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Hao Zhou, Pingjun Zhu, Jin Wang, Hong Zhu, Jun Ren, Yundai Chen
Disturbed mitochondrial homeostasis contributes to the pathogenesis of cardiac ischemia reperfusion (IR) injury, although the underlying mechanism remains elusive. Here, we demonstrated that casein kinase 2α (CK2α) was upregulated following acute cardiac IR injury. Increased CK2α was shown to be instrumental to mitochondrial damage, cardiomyocyte death, infarction area expansion and cardiac dysfunction, whereas cardiac-specific CK2α knockout (CK2αCKO ) mice were protected against IR injury and mitochondrial damage...
March 14, 2018: Cell Death and Differentiation
Yufeng Li, Zhiwei Liu, Yiqian Zhang, Qixiang Zhao, Xiaoyu Wang, Peng Lu, Hao Zhang, Zhu Wang, Hongyan Dong, Zhongming Zhang
Pigment epithelial-derived factor (PEDF) is known to exert diverse physiological activities. Previous studies suggest that hypoxia could induce mitophagy. Astoundingly, under hypoxic condition, we found that PEDF decreased the mitochondrial density of cardiomyocytes. In this study, we evaluated whether PEDF could decrease the mitochondrial density and play a protective role in hypoxic cardiomyocytes via promoting mitophagy. Immunostaining and western blotting were used to analyze mitochondrial density and mitophagy of hypoxic cardiomyocytes...
March 6, 2018: International Journal of Molecular Medicine
Xin Wang, Xiqiong Han, Naifeng Liu
No abstract text is available yet for this article.
August 2017: Atherosclerosis
Juan Pablo Muñoz, Antonio Zorzano
No abstract text is available yet for this article.
December 5, 2017: Circulation
Shengnan Wu, Qiulun Lu, Qilong Wang, Ye Ding, Zejun Ma, Xiaoxiang Mao, Kai Huang, Zhonglin Xie, Ming-Hui Zou
BACKGROUND: FUN14 domain containing 1 (FUNDC1) is a highly conserved outer mitochondrial membrane protein. The aim of this study is to examine whether FUNDC1 modulates the mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), mitochondrial morphology, and function in cardiomyocytes and intact hearts. METHODS: The impacts of FUNDC1 on MAMs formation and cardiac functions were studied in mouse neonatal cardiomyocytes, in mice with cardiomyocyte-specific Fundc1 gene knockout ( Fundc1 f/Y /Cre αMyHC+/- ), and in the cardiac tissues of the patients with heart failure...
December 5, 2017: Circulation
Xiaomei Wu, Fei-Hua Wu, Qianrong Wu, Shu Zhang, Suping Chen, Matthew Sima
As animals evolved to use oxygen as the main strategy to produce ATP through the process of mitochondrial oxidative phosphorylation, the ability to adapt to fluctuating oxygen concentrations is a crucial component of evolutionary pressure. Three mitophagy receptors, FUNDC1, BNIP3 and NIX, induce the removal of dysfunctional mitochondria (mitophagy) under prolonged hypoxic conditions in mammalian cells, to maintain oxygen homeostasis and prevent cell death. However, the evolutionary origins and structure-function relationships of these receptors remain poorly understood...
2017: Frontiers in Physiology
Hao Zhou, Dandan Li, Pingjun Zhu, Shunying Hu, Nan Hu, Sai Ma, Ying Zhang, Tianwen Han, Jun Ren, Feng Cao, Yundai Chen
Platelet activation is a major (patho-) physiological mechanism that underlies ischemia/reperfusion (I/R) injury. In this study, we explored the molecular signals for platelet hyperactivity and investigated the beneficial effects of melatonin on platelet reactivity in response to I/R injury. After reperfusion, peroxisome proliferator-activated receptor γ (PPARγ) was progressively downregulated in patients with acute myocardial infarction undergoing coronary artery bypass grafting (CABG) surgery and in mice with I/R injury model...
November 2017: Journal of Pineal Research
Hao Zhou, Pingjun Zhu, Jun Guo, Nan Hu, Shuyi Wang, Dandan Li, Shunying Hu, Jun Ren, Feng Cao, Yundai Chen
Ripk3-required necroptosis and mitochondria-mediated apoptosis are the predominant types of cell death that largely account for the development of cardiac ischemia reperfusion injury (IRI). Here, we explored the effect of Ripk3 on mitochondrial apoptosis. Compared with wild-type mice, the infarcted area in Ripk3-deficient (Ripk3(-/-)) mice had a relatively low abundance of apoptotic cells. Moreover, the loss of Ripk3 protected the mitochondria against IRI and inhibited caspase9 apoptotic pathways. These protective effects of Ripk3 deficiency were relied on mitophagy activation...
