WDR26/MIP2 interacts with VDAC1 and regulates VDAC1 expression levels in H9c2 cells

Jiang, Lei; Wang, Hao; Guang-bin, Chen; Feng, Yan; Zou, Jian; Liu, Meidong; Liu, Ke; Wang, Nian; Zhang, Huali; Wang, Kangkai; Xiao, Xianzhong

doi:10.1016/j.freeradbiomed.2017.12.015

Cited by 12 publications

(8 citation statements)

References 48 publications

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“…Our study demonstrated that VDAC1 knockdown weakened BPA-exposed cell apoptosis and attenuated BPA-inhibited cell viability of spermatogonia. A study found that VDAC1 silencing protectes cardiomyocyte from cytotoxic effect of H 2 O 2 as evidenced by reducing in LDH activity and dead cell number (Jiang et al, 2018). Knockdown of VDAC1 inhibits cell death on in vitro model of oxidative stress (de Sousa et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of VDAC1 prevents oxidative stress and apoptosis induced by bisphenol A in spermatogonia via AMPK/mTOR signaling pathway

Wang

Liu

et al. 2023

J. Toxicol. Sci.

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Bisphenol A (BPA), one of the main components of industrial products, is clinically associated with the increased male infertility rate. However, the underlying molecular mechanism of the BPA-resulted reproductive toxicity is not fully elucidated. Voltage-dependent anion channel 1 (VDAC1) is a pore protein and located at the outer mitochondrial membrane. As a mitochondrial gatekeeper, VDAC1 controls the release of reactive oxygen species (ROS) and the metabolic and energetic functions of mitochondria, and serves as a critical player in mitochondrial-mediated apoptosis. Herein, we explored the role of VDAC1 in BPA-induced apoptosis of spermatogonia. The results showed that BPA increased spermatogonia cell line GC-1 spg cell apoptosis and intracellular ROS level, and suppressed AMPK/mTOR signaling pathway at a dose of 80 μM for 48 hr. Lentivirus-mediated short hairpin RNA targeting VDAC1 (Lv-shVDAC1) silenced VDAC1 expression and enhanced BPA-restricted cell viability. Knockdown of VDAC1 inhibited the apoptosis of BPA-treated GC-1 spg cells determined by with changes of the expressions of pro-apoptotic and anti-apoptotic proteins. Knockdown of VDAC1 also alleviated the BPA-triggered intracellular ROS generation and oxidative stress. Moreover, silence of VDAC1 increased AMPKα1/2 phosphorylation and suppressed mTOR phosphorylation under BPA exposure. Dorsomorphin, an AMPK inhibitor, partially abolished the effects of VDAC1 gene silencing on BPA-stimulated GC-1 spg cells. In conclusion, inhibition of VDAC1 attenuated the BPA-induced oxidative stress and apoptosis and promoted the cell viability in spermatogonia through modulating AMPK/mTOR signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Inhibition of VDAC1 prevents oxidative stress and apoptosis induced by bisphenol A in spermatogonia via AMPK/mTOR signaling pathway

Wang

Liu

et al. 2023

J. Toxicol. Sci.

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“…MIP2 is located in mitochondria, one of the WDR26 subtypes, and protects cells from oxidative stress. The co-IP assay was used to isolate the MIP2 protein complex from the rat heart, and mass spectrometry analysis showed that there was an interaction between Vdac1 and MIP2 26 . Overexpression of MIP2 reduced the increase and cell damage of HO-induced Vdac1, while the loss of MIP2 aggravated the increase and cell damage of HO-treated H9c2 cells 26,27 .…”

Section: Discussionmentioning

confidence: 99%

“…The co-IP assay was used to isolate the MIP2 protein complex from the rat heart, and mass spectrometry analysis showed that there was an interaction between Vdac1 and MIP2 26 . Overexpression of MIP2 reduced the increase and cell damage of HO-induced Vdac1, while the loss of MIP2 aggravated the increase and cell damage of HO-treated H9c2 cells 26,27 . The protective effect of MIP2 on antioxidant stress of cardiomyocytes was partly related to the interaction with Vdac1, thus inhibiting its expression.…”

