no. 11 (January 7, 2003): 9850–55. http://dx.doi.org/10.1074/jbc.m210811200.

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Cho, Young-Min, Seon-Mi Lee, Young-Hwa Kim, Geon-Uk Jeon, Jee-Hy Sung, Heon-Sang Jeong, and Jun-Soo Lee. "Defatted Grape Seed Extracts Suppress Adipogenesis in 3T3-L1 Preadipocytes." Journal of the Korean Society of Food Science and Nutrition 39, no. 6 (June 30, 2010): 927–31. http://dx.doi.org/10.3746/jkfn.2010.39.6.927.

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McNelis, Joanne C., Konstantinos N. Manolopoulos, Laura L. Gathercole, Iwona J. Bujalska, Paul M. Stewart, Jeremy W. Tomlinson, and Wiebke Arlt. "Dehydroepiandrosterone exerts antiglucocorticoid action on human preadipocyte proliferation, differentiation, and glucose uptake." American Journal of Physiology-Endocrinology and Metabolism 305, no. 9 (November 1, 2013): E1134—E1144. http://dx.doi.org/10.1152/ajpendo.00314.2012.

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Glucocorticoids increase adipocyte proliferation and differentiation, a process underpinned by the local reactivation of inactive cortisone to active cortisol within adipocytes catalyzed by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). The adrenal sex steroid precursor dehydroepiandrosterone (DHEA) has been shown to inhibit 11β-HSD1 in murine adipocytes; however, rodent adrenals do not produce DHEA physiologically. Here, we aimed to determine the effects and underlying mechanisms of the potential antiglucocorticoid action of DHEA and its sulfate ester DHEAS in human preadipocytes. Utilizing a human subcutaneous preadipocyte cell line, Chub-S7, we examined the metabolism and effects of DHEA in human adipocytes, including adipocyte proliferation, differentiation, 11β-HSD1 expression, and activity and glucose uptake. DHEA, but not DHEAS, significantly inhibited preadipocyte proliferation via cell cycle arrest in the G1 phase independent of sex steroid and glucocorticoid receptor activation. 11β-HSD1 oxoreductase activity in differentiated adipocytes was inhibited by DHEA. DHEA coincubated with cortisone significantly inhibited preadipocyte differentiation, which was assessed by the expression of markers of early ( LPL) and terminal ( G3PDH) adipocyte differentiation. Coincubation with cortisol, negating the requirement for 11β-HSD1 oxoreductase activity, diminished the inhibitory effect of DHEA. Further consistent with glucocorticoid-opposing effects of DHEA, insulin-independent glucose uptake was significantly enhanced by DHEA treatment. DHEA increases basal glucose uptake and inhibits human preadipocyte proliferation and differentiation, thereby exerting an antiglucocorticoid action. DHEA inhibition of the amplification of glucocorticoid action mediated by 11β-HSD1 contributes to the inhibitory effect of DHEA on human preadipocyte differentiation.
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Molgat, André SD, AnneMarie Gagnon, and Alexander Sorisky. "Preadipocyte apoptosis is prevented by macrophage-conditioned medium in a PDGF-dependent manner." American Journal of Physiology-Cell Physiology 296, no. 4 (April 2009): C757—C765. http://dx.doi.org/10.1152/ajpcell.00617.2008.

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Obesity is associated with macrophage accumulation and inflammation in adipose tissue. Macrophage-secreted factors have been reported to inhibit the differentiation of preadipocytes into adipocytes and to modulate adipogenic extracellular matrix gene expression. To enlarge our understanding of macrophages and the scope of their interactions with preadipocytes, we investigated their effect on preadipocyte survival. Acute exposure of 3T3-L1 preadipocytes to J774A.1 macrophage-conditioned medium (MacCM) stimulated platelet-derived growth factor receptor (PDGFR) tyrosine phosphorylation by 4.1-fold. There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib. Serum-free J774A.1-MacCM or RAW264.7-MacCM completely prevented 3T3-L1 preadipocyte apoptosis normally induced by serum deprivation. Addition of PDGF alone to serum-free control medium was sufficient to prevent 3T3-L1 preadipocyte apoptosis. Inhibition of PDGFR activation by MacCM, either by addition of imatinib or by PDGF immunodepletion of MacCM, effectively disrupted the prosurvival effect. In summary, our data indicate that MacCM promotes preadipocyte survival in a PDGF-dependent manner.
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Kawarasaki, Satoko, Kazuki Matsuo, Hidetoshi Kuwata, Lanxi Zhou, Jungin Kwon, Zheng Ni, Haruya Takahashi, et al. "Screening of flavor compounds using Ucp1-luciferase reporter beige adipocytes identified 5-methylquinoxaline as a novel UCP1-inducing compound." Bioscience, Biotechnology, and Biochemistry 86, no. 3 (December 22, 2021): 380–89. http://dx.doi.org/10.1093/bbb/zbab216.

