Role of SIRT1 and AMPK in mesenchymal stem cells differentiation

Chen, Huiqiang; Liu, Xianbao; Chen, Han; Cao, Jiashu; Zhang, Ling; Hu, Xinyang; Wang, Jiańan

doi:10.1016/j.arr.2013.12.002

Cited by 93 publications

(77 citation statements)

References 124 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The AMPK pathway is an important signal in regulating energy metabolism, and Sirt-1 can activate and regulate AMPK activity [13]. Therefore, we also analyzed liver Sirt-1/AMPK expression and found that HFD obese mice treated with ginkgolide B had significantly promoted Sirt-1 and pAMPK expression compared to the HFD mice.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have found that ACC phosphorylation will decrease and block downstream fatty acid synthase (FAS) expression associated with the synthesis of fatty acid chains [11,12]. Recent reports also describe Sirt-1 as regulating AMPK phosphorylation, leading to increased AMPK activity [13]. Therefore, enhancing the Sirt-1/AMPK pathway would be expected to block fatty acid chain synthesis and reduce hepatocyte lipid accumulation.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

View full text Add to dashboard Cite

Ginkgolide B is isolated from Ginkgo biloba leaves. It has multiple biological functions, including alleviating lung injury and ischemic stroke in mice and protecting pancreatic beta cells and improving endothelial dysfunction in diabetic mice. Here we sought to determine whether ginkgolide B ameliorates nonalcoholic fatty liver disease (NALFD) in high-fat diet (HFD)-induced obese mice. We also evaluated whether or not ginkgolide B reduces lipid accumulation of hepatocytes in vitro. C57BL/6 mice were fed with HFD and treated with ginkgolide B by intraperitoneal injection twice a week for last 10 weeks of the 14-week HFD feeding period. In addition, HepG2 cells were treated with oleic acid to establish a fatty liver cell model and exposed to various concentrations of ginkgolide B. Ginkgolide B significantly decreased hepatic lipid accumulation and alleviated steatosis in HFD-induced obese mice. It also reduced body weight and epididymal adipose tissue weight. Serum assay results showed that ginkgolide B inhibited leptin, alanine aminotransferase, and aspartate aminotransferase levels and increased HDL levels compared to obese mice. It also decreased fatty acid synthase expression and increased Sirt-1 and phosphorylation of AMP-activated protein kinase α in liver tissue. Furthermore, ginkgolide B significantly inhibited lipid accumulation and expression of adipogenesis-related proteins and increased adipolysis-associated protein expression in hepatocytes in vitro. These results suggest that ginkgolide B is an effective natural compound for alleviating hepatic lipid accumulation and reducing body weight in obese mice. It also ameliorated NALFD in HFD-induced obese mice. www.impactjournals.com/oncotarget/

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

View full text Add to dashboard Cite

show abstract

“…Although SIRT1 is not required for mHSC function [125], some reports suggest that SIRT1 might be required for both the maintenance and differentiation of mHSCs [126]. In MSCs, SIRT1 activity favors osteogenesis while inhibiting adipogenesis [115]. The accumulated evidence clearly supports the involvement of SIRT1 in the regulation of pluripotency and differentiation processes, although the mechanisms underlying stage and lineage specificities remain obscure.…”

Section: Metabolites and Cofactors: Small Molecules With A Broad Inflmentioning

confidence: 93%

“…As recently reviewed elsewhere, AMPK activity controls the fate of MSCs by favoring osteogenic and inhibiting adipogenic differentiation. The role of AMPK in controlling the differentiation of MSCs may depend on its involvement in multiple pathways, including the ERK pathway, mTOR signaling, Wnt/bcatenin signaling, and energy metabolism [115]. In mHSCs, the constitutively active liver kinase B1 (LKB1), which activates AMPK and AMPK-related kinases (interested readers can refer to [116]) under low-energy conditions, is essential to preserve HSC quiescence [117][118][119].…”

