Poly(ADP-ribose) polymerase 1 accelerates vascular calcification by upregulating Runx2

Cheng Wang (), Wenjing Xu, Jie An, Minglu Liang, Yiqing Li, Fengxiao Zhang, Qiangsong Tong and Kai Huang ()
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Cheng Wang: Huazhong University of Science and Technology
Wenjing Xu: Huazhong University of Science and Technology
Jie An: Huazhong University of Science and Technology
Minglu Liang: Huazhong University of Science and Technology
Yiqing Li: Huazhong University of Science and Technology
Fengxiao Zhang: Huazhong University of Science and Technology
Qiangsong Tong: Huazhong University of Science and Technology
Kai Huang: Huazhong University of Science and Technology

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Vascular calcification is highly prevalent in end-stage renal diseases and is predictive of cardiovascular events and mortality. Poly(ADP-ribose) polymerase 1 (PARP1) inhibition or deletion is vasoprotective in several disease models. Here we show that PARP activity is increased in radial artery samples from patients with chronic renal failure, in arteries from uraemic rats, and in calcified vascular smooth muscle cells (VSMCs) in vitro. PARP1 deficiency blocks, whereas PARP1 overexpression exacerbates, the transdifferentiation of VSMCs from a contractile to an osteogenic phenotype, the expression of mineralization-regulating proteins, and calcium deposition. PARP1 promotes Runx2 expression, and Runx2 deficiency offsets the pro-calcifying effects of PARP1. Activated PARP1 suppresses miRNA-204 expression via the IL-6/STAT3 pathway and thus relieves the repression of its target, Runx2, resulting in increased Runx2 protein. Together, these results suggest that PARP1 counteracts vascular calcification and that therapeutic agents that influence PARP1 activity may be of benefit to treat vascular calcification.

Date: 2019
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DOI: 10.1038/s41467-019-09174-1

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