Neuroendocrine regulation of autophagy by leptin

Malik, Shoaib Ahmad; Mariño, Guillermo; BenYounès, Amena; Shen, Shensi; Harper, Francis; Maiuri, Maria Chiara; Kroemer, Guido

doi:10.4161/cc.10.17.17067

Cited by 50 publications

(53 citation statements)

References 34 publications

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“…93 Not only can autophagy be an essential mediator for caloric restriction-elicited beneficial cardiac response, it also participates in the neuroendocrine regulation of the satiety hormone, leptin. 94 Pharmacological autophagy induction by rapamycin, spermidine and resveratrol may reduce serum leptin levels, whereas genetic inactivation of leptin promotes autophagy in peripheral tissues, including skeletal muscle, heart and liver. Paradoxically, administration of recombinant leptin triggered autophagy, the effect of which was mediated through AMPK activation and mTOR inhibition.…”

Section: Resultsmentioning

confidence: 99%

Autophagy and cardiovascular aging

Nair

Ren

2012

Cell Cycle

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Section: Resultsmentioning

confidence: 99%

Autophagy and cardiovascular aging

Nair

Ren

2012

Cell Cycle

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“…16,17 Abnormal autophagy is implicated in multiple tissues of obesity; 18 for instance, autophagosome formation is enhanced in pancreatic β cells and adipose tissue in obese mice, and enhanced autophagy was observed in advanced glycation end products (AGEs)-induced early injury of human umbilical vein endothelial cells and the process of AGEsinduced proliferation of VSMCs. 19,20 On the other hand, ER stress could trigger autophagic imbalance and defective insulin signaling in mammalian cells.…”

Section: Introductionmentioning

confidence: 99%

Intermittent injections of osteocalcin reverse autophagic dysfunction and endoplasmic reticulum stress resulting from diet-induced obesity in the vascular tissue via the NFκB-p65-dependent mechanism

Zhou¹,

Li²,

Liu³

et al. 2013

Cell Cycle

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“…Leptin is a well-known molecule that promotes cell survival both in vivo and in vitro through various mechanisms [25,26]. In addition, recent research suggested that leptin induced autophagy in cultured human or mouse cell lines [13]. In this study conducted on BMSCs, we showed that leptin knockdown reduced HPC-induced autophagy by decreasing the LC3-II and autophagosomes.…”

Section: Discussionmentioning

confidence: 52%

“…Recent reports of in vivo administration of leptin activating AMP-activated protein kinase (AMPK) phosphorylation in peripheral tissues suggests that it may influence autophagy [11,12]. In vitro studies demonstrated that leptin stimulated autophagy in cultured human or mouse cell lines, a phenomenon that was linked to the activation of AMPK as well as the inhibition of mammalian target of rapamycin (mTOR) [13].…”

mentioning

confidence: 99%

Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosis

Wang

Zhu

et al. 2014

Sci. China Life Sci.

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Autophagy is the basic catabolic progress involved in cell degradation of unnecessary or dysfunctional cellular components. It has been proven that autophagy could be utilized for cell survival under stresses. Hypoxic-preconditioning (HPC) could reduce apoptosis induced by ischemia and hypoxia/serum deprivation (H/SD) in bone marrow-derived mesenchymal stem cells (BMSCs). Previous studies have shown that both leptin signaling and autophagy activation were involved in the protection against apoptosis induced by various stress, including ischemia-reperfusion. However, it has never been fully understood how leptin was involved in the protective effects conferred by autophagy. In the present study, we demonstrated that HPC can induce autophagy in BMSCs by increased LC3-II/LC3-I ratio and autophagosome formation. Interestingly, similar effects were also observed when BMSCs were pretreated with rapamycin. The beneficial effects offered by HPC were absent when BMSCs were incubated with autophagy inhibitor, 3-methyladenine (3-MA). In addition, down-regulated leptin expression by leptin-shRNA also attenuated HPC-induced autophagy in BMSCs, which in turn was associated with increased apoptosis after exposed to sustained H/SD. Furthermore, increased AMP-activated protein kinase phosphorylation and decreased mammalian target of rapamycin phosphorylation that were observed in HPC-treated BMSCs can also be attenuated by down-regulation of leptin expression. Our data suggests that leptin has impact on HPC-induced autophagy in BMSCs which confers protection against apoptosis under H/SD, possibly through modulating both AMPK and mTOR pathway. BMSCs, autophagy, hypoxic-preconditioning, leptin, apoptosis Citation:Wang LH, Hu XY, Zhu W, Jiang Z, Zhou Y, Chen PP, Wang JA. Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosis. Sci China Life Sci, 2014Sci, , 57: 171 -180, doi: 10.1007 Although severe hypoxia can lead to cell death for certain cell types such as endothelial cells, repeated episodes of short periods' exposure to hypoxia (hypoxic-preconditioning) have shown conferring cytoprotective benefits. Research done in our laboratory and others has revealed that hypoxic-preconditioning protects bone marrow-derived mesenchymal stem cells (MSCs) from apoptosis and enhances cell survival after implantation [1,2]. However, the mechanisms underlying the beneficial effects of hypoxia preconditioned MSCs remain unclear. Autophagy is the cellular process responsible for the degradation and removal of damaged organelles and protein aggregates [3]. Autophagy is critical to cell survival. The interruption of autophagy may initiate severe energy metabolism disorder and cell death [4]. Many scientists have reported that activation of autophagy protects MSCs from apoptosis [5]. Recent cancer research demonstrates that hypoxia activates autophagy and promotes tumor cell survival [6]. We hypothesized that hypoxic-preconditioning induces autophagy of bone marrow-derived MSCs (BMS...

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Neuroendocrine regulation of autophagy by leptin

Cited by 50 publications

References 34 publications

Autophagy and cardiovascular aging

Autophagy and cardiovascular aging

Intermittent injections of osteocalcin reverse autophagic dysfunction and endoplasmic reticulum stress resulting from diet-induced obesity in the vascular tissue via the NFκB-p65-dependent mechanism

Increased leptin by hypoxic-preconditioning promotes autophagy of mesenchymal stem cells and protects them from apoptosis

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