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ABSTRACT Uncoupling protein 1 (UCP1) in brown or beige adipocytes is a mitochondrial protein that is expected to enhance whole-body energy expenditure. For the high-throughput screening of UCP1 transcriptional activity regulator, we established a murine inguinal white adipose tissue-derived Ucp1-luciferase reporter preadipocyte line. Using this reporter preadipocyte line, 654 flavor compounds were screened, and a novel Ucp1 expression-inducing compound, 5-methylquinoxaline, was identified. Adipocytes treated with 5-methylquinoxaline showed increased Ucp1 mRNA expression levels and enhanced oxygen consumption. 5-Methylquinoxaline induced Ucp1 expression through peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α), and 5-methylquinoxaline-induced PGC1α activation seemed to be partially regulated by its phosphorylation or deacetylation. Thus, our Ucp1-luciferase reporter preadipocyte line is a useful tool for screening of Ucp1 inductive compounds.
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Dissertations / Theses on the topic "Preadipociti"

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MARMO, ROSA. "Riprogrammazione di preadipociti umani mediante trattamento chimico." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3426538.

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Recent studies have shown that differentiated mammalian cells may de-differentiate by forced expression of defined factors for pluripotency; biomedical research is seeking optimizing techniques for obtaining iPS cells without the use of viral genetic material. The purpose of this work was to obtain iPS cells virus-free using the strategy work proposed below: - Extraction of precursors from adipose tissue of healthy subject and cultured in Preadipocyte Growth Medium or in DMEM added with 10% FCS. - Characterization of these cells by research of specific nuclear, cytoplasmic and surface markers; for this purpose it has been invoked in a series of methods including flow cytometry analysis, molecular and cytochemical (immunofluorescence, Oil Red O) essays; - Treatment of cells with 5-azacitidine 10 μM for 48-96 hours; - Performing tests of cell viability (MTT) and daily observation by light microscopy at to monitor the morphology and growth of cells treated with azacitidine. - Real Time PCR order to characterize the cells "reprogrammed" to molecular level, or to check the over-expression of stem cells genes (OCT-4, Nanog, Sox-2) and the down-regulation of tissue-specific genes. - Evaluation of the expression of transcription factors stem cells specific through Western blot analysis. - Analysis by confocal microscopy and cytometry to define the characteristics morphological and phenotypic of cells treated with demethylating agent and "reprogrammed".
Recenti studi hanno dimostrato che cellule di mammifero differenziate possono de-differenziarsi mediante espressione forzata di definiti fattori per la pluripotenza; la ricerca biomedica sta cercando di ottimizzare le tecniche per l'ottenimento di cellule iPS senza l'uso di materiale genetico virale. Scopo di questo lavoro è stato quello di ottenere cellule iPS virus-free utilizzando la strategia di lavoro proposta di seguito: -Estrazione di precursori da tessuto adiposo di soggetto sano e coltura delle stesse in Preadipocyte Growth Medium o in DMEM addizionato con FCS al 10%. -Caratterizzazione delle stesse cellule mediante ricerca di specifici marcatori nucleari, citoplasmatici e di superficie; a tale scopo ci si è avvalsi di una serie di metodiche tra cui l’analisi citofluorimetrica, saggi citochimici (immunofluorescenza, Oil Red O) e molecolari; -Trattamento delle cellule con 5-azacitidina 10 μM per 48-96 ore; -Esecuzione di saggi di vitalità cellulare (MTT) e osservazione giornaliera mediante microscopia ottica allo scopo di monitorare la morfologia e la crescita delle cellule trattate con azacitidina. -Realizzazione di indagini di Real Time PCR allo scopo di caratterizzare le cellule “riprogrammate” a livello molecolare, ovvero per verificare la sovra-espressione di geni indicatori di staminalità (OCT-4, Nanog, Sox-2) e la down-regolazione di geni tessuto specifici. -Valutazione dell’espressione di fattori di trascrizione specifici delle cellule staminali mediante analisi Western Blot. -Analisi mediante microscopia confocale e citofluorimetria per la definizione delle caratteristiche morfologiche e fenotipiche delle cellule trattate con l’agente demetilante e “riprogrammate”.
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Stasi, Fabio. "Caratterizzazione delle cellule staminali del tessuto adiposo nell'obesità e nel diabete: effetto del calo ponderale." Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3423904.

