ArticleRespiratory research2024
GPS2 ameliorates cigarette smoking-induced pulmonary vascular remodeling by modulating the ras-Raf-ERK axis.
Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- GPS2 regulates embryonic angiogenesis by enhancing endothelial cell survival through stabilizing HOIP.Cell death and differentiation · 2026Article
- Esketamine alleviates COPD-depression comorbidity in rats via MAPK/NF-κB inhibition and gut-lung-brain axis modulation.Journal of neuroinflammation · 2026Article
- Gut microbiota dysbiosis in COPD patients increases the level of queuine in the blood serum abnormally enhancing the viability of lung epithelial cells.Frontiers in immunology · 2026Article
- Impact of cigarette smoke on pulmonary vein and artery volumes in those with current and former smoking status: a quantitative computed tomography analysis.ERJ open research · 2025Article
- The SIRT1/GPS2/AIP1 axis regulates pulmonary vascular permeability in ventilator-induced lung injury.Molecular and cellular biochemistry · 2025Article
- Development of Diagnostic and Predictive Models for COPD Based on Anoikis Resistance.Journal of inflammation research · 2025Article
- The protective role of muscone in the development of COPD.Frontiers in immunology · 2025Article
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8 authors.
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Abstract
backgroundMitogen-activated protein kinase (MAPK)signaling-mediated smoking-associated pulmonary vascular remodeling (PVR) plays an important role in the pathogenesis of group 3 pulmonary hypertension (PH). And G protein pathway suppressor 2 (GPS2) could suppress G-protein signaling such as Ras and MAPK, but its role in cigarette smoking -induced PVR (CS-PVR) is unclear.
methodsAn in vivo model of smoke-exposed rats was constructed to assess the role of GPS2 in smoking-induced PH and PVR. In vitro, the effects of GPS2 overexpression and silencing on the function of human pulmonary arterial smooth cells (HPASMCs) and the underlying mechanisms were explored.
resultsGPS2 expression was downregulated in rat pulmonary arteries (PAs) and HPASMCs after CS exposure. More importantly, CS-exposed rats with GPS2 overexpression had lower right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and wall thickness (WT%) than those without. And enhanced proliferation and migration of HPASMCs induced by cigarette smoking extract (CSE) can be evidently inhibited by overexpressed GPS2. Besides, GPS2siRNA significantly enhanced the proliferation, and migration of HPASMCs as well as activated Ras and Raf/ERK signaling, while these effects were inhibited by zoledronic acid (ZOL). In addition, GPS2 promoter methylation level in rat PAs and HPASMCs was increased after CS exposure, and 5-aza-2-deoxycytidine (5-aza) inhibited CSE-induced GPS2 hypermethylation and downregulation in vitro.
conclusionsGPS2 overexpression could improve the CS-PVR, suggesting that GPS2 might serve as a novel therapeutic target for PH-COPD in the future.
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