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CARD9 蛋白 SUMOylation 调节 HOXB5 核转位和 Parkin 介导的心肌 I/R 损伤中的线粒体自噬。

CARD9 protein SUMOylation regulates HOXB5 nuclear translocation and Parkin-mediated mitophagy in myocardial I/R injury.

机构信息

Department of Medicine, Hunan Traditional Chinese Medical College, Zhuzhou, Hunan, People's Republic of China.

Department of Pathology, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha, Hunan, People's Republic of China.

出版信息

J Cell Mol Med. 2024 Nov;28(21):e70195. doi: 10.1111/jcmm.70195.

DOI:10.1111/jcmm.70195
PMID:39496070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11534265/
Abstract

Myocardial injury induced by ischemia-reperfusion (I/R) remains a difficult clinical problem. However, the exact mechanisms underlying I/R-induced have yet to be clarified. CARD9 is an important cytoplasmic-binding protein. In this study, an immunocoprecipitation assay showed that SUMOylation of the CARD9 protein promoted the binding of CARD9 to HOXB5, but hindered the O-GlcNAc glycosylation of HOXB5, a predicted transcription factor of Parkin and a key factor in mitophagy. O-GlcNAc glycosylation is an important signal for translocation of proteins from the cytoplasm to the nucleus. CARD9 protein SUMOylation is regulated by PIAS3, which is related to I/R-induced myocardial injury. Therefore, we propose that knockdown of PIAS3 inhibits SUMOylation of the CARD9 protein, facilitates the dissociation of CARD9 and HOXB5, which increases the O-GlcNAc-mediated glycosylation of HOXB5, while the resulting HOXB5 nuclear translocation promotes Parkin-induced mitophagy and alleviates myocardial I/R injury.

摘要

缺血再灌注（I/R）引起的心肌损伤仍然是一个临床难题。然而，I/R 诱导损伤的确切机制尚未阐明。CARD9 是一种重要的细胞质结合蛋白。在这项研究中，免疫沉淀实验表明，CARD9 蛋白的 SUMO 化促进了 CARD9 与 HOXB5 的结合，但阻碍了 HOXB5 的 O-GlcNAc 糖基化，HOXB5 是 Parkin 的一个预测转录因子，也是线粒体自噬的关键因素。O-GlcNAc 糖基化是蛋白质从细胞质向核内易位的重要信号。CARD9 蛋白的 SUMO 化受 PIAS3 调节，PIAS3 与 I/R 诱导的心肌损伤有关。因此，我们提出敲低 PIAS3 抑制 CARD9 蛋白的 SUMO 化，促进 CARD9 和 HOXB5 的解离，增加 HOXB5 的 O-GlcNAc 介导的糖基化，而由此产生的 HOXB5 核转位促进 Parkin 诱导的线粒体自噬，减轻心肌 I/R 损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5899/11534265/507934e365cf/JCMM-28-e70195-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5899/11534265/1914b6f0e674/JCMM-28-e70195-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5899/11534265/507934e365cf/JCMM-28-e70195-g002.jpg

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