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

Yuanbin Li, Yuting Tang, Xu Yan, Hui Lin, Wanjin Jiang, Luwei Zhang, Hu Zhao, Zhuang Chen
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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.

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CARD9 蛋白 SUMOylation 在心肌 I/R 损伤中调控 HOXB5 核转位和 Parkin 介导的有丝分裂。
缺血再灌注(I/R)诱发的心肌损伤仍然是一个棘手的临床问题。然而,I/R诱导的确切机制尚未明确。CARD9 是一种重要的细胞质结合蛋白。在这项研究中,免疫共沉淀试验显示,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,而HOXB5是预测的Parkin转录因子,也是有丝分裂的关键因素。O-GlcNAc 糖基化是蛋白质从细胞质转位到细胞核的重要信号。CARD9 蛋白的 SUMOylation 受 PIAS3 的调控,而 PIAS3 与 I/R 诱导的心肌损伤有关。因此,我们认为,PIAS3的敲除抑制了CARD9蛋白的SUMO化,促进了CARD9和HOXB5的解离,从而增加了HOXB5的O-GlcNAc介导的糖基化,而由此产生的HOXB5核转位促进了Parkin诱导的有丝分裂,减轻了心肌I/R损伤。
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期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
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