4β-Hydroxywithanolide E and withanolide E from Physalis peruviana L. inhibit adipocyte differentiation of 3T3-L1 cells through modulation of mitotic clonal expansion

2020 ◽  
Vol 75 (1) ◽  
pp. 232-239
Author(s):  
Momochika Kumagai ◽  
Izumi Yoshida ◽  
Takashi Mishima ◽  
Masahiro Ide ◽  
Kazuhiro Fujita ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Clonal Expansion ◽  
Physalis Peruviana ◽  
Mitotic Clonal Expansion ◽  
Withanolide E

scholarly journals Reactive Oxygen Species Facilitate Adipocyte Differentiation by Accelerating Mitotic Clonal Expansion

2009 ◽  
Vol 284 (16) ◽  
pp. 10601-10609 ◽  
Author(s):  
Haemi Lee ◽  
Yoo Jeong Lee ◽  
Hyeonjin Choi ◽  
Eun Hee Ko ◽  
Jae-woo Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Adipocyte Differentiation ◽  
Reactive Oxygen ◽  
Clonal Expansion ◽  
Oxygen Species ◽  
Mitotic Clonal Expansion

Curcumin inhibits adipocyte differentiation through modulation of mitotic clonal expansion

2011 ◽  
Vol 22 (10) ◽  
pp. 910-920 ◽  
Author(s):  
Choon Young Kim ◽  
Thuc T. Le ◽  
Chihyu Chen ◽  
Ji-Xin Cheng ◽  
Kee-Hong Kim
Keyword(s):  
Adipocyte Differentiation ◽  
Clonal Expansion ◽  
Mitotic Clonal Expansion

scholarly journals RNF20 affects porcine adipocyte differentiation via regulation of mitotic clonal expansion

2021 ◽  
Author(s):  
Ying Zhao ◽  
Jianfei Pan ◽  
Chunwei Cao ◽  
Xiaojuan Liang ◽  
Shulin Yang ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Clonal Expansion ◽  
Mitotic Clonal Expansion

Transcription factor HMG box-containing protein 1 (HBP1) modulates mitotic clonal expansion (MCE) during adipocyte differentiation

2017 ◽  
Vol 233 (5) ◽  
pp. 4205-4215 ◽  
Author(s):  
Chien-Yi Chan ◽  
Ping Yu ◽  
Feng-Tzu Chang ◽  
Zih-Hua Chen ◽  
Ming-Fen Lee ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Adipocyte Differentiation ◽  
Clonal Expansion ◽  
Hmg Box ◽  
Mitotic Clonal Expansion

scholarly journals GDE5 inhibition accumulates intracellular glycerophosphocholine and suppresses adipogenesis at a mitotic clonal expansion stage

2019 ◽  
Vol 316 (2) ◽  
pp. C162-C174
Author(s):  
Yuri Okazaki ◽  
Keishi Nakamura ◽  
Shuto Takeda ◽  
Ikumi Yoshizawa ◽  
Fumiyo Yoshida ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Biological Significance ◽  
Clonal Expansion ◽  
Organic Osmolytes ◽  
Differentiation Markers ◽  
Phosphocholine Cytidylyltransferase ◽  
Lactate Dehydrogenase Release ◽  
Choline Metabolism ◽  
Intracellular Amino Acids ◽  
Mitotic Clonal Expansion

Mammalian glycerophosphodiesterases (GDEs) were recently shown to be involved in multiple cellular signaling pathways. This study showed that decreased GDE5 expression results in accumulation of intracellular glycerophosphocholine (GPC), showing that GDE5 is actively involved in GPC/choline metabolism in 3T3-L1 adipocytes. Using 3T3-L1 adipocytes, we further studied the biological significance of GPC/choline metabolism during adipocyte differentiation. Inhibition of GDE5 suppressed the formation of lipid droplets, which is accompanied by the decreased expression of adipocyte differentiation markers. We further showed that the decreased GDE5 expression suppressed mitotic clonal expansion (MCE) of preadipocytes. Decreased expression of CTP: phosphocholine cytidylyltransferase (CCTβ), a rate-limiting enzyme for phosphatidylcholine (PC) synthesis, is similarly able to inhibit MCE and PC synthesis; however, the decreased GDE5 expression resulted in accumulation of intracellular GPC but did not affect PC synthesis. Furthermore, we showed that mRNAs of proteoglycans and transporters for organic osmolytes are significantly upregulated and that intracellular amino acids and urea levels are altered in response to GDE5 inhibition. Finally, we showed that reduction of GDE5 expression increased lactate dehydrogenase release from preadipocytes. These observations indicate that decreased GDE5 expression can suppress adipocyte differentiation not through the PC pathway but possibly by intracellular GPC accumulation. These results provide insight into the roles of mammalian GDEs and their dependence upon osmotic regulation by altering intracellular GPC levels.

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