Depalmitoylase ABHD17B promotes vascular smooth muscle cells calcification in chronic kidney disease vascular calcification through interaction with BRG1

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Depalmitoylase ABHD17B promotes vascular smooth muscle cells calcification in chronic kidney disease vascular calcification through interaction with BRG1

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Co-author 1

Guisen Li guisenli@163.com University of Electronic Science and Technology of China Department of Nephrology, Sichuan Provincial People’s Hospital Chengdu China *

Co-author 2

Lin Xiong 582591080@qq.com University of Electronic Science and Technology of China Department of Nephrology, Sichuan Provincial People’s Hospital Chengdu China -

Co-author 3

Linming Huang liminghuang1@163.com University of Electronic Science and Technology of China Department of Nephrology, Sichuan Provincial People’s Hospital Chengdu China -

Co-author 4

Yi Li brittnay@163.com University of Electronic Science and Technology of China Department of Nephrology, Sichuan Provincial People’s Hospital Chengdu China -

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Li Wang scwangli62@163.com University of Electronic Science and Technology of China Department of Nephrology, Sichuan Provincial People’s Hospital Chengdu China -

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Introduction

Vascular calcification is a common complication of chronic kidney disease, and its pathogenesis is complex and still not fully elucidated. Osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) is critical for vascular calcification in CKD. It has been reported that S-palmitoylation of proteins is involved in the regulation of osteoblast differentiation and atherosclerosis. However, the role of S-palmitoylation in vascular calcification in chronic kidney disease remains unclear. The purpose of this study was to preliminarily investigate the role of S-palmitoylation and its related important molecules on vascular calcification in chronic kidney disease.

Methods

In vivo, rats underwent 5/6 nephrectomy combined with a high-phosphorus diet to induce a vascular calcification model in CKD rats. In vitro, the calcification and osteogenic transdifferentiation of VSMCs induced by 10 mM β-glycerophosphate and 1.5 mM CaCl2. In addition, VSMCs were treated with palmitoylase pan-inhibitor 2-BP and depalmitoylase pan-inhibitor Palm-B to intervene in protein palmitoylation. The depalmitoylase ABHD17B was identified as a potential target by Data-independent acquisition (DIA)-based quantitative proteomics analysis of VSMCs. Subsequently, we investigated the expression pattern of ABHD17B in the aorta of hemodialysis patients and a vascular calcification model in CKD rats, and the effect of ABHD17B on calcification and osteogenic transdifferentiation of VSMCs. Finally, we performed molecular docking and immunoprecipitation to explore the potential mechanisms by which ABHD17B regulates calcification of VSMCs.

Results

Under calcifying conditions, calcification and osteogenic transdifferentiation of VSMCs were exacerbated by 2-BP and inhibited by Palm-B treatment. The expression of ABHD17B was increased in calcified VSMCs and calcified arteries in rat underwent 5/6 nephrectomy combined with a high-phosphorus diet, as well as calcified arteries from patients with hemodialysis presenting vascular calcification. Importantly, silencing ABHD17B expression inhibited VSMCs calcification and osteogenic transdifferentiation, whereas transfection of plasmids expressing ABHD17B promoted calcification of VSMCs. Mechanistically, the Cys1205 residue of Brahma related gene 1 (BRG1) can undergo S-palmitoylation modification. ABHD17B interacted with BRG1 and synergistically promote VSMCs calcification. Interestingly, the Cys1205 residue of BRG1 is involved in the interaction between ABHD17 and BRG1 and affects its synergistic pro-calcification effect on VSMCs.

Conclusion

Protein S-palmitoylation modification is closely associated with vascular calcification in CKD, and ABHD17B might be a novel potential target for the prevention and treatment of vascular calcification in CKD.

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