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INTRODUCTION: The Stromal Vascular Fraction (SVF) of human adipose tissue (AT) contains different subpopulations identified by specific CD membrane markers. We focused on the role of preadipocytes (CD34+/CD31-/CD45-), endothelial precursors (CD34+/CD31+/CD45-) and pericytes (CD146+) in obesity and AT remodeling, and the possible pathological correlation between the preadipocyte content and obesity development. MATERIALS AND METHODS: Abdominal subcutaneous (SAT) and visceral AT (VAT) were obtained from 7 obese and 6 obese/diabetic patients underwent sleeve gastrectomy, 7 obese patients underwent plastic surgery or cholecystectomy after a >10kg weight loss. SVF was isolated by collagenase digestion and characterized measuring the co-expression of CD34, CD90, CD73, CD13, CD29, CD271, CD31, CD146 by flow cytometry. We evaluated the expression profiles by qPCR, adipogenic potential, proliferation capacity and morphological features during culture. We sorted by FACS the different subpopulations and in vitro evaluated their adipogenic and angiogenic potential. RESULTS: The flow cytometric analysis revealed a higher % of preadipocytes in VAT than in SAT, with significant differences in obese DM2 (41.9 % ± 3.2 % VAT vs 23.1 % ± 2.9 % SAT) and a significant increase in preadipocytes in SAT of post-obese, up to 70%. Are rather higher percentages of endothelial precursors in SAT than in VAT, for both categories of patients. SVF cells are positive for most of the markers of mesenchymal stem cells (CD13, CD29, CD90, CD73) with the exception of CD271 which shows differences between the two fat depots analyzed. Finally, there is a higher content of CD146+/CD31-/ CD34- pericytes in SAT of the obese and obese DM2, and a greater portion of cells CD146+/CD31+/CD34- especially in SAT of the obese with DM2. The SVF ex vivo (P0) shows the higher adipogenic potential that decreases during the passages in culture (P1-P4) along with the down-regulation of CD34 mRNA and Zfp423, and the up-regulation of CD90. We observed an increase in cell size and nuclear dimensions, along with changes in cytoskeletal structures. The subpopulation of preadipocytes showed the highest adipogenic potential. CONCLUSIONS: the VAT of obese and obese DM2, with a higher content of preadipocytes shows more hyperplastic features than SAT, which having a greater number of endothelial progenitor cells and pericytes has more pro-angiogenic features. However, under conditions of weight loss that occurs in obese patients following surgical treatment, SAT acquires the characteristics of the VAT in the conditions of obesity, increasing the content in preadipocytes. The loss of adipogenic potential associated with the down-regulation of CD34, and the presence of this marker in preadipocytes of SVF demonstrates its strong involvement in adipogenesis. SVF cells undergo deep morphological changes during expansion in vitro, suggesting a possible connection between the cytoskeletal structures and the expression of stem cell markers.
INTRODUZIONE: la frazione vasculo stromale (SVF) del tessuto adiposo umano contiene differenti sottopopolazioni identificate da specifici marcatori di membrana (CD). Abbiamo focalizzato l’attenzione sul ruolo dei preadipociti (CD34+/CD31-/CD45-), precursori endoteliali (CD34+/CD31+/CD45-) e periciti (CD146+) nell’obesità e rimodellamento del tessuto adiposo, e la possibile correlazione patologica nel contenuto di preadipociti nello sviluppo dell’obesità. MATERIALI E METODI: tessuto adiposo sottocutaneo addominale (SAT) e viscerale (VAT) sono stati prelevati da 7 pazienti obesi e 6 pazienti obesi con diabete mellito di tipo 2 (DM2) sottoposti a bendaggio gastrico, 7 pazienti post-obesi sottoposti ad operazione di chirurgia plastica (addominoplastica) dopo calo ponderale superiore ai 10 Kg. La SVF è isolata mediante digestione enzimatica con collagenasi e caratterizzata misurando la co-espressione del CD34 con il CD90, CD73, CD13, CD29, CD271, CD31, CD146 mediante citofluorimetria. Abbiamo valutato i profili di espressione genica mediante qPCR, analisi del potenziale adipogenico, capacità proliferativa e caratteristiche morfologiche durante i passaggi in coltura. Abbiamo effettuato sorting mediante FACS delle differenti sottopopolazioni della SVF e valutato in vitro il loro potenziale adipogenico. RISULTATI: Le analisi citofluorimetriche hanno rivelato una % più alta di preadipociti nel VAT rispetto al SAT, con differenze significative nei pazienti obesi DM2 (41.9% ± 3.2% VAT vs 23.1% ± 2.9% SAT) e un consistente incremento dei preadipociti nel SAT dei post-obesi, fino al 70%. Risultano invece percentuali maggiori di precursori endoteliali nel SAT rispetto al VAT, per entrambe le categorie di pazienti. Le cellule della SVF risultano positive per la maggior parte dei marcatori delle staminali mesenchimali (CD13, CD29, CD90, CD73) ad eccezione del CD271 il quale mostra differenze tra i due depositi adiposi analizzati. Infine, vi è un contenuto maggiore di periciti CD146+/CD31-/CD34- nel SAT degli obesi e degli obesi DM2, e un quantitativo superiore di cellule CD146+/CD31+/CD34- soprattutto nel SAT degli obesi affetti da DM2. La SVF ex-vivo (P0) mostra il potenziale adipogenico più elevato che diminuisce durante i passaggi in coltura (P1-P4) insieme alla down-regolazione dell’mRNA del CD34 e di Zfp423, e alla up-regolazione del CD90. Abbiamo osservato un incremento nelle dimensioni cellulari e nucleari, insieme a cambiamenti delle strutture citoscheletriche. La frazione dei preadipociti ha mostrato il più alto potenziale adipogenico. CONCLUSIONI: il VAT degli obesi e degli obesi DM2, con un contenuto maggiore di preadipociti dimostra possedere maggiori caratteristiche iperplastiche rispetto al SAT, il quale avendo un numero maggiore di precursori endoteliali e di periciti presenta maggiori caratteristiche pro-angiogeniche. Tuttavia, in condizioni di calo ponderale che avviene nei pazienti obesi in seguito a trattamento chirurgico, il SAT acquisisce le caratteristiche del VAT nelle condizioni di obesità, aumentando il contenuto in preadipociti. La perdita del potenziale adipogenico associata alla down-regolazione del CD34, e la presenza di tale marcatore nei preadipociti della SVF dimostra un suo forte coinvolgimento nell’adipogenesi. Le cellule della SVF vanno incontro a profondi cambiamenti morfologici durante l’espansione in vitro, suggerendo una possibile connessione tra le strutture citoscheletriche e l’espressione di marcatori della staminalità.
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Hutley, Louise Joyce. "Human preadipocyte proliferation and differentiation." Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/37117/6/37117_Digitised_Thesis.pdf.

