Mitophagy protects SH-SY5Y neuroblastoma cells against the TNFα-induced inflammatory injury: Involvement of microRNA-145 and Bnip3

Liu, Huawei; Huang, Haitao; Li, Runxin; Bi, Wenting; Lin, Feng; Lingling, E; Hu, Min; Wei, Wen Bin

doi:10.1016/j.biopha.2018.10.123

Cited by 25 publications

(10 citation statements)

References 58 publications

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“…Studies show that mitophagy plays a protective role in liver [ 17 ] and lung [ 18 , 19 ]. In the brain and heart, however, the role of mitophagy remains elusive, it can be protective or detrimental [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury

et al. 2020

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In the present study, we hypothesized that hypoxia-inducible factor 1α (HIF-1α)-mediated mitophagy plays a protective role in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI). Mitophagy was evaluated by measuring the changes of mitophagy flux, mitochondria DNA copy number, and the changes of mitophagy-related proteins including translocase of outer mitochondrial membrane 20 (TOMM20), cytochrome c oxidase IV (COX IV), microtubule-associated protein 1 light chain 3B (LC3B), and mitochondria adaptor nucleoporin p62 in HK2 cells, a human tubular cell line. Results show that HIF-1α knockout significantly attenuated hypoxia/reoxygenation (H/R)-induced mitophagy, aggravated H/R-induced apoptosis, and increased the production of reactive oxygen species (ROS). Similarly, H/R induced significantly increase in Bcl-2 19-kDa interacting protein 3 (BNIP3), a downstream regulator of HIF-1α. Notably, BNIP3 overexpression reversed the inhibitory effect of HIF-1α knockout on H/R-induced mitophagy, and prevented the enhancing effect of HIF-1α knockout on H/R-induced apoptosis and ROS production. For in vivo study, we established HIF-1α flox/flox ; cadherin-16-cre mice in which tubular HIF-1α was specifically knockout. It was found that tubular HIF-1α knockout significantly inhibited I/R-induced mitophagy, and aggravated I/R-induced tubular apoptosis and kidney damage. In contrast, adenovirus-mediated BNIP3 overexpression significantly reversed the decreased mitophagy, and prevented enhanced kidney damage in tubular HIF-1α knockout mice with I/R injury. In summary, our study demonstrated that HIF-1α-BNIP3-mediated mitophagy in tubular cells plays a protective role through inhibition of apoptosis and ROS production in acute kidney damage.

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Section: Introductionmentioning

confidence: 99%

HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury

et al. 2020

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“…Jin et al reported that the HIF-1 α /BNIP3 signaling pathway is associated with BDNF/TrkB-induced mitophagy in brain microvascular endothelial cell injury [ 61 ]. A valuable article pointed out that BNIP3-mediated mitophagy protects SH-SY5Y neuroblastoma cells against TNF α -induced inflammatory injury [ 62 ]. O'Sullivan et al revealed the functional importance of BNIP3-mediated mitophagy in promoting the generation of natural killer cell memory [ 63 ].…”

Section: Mitophagymentioning

confidence: 99%

The Role of Mitophagy in Regulating Cell Death

Zhang

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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Mitochondria are multifaceted organelles that serve to power critical cellular functions, including act as power generators of the cell, buffer cytosolic calcium overload, production of reactive oxygen species, and modulating cell survival. The structure and the cellular location of mitochondria are critical for their function and depend on highly regulated activities such as mitochondrial quality control (MQC) mechanisms. The MQC is regulated by several sets of processes: mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy, and other mitochondrial proteostasis mechanisms such as mitochondrial unfolded protein response (mtUPR) or mitochondrial-derived vesicles (MDVs). These processes are important for the maintenance of mitochondrial homeostasis, and alterations in the mitochondrial function and signaling are known to contribute to the dysregulation of cell death pathways. Recent studies have uncovered regulatory mechanisms that control the activity of the key components for mitophagy. In this review, we discuss how mitophagy is controlled and how mitophagy impinges on health and disease through regulating cell death.

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“…BNIP3 (B Lymphoma-2 gene/adenovirus E1B interacting protein 3) and NIX (BNIP3L) are pro-apoptotic mitochondrial proteins located in the outer membrane of mitochondria (Kubli et al, 2007;Liu et al, 2019;Xu et al, 2019), they have 56% homology in amino acid sequence. Under certain conditions, the LIR sequence interacts with the recruited autophagy related protein, LC3, to form an autophagosome to clear the damaged mitochondria (Springer and Macleod, 2016;Šprung et al, 2018;Roperto et al, 2019).…”

Section: Bnip3/nix Pathway In Mitochondrial Autophagymentioning

confidence: 99%

Research Progress on the Mechanism of Mitochondrial Autophagy in Cerebral Stroke

Yang

Lü

et al. 2021

Front. Aging Neurosci.

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Mitochondrial autophagy is an early defense and protection process that selectively clears dysfunctional or excessive mitochondria through a distinctive mechanism to maintain intracellular homeostasis. Mitochondrial dysfunction during cerebral stroke involves metabolic disbalance, oxidative stress, apoptosis, endoplasmic reticulum stress, and abnormal mitochondrial autophagy. This article reviews the research progress on the mechanism of mitochondrial autophagy in ischemic stroke to provide a theoretical basis for further research on mitochondrial autophagy and the treatment of ischemic stroke.

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Mitophagy protects SH-SY5Y neuroblastoma cells against the TNFα-induced inflammatory injury: Involvement of microRNA-145 and Bnip3

Cited by 25 publications

References 58 publications

HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury

HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury

The Role of Mitophagy in Regulating Cell Death

Research Progress on the Mechanism of Mitochondrial Autophagy in Cerebral Stroke

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