{"title":"STOML2敲低通过MAPK途径抑制pdgf - bb诱导的气道平滑肌细胞的炎症和气道重塑","authors":"Zhen Li, Songbai Zhu","doi":"10.1080/02770903.2025.2546358","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. Abnormal proliferation and migration of human airway smooth muscle cells (HASMCs), induced by platelet-derived growth factor BB (PDGF-BB), are associated with the occurrence and progression of asthma. In this study, we aim to investigate the expression and molecular mechanisms of stomatin-like protein-2 (STOML2) in airway remodeling in asthma.</p><p><strong>Methods: </strong>PDGF-BB-stimulated HASMCs were used as the asthma cell model. STOML2 expression levels in the serum of patients with asthma and healthy controls were measured using qRT-PCR. Additionally, qRT-PCR and western blotting were used to measure STOML2, E-cadherin, and N-cadherin expression in HASMCs. Extracellular matrix components were detected by western blot assay. The viability and migration of HASMCs were analyzed using MTT and Transwell assays. Tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 contents were evaluated using the corresponding kits. The key molecules of the p38 mitogen-activated protein kinase (p38 MAPK) pathway (p38 and p38) were determined using western blotting.</p><p><strong>Results: </strong>Increased STOML2 expression was observed in both patients with asthma and PDGF-BB-treated HASMCs. STOML2 knockdown inhibits STOML2 expression in HASMCs. PDGF-BB induced proliferation, migration, extracellular matrix deposition, inflammatory responses, and p38 MAPK pathway activation in HASMCs. However, the opposite effects were observed following STOML2 knockdown or SB-203580 treatment, respectively. Furthermore, P79350 treatment reversed the effect of STOML2 knockdown.</p><p><strong>Conclusions: </strong>Our results showed that silencing STOML2 inhibits inflammation and airway remodeling in PDGF-BB-stimulated HASMCs via the p38 MAPK pathway. Thus, STOML2 is a promising therapeutic target for the treatment of asthma.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-10"},"PeriodicalIF":1.3000,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"STOML2 knockdown inhibits inflammation and airway remodeling of PDGF-BB-induced airway smooth-muscle cells by the MAPK pathway.\",\"authors\":\"Zhen Li, Songbai Zhu\",\"doi\":\"10.1080/02770903.2025.2546358\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. Abnormal proliferation and migration of human airway smooth muscle cells (HASMCs), induced by platelet-derived growth factor BB (PDGF-BB), are associated with the occurrence and progression of asthma. In this study, we aim to investigate the expression and molecular mechanisms of stomatin-like protein-2 (STOML2) in airway remodeling in asthma.</p><p><strong>Methods: </strong>PDGF-BB-stimulated HASMCs were used as the asthma cell model. STOML2 expression levels in the serum of patients with asthma and healthy controls were measured using qRT-PCR. Additionally, qRT-PCR and western blotting were used to measure STOML2, E-cadherin, and N-cadherin expression in HASMCs. Extracellular matrix components were detected by western blot assay. The viability and migration of HASMCs were analyzed using MTT and Transwell assays. Tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 contents were evaluated using the corresponding kits. The key molecules of the p38 mitogen-activated protein kinase (p38 MAPK) pathway (p38 and p38) were determined using western blotting.</p><p><strong>Results: </strong>Increased STOML2 expression was observed in both patients with asthma and PDGF-BB-treated HASMCs. STOML2 knockdown inhibits STOML2 expression in HASMCs. PDGF-BB induced proliferation, migration, extracellular matrix deposition, inflammatory responses, and p38 MAPK pathway activation in HASMCs. However, the opposite effects were observed following STOML2 knockdown or SB-203580 treatment, respectively. Furthermore, P79350 treatment reversed the effect of STOML2 knockdown.</p><p><strong>Conclusions: </strong>Our results showed that silencing STOML2 inhibits inflammation and airway remodeling in PDGF-BB-stimulated HASMCs via the p38 MAPK pathway. Thus, STOML2 is a promising therapeutic target for the treatment of asthma.</p>\",\"PeriodicalId\":15076,\"journal\":{\"name\":\"Journal of Asthma\",\"volume\":\" \",\"pages\":\"1-10\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-08-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Asthma\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/02770903.2025.2546358\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Asthma","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/02770903.2025.2546358","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ALLERGY","Score":null,"Total":0}
STOML2 knockdown inhibits inflammation and airway remodeling of PDGF-BB-induced airway smooth-muscle cells by the MAPK pathway.
Objective: Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. Abnormal proliferation and migration of human airway smooth muscle cells (HASMCs), induced by platelet-derived growth factor BB (PDGF-BB), are associated with the occurrence and progression of asthma. In this study, we aim to investigate the expression and molecular mechanisms of stomatin-like protein-2 (STOML2) in airway remodeling in asthma.
Methods: PDGF-BB-stimulated HASMCs were used as the asthma cell model. STOML2 expression levels in the serum of patients with asthma and healthy controls were measured using qRT-PCR. Additionally, qRT-PCR and western blotting were used to measure STOML2, E-cadherin, and N-cadherin expression in HASMCs. Extracellular matrix components were detected by western blot assay. The viability and migration of HASMCs were analyzed using MTT and Transwell assays. Tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 contents were evaluated using the corresponding kits. The key molecules of the p38 mitogen-activated protein kinase (p38 MAPK) pathway (p38 and p38) were determined using western blotting.
Results: Increased STOML2 expression was observed in both patients with asthma and PDGF-BB-treated HASMCs. STOML2 knockdown inhibits STOML2 expression in HASMCs. PDGF-BB induced proliferation, migration, extracellular matrix deposition, inflammatory responses, and p38 MAPK pathway activation in HASMCs. However, the opposite effects were observed following STOML2 knockdown or SB-203580 treatment, respectively. Furthermore, P79350 treatment reversed the effect of STOML2 knockdown.
Conclusions: Our results showed that silencing STOML2 inhibits inflammation and airway remodeling in PDGF-BB-stimulated HASMCs via the p38 MAPK pathway. Thus, STOML2 is a promising therapeutic target for the treatment of asthma.
期刊介绍:
Providing an authoritative open forum on asthma and related conditions, Journal of Asthma publishes clinical research around such topics as asthma management, critical and long-term care, preventative measures, environmental counselling, and patient education.