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Obesity represents a major health, social and economic burden to many developing and Westernized communities, with the prevalence increasing at a rate exceeding almost all other medical conditions. Despite major recent advances in our understanding of adipose tissue metabolism and dynamics, we still have limited insight into the regulation of adipose tissue mass in humans. Any significant increase in adipose tissue mass requires proliferation and differentiation of precursor cells (preadipocytes) present in the stromo-vascular compartment of adipose tissue. These processes are very complex and an increasing number of growth factors and hormones have been shown to modulate the expression of genes involved in preadipocyte proliferation and differentiation. A number of transcription factors, including the C/EBP family and PP ARy, have been identified as integral to adipose tissue development and preadipocyte differentiation. Together PP ARy and C/EBPa regulate important events in the activation and maintenance of the terminally differentiated phenotype. The ability of PP ARy to increase transcription through its DNA recognition site is dependent on the binding of ligands. This suggests that an endogenous PP ARy ligand may be an important regulator of adipogenesis. Adipose tissue functions as both the major site of energy storage in the body and as an endocrine organ synthesizing and secreting a number of important molecules involved in regulation of energy balance. For optimum functioning therefore, adipose tissue requires extensive vascularization and previous studies have shown that growth of adipose tissue is preceded by development of a microvascular network. This suggests that paracrine interactions between constituent cells in adipose tissue may be involved in both new capillary formation and fat cell growth. To address this hypothesis the work in this project was aimed at (a) further development of a method for inducing preadipocyte differentiation in subcultured human cells; (b) establishing a method for simultaneous isolation and separate culture of both preadipocytes and microvascular endothelial cells from the same adipose tissue biopsies; (c) to determine, using conditioned medium and co-culture techniques, if endothelial cell-derived factors influence the proliferation and/or differentiation of human preadipocytes; and (d) commence characterization of factors that may be responsible for any observed paracrine effects on aspects of human adipogenesis. Major findings of these studies were as follows: (A) Inclusion of either linoleic acid (a long-chain fatty acid reported to be a naturally occurring ligand for PP ARy) or Rosiglitazone (a member of the thiazolidinedione class of insulin-sensitizing drugs and a synthetic PPARy ligand) in differentiation medium had markedly different effects on preadipocyte differentiation. These studies showed that human preadipocytes have the potential to accumulate triacylglycerol irrespective of their stage of biochemical differentiation, and that thiazolidinediones and fatty acids may exert their adipogenic and lipogenic effects via different biochemical pathways. It was concluded that Rosiglitazone is a more potent inducer of human preadipocyte differentiation than linoleic acid. (B) A method for isolation and culture of both endothelial cells and preadipocytes from the same adipose tissue biopsy was developed. Adipose-derived microvascular endothelial cells were found to produce factor/s, which enhance both proliferation and differentiation of human preadipocytes. (C) The adipogenic effects of microvascular endothelial cells can be mimicked by exposure of preadipocytes to members of the Fibroblast Growth Factor family, specifically ~-ECGF and FGF-1. (D) Co-culture of human preadipocytes with endothelial cells or exposure of preadipocytes to either ~-ECGF or FGF-1 were found to 'prime' human preadipocytes, during their proliferative phase of growth, for thiazolidinedione-induced differentiation. (E) FGF -1 was not found to be acting as a ligand for PP ARy in this system. Findings from this project represent a significant step forward in our understanding of factors involved in growth of human adipose tissue and may lead to the development of therapeutic strategies aimed at modifying the process. Such strategies would have potential clinical utility in the treatment of obesity and obesity related disorders such as Type II Diabetes.
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Peshdary, Vian. "Effect of Glucose on Human Adipogenesis and its Regulation by Macrophages." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35051.

