NIPSNAP3A regulates cellular homeostasis by modulating mitochondrial dynamics.

Autor: Yan R; Department of Emergency and Critical Disease, Songjiang Research Institute, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China., Chen L; Department of Emergency and Critical Disease, Songjiang Research Institute, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China., Cai Z; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China., Tang J; Cixi Biomedical Research Institute, Wenzhou Medical University, Zhejiang 315302, China., Zhu Y; Cixi Biomedical Research Institute, Wenzhou Medical University, Zhejiang 315302, China., Li Y; Institute of Precision Medicine, Jining Medical University, Jining 272067, China., Wang X; Department of Emergency and Critical Disease, Songjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 201600, China. Electronic address: 734001472@shsmu.edu.cn., Ruan Y; Department of Emergency and Critical Disease, Songjiang Research Institute, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address: yuruan@sjtu.edu.cn., Han Q; Department of Emergency and Critical Disease, Songjiang Research Institute, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201600, China; Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China. Electronic address: qihan8@shsmu.edu.cn.
Jazyk: angličtina
Zdroj: Gene [Gene] 2025 Jan 15; Vol. 933, pp. 148976. Date of Electronic Publication: 2024 Oct 01.
DOI: 10.1016/j.gene.2024.148976
Abstrakt: Mitochondria are essential for cell metabolism and survival as they produce the majority of cellular ATP through oxidative phosphorylation as well as regulate critical processes such as cell proliferation and apoptosis. NIPSNAP family of proteins are predominantly mitochondrial matrix proteins. However, the molecular and cellular functions of the NIPSNAPs, particularly NIPSNAP3A, have remained elusive. Here, we demonstrated that NIPSNAP3A knockdown in HeLa cells inhibited their proliferation and migration and attenuated apoptosis induced by Actinomycin D (Act-D). These findings suggested a complex relationship between cellular processes and mitochondrial functions, mediated by NIPSNAP3A. Further investigations revealed that NIPSNAP3A knockdown not only inhibited mitochondrial fission through reduction of DRP1-S616, but also suppressed cytochrome c release in apoptosis. Collectively, our findings highlight the critical role of NIPSNAP3A in coordinating cellular processes, likely through its influence on mitochondrial dynamics.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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