Section: Nutrient-and Energy-sensing Pathways: a Complex Connection Bmentioning

confidence: 99%

Connecting Mitochondria, Metabolism, and Stem Cell Fate

Wanet

Arnould

Najimi

et al. 2015

Stem Cells and Development

260

216

View full text Add to dashboard Cite

As sites of cellular respiration and energy production, mitochondria play a central role in cell metabolism. Cell differentiation is associated with an increase in mitochondrial content and activity and with a metabolic shift toward increased oxidative phosphorylation activity. The opposite occurs during reprogramming of somatic cells into induced pluripotent stem cells. Studies have provided evidence of mitochondrial and metabolic changes during the differentiation of both embryonic and somatic (or adult) stem cells (SSCs), such as hematopoietic stem cells, mesenchymal stem cells, and tissue-specific progenitor cells. We thus propose to consider those mitochondrial and metabolic changes as hallmarks of differentiation processes. We review how mitochondrial biogenesis, dynamics, and function are directly involved in embryonic and SSC differentiation and how metabolic and sensing pathways connect mitochondria and metabolism with cell fate and pluripotency. Understanding the basis of the crosstalk between mitochondria and cell fate is of critical importance, given the promising application of stem cells in regenerative medicine. In addition to the development of novel strategies to improve the in vitro lineage-directed differentiation of stem cells, understanding the molecular basis of this interplay could lead to the identification of novel targets to improve the treatment of degenerative diseases.

show abstract

“…AMPKα activation can inhibit lipid biosynthesis, accelerating the decomposition of lipid to reducing liver fat accumulation [10]. Sirt1 is an NAD-dependent deacetylase and has been reported to have many beneficial effects for controlled glucose homeostasis, lipid metabolism, and insulin resistance in the liver tissue of obese mice [12]. In our current experiment, we found that HFD obese mice treated with fisetin express increased level of sirt1 and pAMPKα in liver tissue, and FL83B hepatocyte experiments demonstrated that fisetin significantly promotes sirt1 and pAMPKα expression in vitro.…”

Section: Fig 10mentioning

confidence: 99%

Fisetin Protects Against Hepatic Steatosis Through Regulation of the Sirt1/AMPK and Fatty Acid β-Oxidation Signaling Pathway in High-Fat Diet-Induced Obese Mice

Liou

Wei

Chen

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Fisetin is a naturally abundant flavonoid isolated from various fruits and vegetables that was recently identified to have potential biological functions in improving allergic airway inflammation, as well as anti-oxidative and anti-tumor properties. Fisetin has also been demonstrated to have anti-obesity properties in mice. However, the effect of fisetin on nonalcoholic fatty liver disease (NAFLD) is still elusive. Thus, the present study evaluated whether fisetin improves hepatic steatosis in high-fat diet (HFD)-induced obese mice and regulates lipid metabolism of FL83B hepatocytes in vitro. Methods: NAFLD was induced by HFD in male C57BL/6 mice. The mice were then injected intraperitoneally with fisetin for 10 weeks. In another experiment, FL83B cells were challenged with oleic acid to induce lipid accumulation and treated with various concentrations of fisetin. Results: NAFLD mice treated with fisetin had decreased body weight and epididymal adipose tissue weight compared to NAFLD mice. Fisetin treatment also reduced liver lipid droplet and hepatocyte steatosis, alleviated serum free fatty acid, and leptin concentrations, significantly decreased fatty acid synthase, and significantly increased phosphorylation of AMPKα and the production of sirt-1 and carnitine palmitoyltransferase I in the liver tissue. In vitro, fisetin decreased lipid accumulation and increased lipolysis and β-oxidation in hepatocytes. Conclusion: This study suggests that fisetin is a potential novel treatment for alleviating hepatic lipid metabolism and improving NAFLD in mice via activation of the sirt1/AMPK and β-oxidation pathway.

show abstract

Role of SIRT1 and AMPK in mesenchymal stem cells differentiation

Cited by 93 publications

References 124 publications

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Connecting Mitochondria, Metabolism, and Stem Cell Fate

Fisetin Protects Against Hepatic Steatosis Through Regulation of the Sirt1/AMPK and Fatty Acid β-Oxidation Signaling Pathway in High-Fat Diet-Induced Obese Mice

Contact Info

Product

Resources

About