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Adipose tissue expands via differentiation of preadipocytes into adipocytes (adipogenesis) and/or hypertrophy of existing adipocytes. A low adipogenic capacity promotes adipocyte hypertrophy, causing inflammatory macrophage accumulation and insulin resistance. Macrophage-conditioned medium (MacCM) inhibits adipogenesis and promotes adipocyte inflammation, but it is unknown if these effects are altered by high glucose (HG) versus normal glucose (NG) concentrations. The effect of HG on adipogenesis was assessed. Human subcutaneous abdominal preadipocytes were induced to differentiate in HG or NG conditions. HG did not affect adipogenesis. HG increased ChREBP-β mRNA and protein levels, and increased GLUT4 mRNA, in differentiated adipocytes. It did not change mRNA levels of ACC, SCD, and FAS. The increase in ChREBP-β mRNA was positively correlated with HG-induced increase in GLUT4 mRNA. The effect of HG-MacCM versus NG-MacCM on human adipogenesis and adipocyte inflammation was compared. Human monocyte-derived macrophages (MDM) were placed in NG or HG glucose for 24 hours to generate MacCM. HG-MacCM, but not NG-MacCM inhibited triacylglycerol accumulation and protein expression of PPARγ during human adipogenesis. Preadipocytes differentiated in HG-MacCM displayed a more pro-inflammatory phenotype, as assessed by increased MCP-1 and IL-6 and reduced adiponectin mRNA expression. HG increased phosphorylation of IKK-β and decreased protein expression of IκBα in MDMs. In addition, HG reduced protein expression of PPARγ in MDMs. The pro-inflammatory effect of HG-MacCM on MCP-1 expression in adipocytes was partially inhibited when MDMs were treated with sc-514 (IKKβ inhibitor). My data demonstrate that HG-induced expression of ChREBP-β in adipocytes may be associated with increased GLUT4 mRNA. The anti-adipogenic and pro-inflammatory effects of HG-MacCM are more potent than NG-MacCM. This suggests the possibility that adipose tissue cellular remodeling in vivo may be altered with hyperglycemia.
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Hattingh, Anna C. "The anti-ageing potential of rooibos: preserving preadipocyte funtion." Thesis, Nelson Mandela Metropolitan University, 2015. http://hdl.handle.net/10948/7804.

