Chrysanthemum indicum suppresses adipogenesis by inhibiting mitotic clonal expansion in 3T3‐L1 preadipocytes

2021 ◽  
Author(s):  
Won‐Ju Kim ◽  
Hyung‐Seok Yu ◽  
Won‐Young Bae ◽  
Kyung Yuk Ko ◽  
Kyung‐Hoon Chang ◽  
...  
Keyword(s):  
Clonal Expansion ◽  
Chrysanthemum Indicum ◽  
Mitotic Clonal Expansion

scholarly journals Adipogenic function of tetranectin mediated by enhancing mitotic clonal expansion via ERK signaling

BMB Reports ◽  
2021 ◽  
Vol 54 (7) ◽  
pp. 374-379
Author(s):  
Seulgi Go ◽  
Jihyun Park ◽  
Safikur Rahman ◽  
Juno Jin ◽  
Inho Choi & Jihoe Kim
Keyword(s):  
Clonal Expansion ◽  
Erk Signaling ◽  
Mitotic Clonal Expansion

scholarly journals CD90 serves as differential modulator of subcutaneous and visceral adipose-derived stem cells by regulating AKT activation that influences adipose tissue and metabolic homeostasis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhenzhen Pan ◽  
Zixin Zhou ◽  
Huiying Zhang ◽  
Hui Zhao ◽  
Peixuan Song ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Metabolic Disorders ◽  
Adipogenic Differentiation ◽  
Clonal Expansion ◽  
S Phase ◽  
Adipose Derived Stem Cells ◽  
Akt Activation ◽  
Adipocyte Hypertrophy ◽  
Mitotic Clonal Expansion ◽  
Visceral Adipose

Abstract Background White adipose tissue includes subcutaneous and visceral adipose tissue (SAT and VAT) with different metabolic features. SAT protects from metabolic disorders, while VAT promotes them. The proliferative and adipogenic potentials of adipose-derived stem cells (ADSCs) are critical for maintaining adipose tissue homeostasis through driving adipocyte hyperplasia and inhibiting pathological hypertrophy. However, it remains to be elucidated the critical molecules that regulate different potentials of subcutaneous and visceral ADSCs (S-ADSCs, V-ADSCs) and mediate distinct metabolic properties of SAT and VAT. CD90 is a glycosylphosphatidylinositol-anchored protein on various cells, which is also expressed on ADSCs. However, its expression patterns and differential regulation on S-ADSCs and V-ADSCs remain unclear. Methods S-ADSCs and V-ADSCs were detected for CD90 expression. Proliferation, colony formation, cell cycle, mitotic clonal expansion, and adipogenic differentiation were assayed in S-ADSCs, V-ADSCs, or CD90-silenced S-ADSCs. Glucose tolerance test and adipocyte hypertrophy were examined in mice after silencing of CD90 in SAT. CD90 expression and its association with CyclinD1 and Leptin were analyzed in adipose tissue from mice and humans. Regulation of AKT by CD90 was detected using a co-transfection system. Results Compared with V-ADSCs, S-ADSCs expressed high level of CD90 and showed increases in proliferation, mitotic clonal expansion, and adipogenic differentiation, together with AKT activation and G1-S phase transition. CD90 silencing inhibited AKT activation and S phase entry, thereby curbing proliferation and mitotic clonal expansion of S-ADSCs. In vivo CD90 silencing in SAT inhibited S-ADSC proliferation, which caused adipocyte hypertrophy and glucose intolerance in mice. Furthermore, CD90 was highly expressed in SAT rather than in VAT in human and mouse, which had positive correlation with CyclinD1 but negative correlation with Leptin. CD90 promoted AKT activation through recruiting its pleckstrin homology domain to plasma membrane. Conclusions CD90 is differentially expressed on S-ADSCs and V-ADSCs, and plays critical roles in ADSC proliferation, mitotic clonal expansion, and hemostasis of adipose tissue and metabolism. These findings identify CD90 as a crucial modulator of S-ADSCs and V-ADSCs to mediate distinct metabolic features of SAT and VAT, thus proposing CD90 as a valuable biomarker or target for evaluating ADSC potentials, monitoring or treating obesity-associated metabolic disorders.

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

scholarly journals A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 331 ◽  
Author(s):  
Xin Wang ◽  
Min Liu ◽  
Guo He Cai ◽  
Yan Chen ◽  
Xiao Chen Shi ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Early Stage ◽  
Lipid Synthesis ◽  
Clonal Expansion ◽  
Inhibitory Effect ◽  
Limiting Factor ◽  
Stat3 Signaling Pathway ◽  
Mitotic Clonal Expansion

The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of lactucin. Compared to controls, lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of lactucin in these cells. Together, our results provide the indication that lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.

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