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DRG2 Depletion Promotes Endothelial Cell Senescence and Vascular Endothelial Dysfunctionopen access

Authors
Le, Anh-NhungPark, Seong-SoonLe, Minh-XuanLee, Unn HwaKo, Byung KyunLim, Hye RyeongYu, RiChoi, Seong HeeLee, Byung JuHam, Soo-YounHa, Chang ManPark, Jeong Woo
Issue Date
Mar-2022
Publisher
Multidisciplinary Digital Publishing Institute (MDPI)
Keywords
DRG2; endothelial cells; senescence; angiogenesis; vascular dysfunction
Citation
International Journal of Molecular Sciences, v.23, no.5
Journal Title
International Journal of Molecular Sciences
Volume
23
Number
5
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/245
DOI
10.3390/ijms23052877
ISSN
1661-6596
Abstract
Endothelial cell senescence is involved in endothelial dysfunction and vascular diseases. However, the detailed mechanisms of endothelial senescence are not fully understood. Here, we demonstrated that deficiency of developmentally regulated GTP-binding protein 2 (DRG2) induces senescence and dysfunction of endothelial cells. DRG2 knockout (KO) mice displayed reduced cerebral blood flow in the brain and lung blood vessel density. We also determined, by Matrigel plug assay, aorta ring assay, and in vitro tubule formation of primary lung endothelial cells, that deficiency in DRG2 reduced the angiogenic capability of endothelial cells. Endothelial cells from DRG2 KO mice showed a senescence phenotype with decreased cell growth and enhanced levels of p21 and phosphorylated p53, gamma H2AX, senescence-associated beta-galactosidase (SA-beta-gal) activity, and senescence-associated secretory phenotype (SASP) cytokines. DRG2 deficiency in endothelial cells upregulated arginase 2 (Arg2) and generation of reactive oxygen species. Induction of SA-beta-gal activity was prevented by the antioxidant N-acetyl cysteine in endothelial cells from DRG2 KO mice. In conclusion, our results suggest that DRG2 is a key regulator of endothelial senescence, and its downregulation is probably involved in vascular dysfunction and diseases.
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연구본부 > 신경·혈관 단위체 연구그룹 > 1. Journal Articles
연구전략실 > 연구전략실 > 1. Journal Articles
연구전략실 > 첨단뇌연구장비센터 > 1. Journal Articles

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