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Treatments with natural products rich in anti-oxidants have attracted remarkable interest in the cosmetic and pharmaceutical industry to combat oxidative stress and reverse the effects of ageing. Rooibos (Aspalathus linearis) is a South African fynbos plant, well-known for its strong anti-oxidant capacity and use in many cosmetic products. However, little published research exists on its potential as an anti-ageing treatment. The anti-ageing properties of fermented and green rooibos were investigated using an in vitro cell culture model designed to evaluate the involvement of mitochondrial dysfunction in the age related decline in preadipocyte function. Mitochondrial DNA (mtDNA) deficient preadipocytes, ρ0 3T3-L1preadipocytes, were generated following continuous long-term exposure to sub lethal concentrations of ethidium bromide (EtBr). Depletion of the mtDNA resulted in a significantly reduced mitochondrial membrane potential, rate of proliferation in culture, as well as an increased glucose utilization and lactate production. Treatment with the green rooibos (100 μg/mL) stimulated cell growth rates for both the wildtype and mutant cell lines. MtDNA depleted cells showed arrest in the G1 phase (48.8 ± 3.34%) compared to wildtype cells (44.6 ± 1.38%), which was significantly attenuated after treatment with green rooibos for mutant (42.0 ± 0.83%) and wildtype (36.5 ± 5.80%) treated cells. The results obtained for glucose utilization and lactate production, indicated a significant increase in glucose utilization along with a concomitant increase in lactate production after treatment with both green and fermented rooibos for wildtype and mutant cell lines. A significant improvement in mitochondrial membrane potential was also later observed after treatment with green and fermented rooibos on both the wildtype and mutant cell lines. The results obtained indicate that rooibos extracts, particularly the green rooibos, exhibit effects which preserve the functional capacity of preadipocytes exposed to ageing related insults, and indicate that rooibos could cause a metabolic shift in cells redirecting carbon flow away from mitochondrial metabolism, and towards lactate production and consequently, cells become resistant to mitochondrial dysfunction.
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Molgat, André. "The Effect of Macrophage-secreted Factors on Preadipocyte Survival." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23628.

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Adipose tissue (AT) expansion and remodeling that maintains healthy function relies on stromal preadipocytes capable of differentiating into new adipocytes (adipogenesis). During chronic positive energy balance, a relative deficit in adipogenesis, from either a decrease in preadipocyte number or their capacity to differentiate, leads to excessive adipocyte hypertrophy and AT dysfunction. AT contains macrophages whose number and activation state is dynamically regulated with changes in AT mass. This study aims to investigate the effect of macrophage-secreted factors on preadipocyte survival. To assess the effect of macrophage-secreted factors on preadipocytes, murine 3T3-L1 preadipocytes or human primary preadipocytes were incubated with macrophage-conditioned medium (MacCM), prepared from either murine (J774A.1, RAW264.7, bone marrow-derived) or human (THP-1, monocyte-derived) macrophage models, respectively. MacCM inhibited preadipocyte apoptosis and activated pro-survival signaling in both preadipocyte models. Inhibition of PDGFR, Akt, or ERK1/2 reduced the pro-survival effect of MacCM in 3T3-L1 preadipocytes. Inhibition of reactive oxygen species (ROS) generation, or enhancement of ROS clearance, reduced MacCM-dependent 3T3-L1 preadipocyte survival. Whereas anti-inflammatory activated macrophages retained the ability to prevent preadipocyte apoptosis, pro-inflammatory activated macrophages did not. TNF-α immunoneutralization restored the survival activity of pro-inflammatory MacCM on 3T3-L1 preadipocytes. These studies reveal a novel pro-survival effect of MacCM on preadipocytes, and identify signaling molecules (PDGF, Akt, ERK1/2, and ROS) that underlie this action. Macrophage activation was found to regulate the pro-survival activity of MacCM. These in vitro cell culture studies are consistent with a model in which the extent of preadipocyte apoptosis in vivo may determine preadipocyte number and the ability of AT to expand while maintaining healthy function during chronic positive energy balance.
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El, Bilali Jason. "Effects of Chronic Insulin and High Glucose on Insulin-Stimulated Responses in Human Preadipocytes." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34109.

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The preadipocyte is crucial for healthy adipose tissue (AT) remodeling, and insulin resistance in these cells may contribute to AT dysfunction. Chronic exposure to insulin and high glucose induces insulin resistance in the 3T3-L1 mouse adipocyte cell line in vitro, however, whether this occurs in human preadipocytes is not known. To investigate this, human preadipocytes were isolated from subcutaneous AT obtained from 6 female patients undergoing elective surgery (Research Ethics Board-approved). Human preadipocytes were incubated in 5 mM glucose or 25 mM glucose in the presence or absence of 0.6 nM insulin for 48 hours, followed by acute 100 nM insulin stimulation. 25 mM glucose + 0.6 nM insulin inhibited insulin-stimulated tyrosine phosphorylation of IR-β (77%) and IRS-1 (81%) compared to NG (p<0.01), however, insulin-stimulated Ser473 Akt phosphorylation was not affected. 25 mM glucose and/or 0.6 nM insulin did not significantly change levels of pro-inflammatory adipokines. 25 mM glucose and/or 0.6 nM, prior to and/or during 14 days of adipogenic induction, did not affect levels of adipogenic markers or intracellular triglyceride accumulation.
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Nguyen, Anh Thu. "Effects of the HIV-1 protease inhibitor ritonavir on preadipocyte differentiation." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9001.

