Salidroside mediated stabilization of Bcl -xL prevents mitophagy in CA3 hippocampal neurons during hypoxia

Biswal, Suryanarayan; Barhwal, Kalpana; Das, Debarati; Dhingra, Richa; Dhingra, Nilima; Nag, Tapas Chanda; Hota, Sunil Kumar

doi:10.1016/j.nbd.2018.04.019

Cited by 24 publications

(9 citation statements)

References 33 publications

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“…However, other previous studies have also suggested that salidroside can increase hypoxia and hydrogen peroxide-induced autophagy in pulmonary arterial smooth muscle cells and human umbilical vein endothelial cells through downregulation of mTOR signaling (57,58). Salidroside has also been documented to inhibit autophagy in primary cortical neurons of neonatal Sprague-Dawley rats exposed to glutamate (59) and suppress the mitophagy process in the hippocampal CA3 neurons after chronic hypobaric hypoxia injury (60). Additionally, salidroside alleviated hepatic autophagy in mouse models of hepatic ischemia-reperfusion injury and hepatic fibrosis (61,62).…”

Section: Discussionmentioning

confidence: 94%

Rhodiola Crenulata ameliorates exhaustive exercise‑induced fatigue in mice by suppressing mitophagy in skeletal muscle

et al. 2020

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The aim of present study was to evaluate the potential effects of Rhodiola crenulata oral liquid (RCOL) on exhaustive exercise (EE)-induced fatigue in mice. Male Institute of Cancer Research mice from five treatment groups (n=10 per group) were orally administered with sterilized water for the Control and EE groups and/or RCOL at doses of 1.02, 3.03 and 6.06 ml/kg/day, once daily for 2 weeks. Anti-fatigue activity was subsequently evaluated by measuring the levels of creatine kinase (CK), lactic acid (LA), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and total anti-oxidative capability (T-AOC). Histopathology was assessed using hematoxylin and eosin staining. Ultrastructures of mitochondria were observed by transmission electron microscopy. Energy supply capacity was assessed using citrate synthase (CS), succinate dehydrogenase (SDH), Na +-K +-ATPase, and liver and quadriceps glycogen content assays. Expression levels of mRNA and protein associated with mitophagy in the skeletal muscle were measured by reverse transcription-quantitative PCR and western blotting, respectively. RCOL was observed to markedly inhibit fatigue-induced oxidative stress by increasing the activities of SOD, CAT and T-AOC, whilst reducing the accumulation of LA, CK, LDH and MDA. Histological analysis of the quadriceps femoris tissue suggested increased numbers of muscle fibers in the RCOL groups compared with those in the EE group. RCOL administration was found to reverse EE-induced mitochondrial structural damage and alleviated defects inflicted onto the energy supply mechanism by increasing CS, SDH, Na +-K +-ATPase and glycogen levels. Additionally, RCOL reduced the protein expression of PTEN-induced kinase 1 (PINK1), Parkin, microtubule-associated proteins 1A/1B light chain 3, sequestosome 1 and ubiquitin, whilst lowering the gene expression of PINK1 and Parkin. Taken together, results from the present study clarified the anti-fatigue effect of RCOL, where the underlying mechanism may be associated with increased antioxidant activity, enhanced energy production and the inhibition of mitophagy by suppressing the PINK1/Parkin signaling pathway.

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Section: Discussionmentioning

confidence: 94%

Rhodiola Crenulata ameliorates exhaustive exercise‑induced fatigue in mice by suppressing mitophagy in skeletal muscle

et al. 2020

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“…While under hypoxia condition, BCL2L1 is hydrolyzed, and PGAM5 is released. Activated PGAM5 dephosphorylates FUNDC1 at S13 and promotes the interaction between FUNDC1 and LC3, thereby inducing mitophagy ( Wu et al, 2014a ; Kuang et al, 2016 ; Biswal et al, 2018 ). In addition, FUNDC1 is phosphorylated by unc-51 like autophagy activating kinase 1 (ULK1) at S17 site under hypoxic condition ( Wu et al, 2014b ).…”

Section: The Regulatory Proteins Of Fundc1-mediated Mitophagymentioning

confidence: 99%

The multi-faced role of FUNDC1 in mitochondrial events and human diseases

Tan

Liu

Wang

et al. 2022

Front. Cell Dev. Biol.

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Mitophagy plays a vital role in the selective elimination of dysfunctional and unwanted mitochondria. As a receptor of mitophagy, FUN14 domain containing 1 (FUNDC1) is attracting considerably critical attention. FUNDC1 is involved in the mitochondria fission, the clearance of unfolded protein, iron metabolism in mitochondria, and the crosstalk between mitochondria and endoplasmic reticulum besides mitophagy. Studies have demonstrated that FUNDC1 is associated with the progression of ischemic disease, cancer, and metabolic disease. In this review, we systematically examine the recent advancements in FUNDC1 and the implications of this protein in health and disease.

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“…13 Recent studies suggested that mitochondrial protein FUNDC1 might mediate mitophagy and act a crucial part in the selective clearance of damaged mitochondria. 14,15 In mitochondria, ULK1 phosphorylates mitochondria membrane protein Fun14 domain containing protein 1 (FUNDC1) to enhance FUNDC1 binding to microtubule-associated protein light chain 3 (LC3) to induce autophagy. 16 Therefore, we hypothesized that EA treatment might protect neuronal cells from I/R injury by activating the mTOR signaling to suppress ULK1/FUNDC1/LC3Àdependent autophagy.…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture Pretreatment Alleviates Cerebral Ischemia-Reperfusion Injury by Regulating Mitophagy via mTOR-ULK1/FUNDC1 Axis in Rats

Tian

Zhu

Zhou

et al. 2022

Journal of Stroke and Cerebrovascular Diseases

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Salidroside mediated stabilization of Bcl -xL prevents mitophagy in CA3 hippocampal neurons during hypoxia

Cited by 24 publications

References 33 publications

Rhodiola Crenulata ameliorates exhaustive exercise‑induced fatigue in mice by suppressing mitophagy in skeletal muscle

Rhodiola Crenulata ameliorates exhaustive exercise‑induced fatigue in mice by suppressing mitophagy in skeletal muscle

The multi-faced role of FUNDC1 in mitochondrial events and human diseases

Electroacupuncture Pretreatment Alleviates Cerebral Ischemia-Reperfusion Injury by Regulating Mitophagy via mTOR-ULK1/FUNDC1 Axis in Rats

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