Section: Discussionmentioning

confidence: 99%

Salvianic Acid A Sodium Promotes the Recovery of Motor Function After Spinal Cord Injury in Rats by Reducing Microglia Inflammation through Regulating MIP2/Vdac1/Ndufa12 Signaling Axis

Liu

Zhao

et al. 2020

Orthopaedic Surgery

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Objective: To clarify the effects on and the mechanism of salvianic acid A sodium (SAAS) in the recovery of motor function after spinal cord injury. Methods: In vivo and in vitro experiments were carried out in this research to determine the effects of SAAS on tissue damage, neuron survival, microglia polarization, and inflammation after spinal cord injury (SCI). Differentially expressed genes treated with SAAS were screened by transcriptome sequencing, and the molecular mechanism was investigated simultaneously. Results: The results revealed that SAAS could promote type M2 polarization of microglia and reduce the proportion of type M1. In this way, it reduced the secretion and expression of inflammatory factors. Compared with Lipopolysaccharides(LPS), 345 genes were upregulated and 407 genes were downregulated in the LPS + SAAS treatment group. In the SAAS group, expression levels of Ndufa12, IL-6, TNF-α, and Vdac1 were significantly reduced, while a marked elevation was found in MIP2. In addition, results found in an animal model showed that SAAS could obviously facilitate motor function recovery of mice after spinal cord injury, and it had a good protective effect on spinal cord tissue and neuron cells. Conclusion: As a result, the present study clarified both the protective effect of SAAS on neurons after spinal cord injury and the anti-inflammatory effect of microglia, which is expected to serve as a theoretical basis for clinical treatment.

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“…One of the VDAC1 regulated mechanisms is to protect cardiac function by inhibiting the expression of VDAC1. For example, in H 2 O 2 -treated H9C2 cells, MIP2 can bind to VDAC1 and inhibit its expression, alleviating H 2 O 2 -induced cell damage ( 50 ).…”

Section: Production Of Ros At Mamsmentioning

confidence: 99%

The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases

Zhao

Li²,

Li³

et al. 2022

Front. Cardiovasc. Med.

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Reactive oxygen species (ROS) metabolism is essential for the homeostasis of cells. Appropriate production of ROS is an important signaling molecule, but excessive ROS production can damage cells. ROS and ROS-associated proteins can act as damage associated molecular pattern molecules (DAMPs) to activate the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in cardiovascular diseases. Previous studies have shown that there are connected sites, termed mitochondria-associated membranes (MAMs), between mitochondria and the endoplasmic reticulum. In cardiovascular disease progression, MAMs play multiple roles, the most important of which is the ability to mediate ROS generation, which further activates the NLPR3 inflammasome, exacerbating the progression of disease. In this review, the following topics will be covered: 1. Molecular structures on MAMs that can mediate ROS generation; 2. Specific mechanisms of molecule-mediated ROS generation and the molecules' roles in cardiovascular disease, 3. The effects of MAMs-mediated ROS on the NLRP3 inflammasome in cardiovascular disease. The purpose of this review is to provide a basis for subsequent clinical treatment development.

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WDR26/MIP2 interacts with VDAC1 and regulates VDAC1 expression levels in H9c2 cells

Cited by 12 publications

References 48 publications

Inhibition of VDAC1 prevents oxidative stress and apoptosis induced by bisphenol A in spermatogonia via AMPK/mTOR signaling pathway

Inhibition of VDAC1 prevents oxidative stress and apoptosis induced by bisphenol A in spermatogonia via AMPK/mTOR signaling pathway

Salvianic Acid A Sodium Promotes the Recovery of Motor Function After Spinal Cord Injury in Rats by Reducing Microglia Inflammation through Regulating MIP2/Vdac1/Ndufa12 Signaling Axis

The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases

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