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HIV-1 protease inhibitor therapy is associated with a novel lipodystrophy syndrome characterized by truncal adiposity, peripheral fat atrophy, dyslipidemia, and type 2 diabetes. The increase in truncal fat may be due to increase in adipocyte number as a result of enhanced preadipocyte differentiation. We show that addition of 10 mug/ml ritonavir to standard differentiation medium enhanced 3T3-L1 preadipocyte differentiation as measured by a 30% increase in triacylglycerol (TG) accumulation and a 50% increase in glycerol 3-phosphate dehydrogenase (GPDH) activity. Although ritonavir partially inhibited protein expression of peroxisome proliferator activated receptor gamma (PPARgamma), CCAAT/enhancer binding protein alpha (C/EBPalpha), and the aP2 gene (which encodes the adipocyte lipid binding protein), it resulted in higher levels of the active form of adipocyte determination and differentiation-dependent factor-1 (ADD-1), also known as sterol regulatory element binding protein 1 (SREBP-1). The enhancing effects of ritonavir on late events of 3T3-L1 preadipocyte differentiation may be mediated by ADD-1/SREBP-1 which has been shown to directly activate transcription of several genes encoding lipogenic enzymes. Preliminary results suggest that ritonavir preferentially enhances differentiation of human preadipocytes derived from abdominal omental but not subcutaneous adipose tissue in primary culture.
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Yarwood, Stephen J. "The cyclic amp signalling system as a regulator of preadipocyte differentiation." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362948.

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Wurst, Ulrike. "Die Regulation von Preadipocyte factor-1 bei Gestationsdiabetes mellitus und Präeklampsie." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-216381.

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Adipositas und die damit verbundenen Begleiterkrankungen zeigen einen deutlichen Anstieg der Prävalenz in der Bevölkerung. Auch für die Schwangerschaft gilt starkes Übergewicht als Risikofaktor für metabolische und vaskuläre Komplikationen wie Gestationsdiabetes mellitus (GDM) und Präeklampsie (PE). In den letzten 20 Jahren wurde eindrücklich nachgewiesen, dass eine Dysregulation von Fettzell-sezernierten Proteinen, sogenannten Adipokinen, ursächlich zu GDM und PE beitragen könnte. Zu Beginn der Dissertation lagen jedoch nur unzureichende Daten über die Regulation des Insulinresistenz-induzierenden, anti-adipogenen und anti-angiogenen Adipokins Preadipocyte factor-1 (Pref-1) bei GDM und PE vor. Die vorliegende Arbeit untersucht daher die Regulation von zirkulierendem Pref-1 bei GDM und PE sowie seine Expression in der Plazenta. Bei 74 Patientinnen mit GDM konnte kein signifikanter Unterschied der Pref-1 Konzentrationen (0.40 µg/l) verglichen zu 74 Gesunden (0.42 µg/l) (p = 0.655) festgestellt werden (Wurst U et al., Cytokine 2015; 71: 161–164). Es zeigte sich in der Kohorte eine unabhängige Assoziation zwischen Pref-1 und Schwangerschaftsalter bei der Blutentnahme, Triglyzeriden, Kreatinin, Body Mass Index und C reaktivem Protein (p < 0.05). In einer Studienkohorte von 51 Schwangeren mit PE wurden signifikant niedrigere Serumspiegel von Pref-1 (0.49 µg/l) im Vergleich zu 51 gesunden Schwangeren (0.68 µg/l) (p < 0.001) gemessen (Schrey S, Wurst U, et al., Cytokine 2015; 75: 338–343). In der multiplen Regressionsanalyse waren PE, Schwangerschaftsalter zum Zeitpunkt der Blutentnahme sowie zirkulierendes Leptin unabhängige Prädiktoren für Pref-1. Im peripartalen Zeitraum zeigte sich ein akuter und deutlicher Abfall von zirkulierendem Pref-1 im mütterlichen Blut und das Adipokin wurde immunhistochemisch im Plazentagewebe nachgewiesen. Die Daten dieser Studien sind vereinbar mit den Hypothesen, dass Pref-1 mit fortschreitender Schwangerschaft zunehmend produziert wird, die Plazenta zur Sekretion des Adipokins aktiv beiträgt sowie das Adipokin bei PE dysreguliert ist. Weiterführende Untersuchungen im Tiermodell sowie prospektive Studien sind notwendig, um die Signifikanz von Pref-1 bei GDM und PE näher zu untersuchen.
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Book chapters on the topic "Preadipociti"

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Stockdale, Frank E., and Darrell Wiens. "Adipocyte, Preadipocyte and Mammary Epithelial Cell Interaction." In Cellular and Molecular Biology of Mammary Cancer, 129–40. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0943-7_8.