July 13, 2017: Redox Biology
Hailing Hou, Puchun Er, Jingjing Cheng, Xiuli Chen, Xiaofeng Ding, Yuwen Wang, Xi Chen, Zhiyong Yuan, Qingsong Pang, Ping Wang, Dong Qian
FUN14 domain containing 1 (FUNDC1) is an important molecule in receptor-dependent mitophagy. However, the roles of FUNDC1 in human cancer biology remain unknown. The aim of this study was to explore the expression and roles of FUNDC1 in cervical cancer. Immunohistochemistry and Western blotting were applied to detect the expression of FUNDC1, and small-hairpin RNA was applied to inhibit the expression of endogenous FUNDC1 in cervical cancer cells. MTT assays and Flow cytometric analysis were applied to examine cell proliferation and apoptosis...
August 2017: Cancer Medicine
Vladimir V Rogov, Alexandra Stolz, Arvind C Ravichandran, Diana O Rios-Szwed, Hironori Suzuki, Andreas Kniss, Frank Löhr, Soichi Wakatsuki, Volker Dötsch, Ivan Dikic, Renwick Cj Dobson, David G McEwan
Through the canonical LC3 interaction motif (LIR), [W/F/Y]-X1-X2-[I/L/V], protein complexes are recruited to autophagosomes to perform their functions as either autophagy adaptors or receptors. How these adaptors/receptors selectively interact with either LC3 or GABARAP families remains unclear. Herein, we determine the range of selectivity of 30 known core LIR motifs towards individual LC3s and GABARAPs. From these, we define a G ABARAP I nteraction M otif (GIM) sequence ([W/F]-[V/I]-X2-V) that the adaptor protein PLEKHM1 tightly conforms to...
August 2017: EMBO Reports
S Y Deng, Y H Ai, H Gong, L Wu, C X Chen, Y M Wang, Z Y Liu, L Huang, Q Y Peng, L N Zhang
Objective: To investigate the effect of neuroglobin on oxygen-glucose deprivation and reoxygenation (OGD/R) induced autophagy in a human neuroblastoma cell line (SH-SY5Y). Methods: SH-SY5Y cells were transfected with plasmids (or vector) to establish a stable cell line of NGB overexpression (OE). After treated with OGD/R, cells were collected for the analyses of mRNA (Atg5, Atg7, BECN1 and FUNDC1) and protein levels of LC3. Furthermore, mitochondrial and cytosolic fractions were isolated for protein levels of PINK1 and Parkin...
May 23, 2017: Zhonghua Yi Xue za Zhi [Chinese medical journal]
Grace Gy Lim, Kah-Leong Lim
Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the selective clearance of mitochondria in the absence of Parkin. In this issue, Bhujabal et al expand the repertoire of Parkin-independent mitophagy receptors to include the anti-apoptotic protein, FKBP8. The authors demonstrate that FKBP8 interacts preferentially with LC3A via its LIR motif to destroy damaged mitochondria...
June 2017: EMBO Reports
Gongyu Xu, Zhenzhen Li, Jinwen Xiao, Fangqing Li, Weiyuan Ye, Haobin Zhao, Qingchun Zhou, Xueping Zhong
Fundc1 is a mitochondrial outer membrane protein and plays important roles in mitochondria fission and hypoxia-induced mitophagy in mammalian cells. However, there is no relevant report of fundc1 in fish. In the present study, we cloned a 942bp fundc1 cDNA from rare minnow. The cDNA, designated as Grfundc1 cDNA, contains an open reading frame (ORF) of 459bp which encodes a polypeptide of 152 amino acid residues. Comparisons of deduced amino acid sequences demonstrated that Grfundc1 was highly homologous with those of other vertebrates...
August 30, 2017: Gene
Ziheng Chen, Sami Siraj, Lei Liu, Quan Chen
Mitophagy is responsible for removal of damaged mitochondria and is therefore a fundamental process in mitochondrial quality control. Both ubiquitin-dependent and receptor-dependent pathways are considered to mediate mitophagy. These distinct mechanisms may be activated in response to distinct mitochondrial stresses. An intriguing question is whether and how crosstalk occurs between the distinct pathways to coordinate mitophagy. We have uncovered a striking piece of evidence to demonstrate that the mitophagy receptor FUNDC1 is a substrate of MARCH5, a mitochondrially localized E3 ubiquitin ligase...
