{"title":"类花粉素蛋白 1 通过调节 MicroRNA-21 减轻肾缺血再灌注损伤","authors":"Guoxiong Lin, Shiquan Chai, Kaibo Mei, Guixiang Xiong, Fanglan Liu, Haifei Mao","doi":"10.1166/jbn.2024.3760","DOIUrl":null,"url":null,"abstract":"A mouse renal ischemia-reperfusion injury (RIRI) model was used to investigate how follistatin-Like Protein 1 (FSTL1) provides renal protection post-RIRI by targeting inflammation, apoptosis, and microRNA (miRNA). RIRI was induced in 8-week-old male C57BL/6 mice, followed by FSTL1 recombinant\n protein treatment. Inflammation and apoptosis in kidney tissues were assessed using ELISA and flow cytometry. A cellular RIRI model was created using hypoxia/reoxygenation (H/R) in HK-2 cells to validate FSTL1’s effects. miRNA-mediated mechanisms were explored using cell transfection\n and dual-luciferase assays. RIRI mice exhibited elevated inflammation and apoptosis, while FSTL1 treatment mitigated these effects. Similarly, FSTL1 attenuated H/R-induced HK-2 cell damage. miR-21 expression decreased in H/R-treated HK-2 cells, which FSTL1 reversed. miR-21 mimic reduced H/R-induced\n HK-2 cell damage, while its inhibition decreased FSTL1’s protection. Notably, miR-21 targeted caspase-7 and suppressed its activity. FSTL1 alleviated mouse RIRI by upregulating miR-21, thereby reducing inflammation and apoptosis in kidney tissues post-RIRI. This study highlights FSTL1’s\n therapeutic potential through the miR-21-mediated regulation of inflammation and apoptosis in RIRI.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Follistatin-Like Protein 1 Alleviates Renal Ischemia-Reperfusion Injury by Regulating MicroRNA-21\",\"authors\":\"Guoxiong Lin, Shiquan Chai, Kaibo Mei, Guixiang Xiong, Fanglan Liu, Haifei Mao\",\"doi\":\"10.1166/jbn.2024.3760\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"A mouse renal ischemia-reperfusion injury (RIRI) model was used to investigate how follistatin-Like Protein 1 (FSTL1) provides renal protection post-RIRI by targeting inflammation, apoptosis, and microRNA (miRNA). RIRI was induced in 8-week-old male C57BL/6 mice, followed by FSTL1 recombinant\\n protein treatment. Inflammation and apoptosis in kidney tissues were assessed using ELISA and flow cytometry. A cellular RIRI model was created using hypoxia/reoxygenation (H/R) in HK-2 cells to validate FSTL1’s effects. miRNA-mediated mechanisms were explored using cell transfection\\n and dual-luciferase assays. RIRI mice exhibited elevated inflammation and apoptosis, while FSTL1 treatment mitigated these effects. Similarly, FSTL1 attenuated H/R-induced HK-2 cell damage. miR-21 expression decreased in H/R-treated HK-2 cells, which FSTL1 reversed. miR-21 mimic reduced H/R-induced\\n HK-2 cell damage, while its inhibition decreased FSTL1’s protection. Notably, miR-21 targeted caspase-7 and suppressed its activity. FSTL1 alleviated mouse RIRI by upregulating miR-21, thereby reducing inflammation and apoptosis in kidney tissues post-RIRI. This study highlights FSTL1’s\\n therapeutic potential through the miR-21-mediated regulation of inflammation and apoptosis in RIRI.\",\"PeriodicalId\":15260,\"journal\":{\"name\":\"Journal of biomedical nanotechnology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-02-01\",\"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.2024.3760\",\"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.2024.3760","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
Follistatin-Like Protein 1 Alleviates Renal Ischemia-Reperfusion Injury by Regulating MicroRNA-21
A mouse renal ischemia-reperfusion injury (RIRI) model was used to investigate how follistatin-Like Protein 1 (FSTL1) provides renal protection post-RIRI by targeting inflammation, apoptosis, and microRNA (miRNA). RIRI was induced in 8-week-old male C57BL/6 mice, followed by FSTL1 recombinant
protein treatment. Inflammation and apoptosis in kidney tissues were assessed using ELISA and flow cytometry. A cellular RIRI model was created using hypoxia/reoxygenation (H/R) in HK-2 cells to validate FSTL1’s effects. miRNA-mediated mechanisms were explored using cell transfection
and dual-luciferase assays. RIRI mice exhibited elevated inflammation and apoptosis, while FSTL1 treatment mitigated these effects. Similarly, FSTL1 attenuated H/R-induced HK-2 cell damage. miR-21 expression decreased in H/R-treated HK-2 cells, which FSTL1 reversed. miR-21 mimic reduced H/R-induced
HK-2 cell damage, while its inhibition decreased FSTL1’s protection. Notably, miR-21 targeted caspase-7 and suppressed its activity. FSTL1 alleviated mouse RIRI by upregulating miR-21, thereby reducing inflammation and apoptosis in kidney tissues post-RIRI. This study highlights FSTL1’s
therapeutic potential through the miR-21-mediated regulation of inflammation and apoptosis in RIRI.