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Rhie, Jong Won, Jin Kyung Song, Paik Kwon Lee, and Sang Tae Ahn. "Implantation of Cultured Preadipocyte Using Chitosan/Alginate Sponge." In Advanced Biomaterials VII, 349–52. Stafa: Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-436-7.349.

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Kirkland, James L., and Charles H. Hollenberg. "Inhibitors of Preadipocyte Replication: Opportunities for the Treatment of Obesity." In Inhibitors of Cell Growth, 177–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72149-6_9.

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Bernlohr, David A., and M. Daniel Lane. "Early Studies on Role of Stearoyl-CoA Desaturase During Preadipocyte Differentiation." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 1–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_1.

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Shamsi, Farnaz, and Yu-Hua Tseng. "Protocols for Generation of Immortalized Human Brown and White Preadipocyte Cell Lines." In Thermogenic Fat, 77–85. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_8.

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Matsubara, Yumiko, Mitsuru Murata, and Yasuo Ikeda. "Culture of Megakaryocytes and Platelets from Subcutaneous Adipose Tissue and a Preadipocyte Cell Line." In Methods in Molecular Biology, 249–58. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-307-3_17.

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Stephens, Jacqueline M., Michelle Butts, Randy Stone, Philip H. Pekala, and David A. Bernlohr. "Regulation of transcription factor mRNA accumulation during 3T3-L1 preadipocyte differentiation by antagonists of adipogenesis." In Cellular Fatty Acid-Binding Proteins II, 63–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3096-1_9.

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Moon, Hyun Seuk, Hong Gu Lee, Ho Hyun Song, Yun Jaie Choi, and Chong Su Cho. "Effect of Collagen Coating on Lipid Accumulation and Differentiation on 3T3-L1 Preadipocyte Treated with Conjugated Linoleic Acid." In Advanced Biomaterials VII, 261–64. Stafa: Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-436-7.261.

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Sul, Hei Sook, Yuhui Wang, and Carolyn Hudak. "Preadipocyte Factor-1 and Adipose Tissue-Specific Secretory Factor/Resistin - Two Secreted Factors from Adipose Tissue: Role in Adipogenesis and Insulin Resistance." In Adipose Tissue in Health and Disease, 231–43. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527629527.ch12.

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Kawada, Teruo, Naohito Aoki, and Etsuro Sugimoto. "Protein Factor Obtained from Rat Adipose Tissue Specifically Permits the Proliferation of 3T3-L1 and OB1771 Preadipocyte Cell Lines in a Completely Defined Serum-Free Medium." In Animal Cell Culture and Production of Biologicals, 197–204. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3550-4_22.

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Conference papers on the topic "Preadipociti"

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Almuraikhi, Shamma, Wael Kafienah, Moataz Bashah, Morana Jaganjac, Houari Abdesselem, Nayef Mazloum, and Mohamed Elrayess. "Insulin Resistance-associated Impairment Of Preadipocyte Differentiation In Human Abdominal Obesity." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0050.

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Elrayess, Mohamed A., Shamma Al Muraikhi, Fatima Al-Khelaifi, Afnan Al-Yafei, Moataz Bashah, and Morana Jaganjac. "The Role of 4-hydroxynonenal in Human Preadipocyte Proliferation and Differentiation." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbop1500.

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Elrayess, Mohamed A., Shamma Al-Muraikhi, Wael Kafienah, Michelle Somerville, Fatima Al-Khelaifi, and Moataz Bashah. "A Dual Role of Il-6 in Bone Marrow and Adipose Tissue-Derived Preadipocyte Differentiation." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2006.

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Wolfson, Benjamin, Ramkishore Gernapudi, Nadire Duru, and Qun Zhou. "Abstract 5067: Preadipocyte exosomes promote early stage breast cancer formation by enhancing cancer stem cell renewal signaling." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5067.

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Kim, HS, M. Jung, SK Choi, and WK Moon. "Abstract P5-03-09: Breast cancer promotion by IL-6-mediated cross-talk between human preadipocyte and breast dutal carcinoma in situ." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p5-03-09.

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