July 3, 2017: Autophagy
Zambarlal Bhujabal, Åsa B Birgisdottir, Eva Sjøttem, Hanne B Brenne, Aud Øvervatn, Sabrina Habisov, Vladimir Kirkin, Trond Lamark, Terje Johansen
Mitophagy, the selective removal of damaged or excess mitochondria by autophagy, is an important process in cellular homeostasis. The outer mitochondrial membrane (OMM) proteins NIX, BNIP3, FUNDC1, and Bcl2-L13 recruit ATG8 proteins (LC3/GABARAP) to mitochondria during mitophagy. FKBP8 (also known as FKBP38), a unique member of the FK506-binding protein (FKBP) family, is similarly anchored in the OMM and acts as a multifunctional adaptor with anti-apoptotic activity. In a yeast two-hybrid screen, we identified FKBP8 as an ATG8-interacting protein...
June 2017: EMBO Reports
Pierre Vigié, Nadine Camougrand
Mitochondria are highly dynamic organelles that provide essential metabolic functions and represent the major bioenergetic hub of eukaryotic cells. Mitochondrial dysfunctions are implicated in numerous diseases. Therefore, maintenance of a healthy pool of mitochondria is required for cellular function and survival. Mitochondrial quality control is achieved through several mechanisms that act at different levels: proteases and chaperones, the Ubiquitin-Proteasome-System (UPS) and mitophagy. Multiple mitophagy-involved programs operate independently or undergo crosstalk, and require modulated receptor activities at the outer membranes of mitochondria...
March 2017: Médecine Sciences: M/S
Weilin Zhang, Sami Siraj, Rong Zhang, Quan Chen
Mitophagy plays pivotal roles in the selective disposal of unwanted mitochondria, and accumulation of damaged mitochondria has been linked to aging-related diseases. However, definitive proof that mitophagy regulates mitochondrial quality in vivo is lacking. It is also largely unclear whether damaged mitochondria are the cause or just the consequence of these diseases. We previously showed that FUNDC1 is a mitophagy receptor that interacts with LC3 to mediate mitophagy in response to hypoxia in cultured cells...
June 3, 2017: Autophagy
Won Hee Jang, Young Joo Jeong, Sun Hee Choi, Sang-Hwa Urm, Dae-Hyun Seog
Kinesin 1 is a member of the kinesin superfamily proteins (KIFs) of microtubule-dependent molecular motor proteins that transport organelles and protein complexes in cells. Kinesin 1 consists of a homo- or hetero-dimer of kinesin heavy chains (KHCs), often, although not always, associated with two kinesin light chains (KLCs). KLCs are non-motor proteins that associate with many different binding proteins and cargoes, but their binding partners have not yet been fully identified. In the present study, a yeast two-hybrid system was used to identify proteins that interact with the tetratricopeptide repeat (TPR) domain of KLC1...
January 2017: Biomedical Reports
Ziheng Chen, Lei Liu, Qi Cheng, Yanjun Li, Hao Wu, Weilin Zhang, Yueying Wang, Sheikh Arslan Sehgal, Sami Siraj, Xiaohui Wang, Jun Wang, Yushan Zhu, Quan Chen
Mitophagy is an essential process for mitochondrial quality control and turnover. It is activated by two distinct pathways, one dependent on ubiquitin and the other dependent on receptors including FUNDC1. It is not clear whether these pathways coordinate to mediate mitophagy in response to stresses, or how mitophagy receptors sense stress signals to activate mitophagy. We find that the mitochondrial E3 ligase MARCH5, but not Parkin, plays a role in regulating hypoxia-induced mitophagy by ubiquitylating and degrading FUNDC1...
March 2017: EMBO Reports
Weilin Zhang, He Ren, Chunling Xu, Chongzhuo Zhu, Hao Wu, Dong Liu, Jun Wang, Lei Liu, Wei Li, Qi Ma, Lei Du, Ming Zheng, Chuanmao Zhang, Junling Liu, Quan Chen
Mitochondrial dysfunction underlies many prevalent diseases including heart disease arising from acute ischemia/reperfusion (I/R) injury. Here, we demonstrate that mitophagy, which selectively removes damaged or unwanted mitochondria, regulated mitochondrial quality and quantity in vivo. Hypoxia induced extensive mitochondrial degradation in a FUNDC1-dependent manner in platelets, and this was blocked by in vivo administration of a cell-penetrating peptide encompassing the LIR motif of FUNDC1 only in wild-type mice...
December 20, 2016: ELife
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