Minjing Li, Yueming Liang, Yeliang Wen, Yaofeng Chen, Jian Liu
{"title":"miR-146a修饰的肺成纤维细胞通过下调早期生长应答因子1抑制转化生长因子β诱导的纤维化进程","authors":"Minjing Li, Yueming Liang, Yeliang Wen, Yaofeng Chen, Jian Liu","doi":"10.1166/jbn.2023.3677","DOIUrl":null,"url":null,"abstract":"This study investigated the role of miR-146a in lung fibrosis, specifically focusing on idiopathic pulmonary fibrosis (IPF), which is characterized by excessive alveolar fibrosis and collagen synthesis. The study aimed to explore the impact and mechanism of miR-146a on lung fibrosis\n using in vitro methods. Human lung fibroblasts (LFs) were transfected with miR-146a mimics and inhibitors to examine their effects. Transforming growth factor-β (TGF-β) was used to activate LFs for 24 hours, while phosphate-buffered saline (PBS)-treated cells\n served as the control group. The transfection efficiency, level of LFs activation, collagen expression, and cell viability were investigated. The results demonstrated that administration of miR-146a mimics attenuated LFs activation and reduced collagen levels by inhibiting the expression of\n EGR1, an important factor involved in cell proliferation and differentiation that is positively associated with fibrogenesis. On the other hand, miR-146a inhibitor increased EGR1 expression, but did not significantly affect LFs activation and collagen expression. Furthermore, rescuing EGR1\n expression reversed the decrease in LFs activation and collagen expression induced by increased levels of miR-146a. These findings indicate that miR-146a overexpression has an anti-fibrotic effect on LFs by inhibiting EGR1 expression, thereby restraining cell activation and reducing collagen\n deposition. Therefore, miR-146a holds promise as a potential therapeutic target for mitigating lung fibrosis diseases.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":" 3","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"miR-146a-Modified Lung Fibroblast Attenuates Transforming Growth Factor Beta-Induced Fibrosis Progress via Downregulation of Early Growth Response Factor 1\",\"authors\":\"Minjing Li, Yueming Liang, Yeliang Wen, Yaofeng Chen, Jian Liu\",\"doi\":\"10.1166/jbn.2023.3677\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This study investigated the role of miR-146a in lung fibrosis, specifically focusing on idiopathic pulmonary fibrosis (IPF), which is characterized by excessive alveolar fibrosis and collagen synthesis. The study aimed to explore the impact and mechanism of miR-146a on lung fibrosis\\n using in vitro methods. Human lung fibroblasts (LFs) were transfected with miR-146a mimics and inhibitors to examine their effects. Transforming growth factor-β (TGF-β) was used to activate LFs for 24 hours, while phosphate-buffered saline (PBS)-treated cells\\n served as the control group. The transfection efficiency, level of LFs activation, collagen expression, and cell viability were investigated. The results demonstrated that administration of miR-146a mimics attenuated LFs activation and reduced collagen levels by inhibiting the expression of\\n EGR1, an important factor involved in cell proliferation and differentiation that is positively associated with fibrogenesis. On the other hand, miR-146a inhibitor increased EGR1 expression, but did not significantly affect LFs activation and collagen expression. Furthermore, rescuing EGR1\\n expression reversed the decrease in LFs activation and collagen expression induced by increased levels of miR-146a. These findings indicate that miR-146a overexpression has an anti-fibrotic effect on LFs by inhibiting EGR1 expression, thereby restraining cell activation and reducing collagen\\n deposition. Therefore, miR-146a holds promise as a potential therapeutic target for mitigating lung fibrosis diseases.\",\"PeriodicalId\":15260,\"journal\":{\"name\":\"Journal of biomedical nanotechnology\",\"volume\":\" 3\",\"pages\":\"\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2023-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biomedical nanotechnology\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1166/jbn.2023.3677\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2023.3677","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
miR-146a-Modified Lung Fibroblast Attenuates Transforming Growth Factor Beta-Induced Fibrosis Progress via Downregulation of Early Growth Response Factor 1
This study investigated the role of miR-146a in lung fibrosis, specifically focusing on idiopathic pulmonary fibrosis (IPF), which is characterized by excessive alveolar fibrosis and collagen synthesis. The study aimed to explore the impact and mechanism of miR-146a on lung fibrosis
using in vitro methods. Human lung fibroblasts (LFs) were transfected with miR-146a mimics and inhibitors to examine their effects. Transforming growth factor-β (TGF-β) was used to activate LFs for 24 hours, while phosphate-buffered saline (PBS)-treated cells
served as the control group. The transfection efficiency, level of LFs activation, collagen expression, and cell viability were investigated. The results demonstrated that administration of miR-146a mimics attenuated LFs activation and reduced collagen levels by inhibiting the expression of
EGR1, an important factor involved in cell proliferation and differentiation that is positively associated with fibrogenesis. On the other hand, miR-146a inhibitor increased EGR1 expression, but did not significantly affect LFs activation and collagen expression. Furthermore, rescuing EGR1
expression reversed the decrease in LFs activation and collagen expression induced by increased levels of miR-146a. These findings indicate that miR-146a overexpression has an anti-fibrotic effect on LFs by inhibiting EGR1 expression, thereby restraining cell activation and reducing collagen
deposition. Therefore, miR-146a holds promise as a potential therapeutic target for mitigating lung fibrosis diseases.