miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway
Renal fibrosis, in particular tubulointerstitial fibrosis, which is characterized by an increased extracellular matrix (ECM) formation and development in the interstitium, is the common end pathway for nearly all progressive kidney disorders. One of the sources for this matrix is the epithelial to m...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
|
| Series: | Applied Bionics and Biomechanics |
| Online Access: | http://dx.doi.org/10.1155/2022/6382323 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832553003552342016 |
|---|---|
| author | Weifeng Feng Huijun Xie Jiong Li Xianxin Yan Shiping Zhu Shengyun Sun |
| author_facet | Weifeng Feng Huijun Xie Jiong Li Xianxin Yan Shiping Zhu Shengyun Sun |
| author_sort | Weifeng Feng |
| collection | DOAJ |
| description | Renal fibrosis, in particular tubulointerstitial fibrosis, which is characterized by an increased extracellular matrix (ECM) formation and development in the interstitium, is the common end pathway for nearly all progressive kidney disorders. One of the sources for this matrix is the epithelial to mesenchymal transition (EMT) from the tabular epithelium. The driving force behind it is some profibrotic growth factors such as transforming growth factor-β (TGF-β) which is responsible for the formation of collagen in renal fibrosis. miR-29c, which is an antifibrotic microRNA, downregulates renal interstitial fibrosis by downregulating the TGF-β and collagen. However, it is not known whether miR-29c mediates the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering within NRK-52E cultures. The main objective of this investigation was to examine the influence of miR-29c on the downregulation of the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering in NRK-52E cultures. This study revealed that miR-29c inhibited TGF-β1 expression in NRK-52E cell cultures. Overexpression of miR-29c significantly inhibits NRK-52E culture proliferation mediated by TGF-β1. miR-29c inhibited the expression of Col-1 and decreased PI3K/Akt phosphorylation. These findings revealed a novel mechanism by which miR29c inhibits the proliferation of renal interstitial fibrotic cultures by downregulating the PI3k-Akt pathway, which is controlled by TGF-β1. |
| format | Article |
| id | doaj-art-adab2ce22a2c439682b21416a6e8bc5a |
| institution | Kabale University |
| issn | 1754-2103 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Applied Bionics and Biomechanics |
| spelling | doaj-art-adab2ce22a2c439682b21416a6e8bc5a2025-02-03T05:57:23ZengWileyApplied Bionics and Biomechanics1754-21032022-01-01202210.1155/2022/6382323miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT PathwayWeifeng Feng0Huijun Xie1Jiong Li2Xianxin Yan3Shiping Zhu4Shengyun Sun5Department of Traditional Chinese MedicineCollege of Traditional Chinese MedicineDepartment of AnatomyCollege of Traditional Chinese MedicineDepartment of Traditional Chinese MedicineDepartment of Traditional Chinese MedicineRenal fibrosis, in particular tubulointerstitial fibrosis, which is characterized by an increased extracellular matrix (ECM) formation and development in the interstitium, is the common end pathway for nearly all progressive kidney disorders. One of the sources for this matrix is the epithelial to mesenchymal transition (EMT) from the tabular epithelium. The driving force behind it is some profibrotic growth factors such as transforming growth factor-β (TGF-β) which is responsible for the formation of collagen in renal fibrosis. miR-29c, which is an antifibrotic microRNA, downregulates renal interstitial fibrosis by downregulating the TGF-β and collagen. However, it is not known whether miR-29c mediates the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering within NRK-52E cultures. The main objective of this investigation was to examine the influence of miR-29c on the downregulation of the TGF-β1-driven PI3K-Akt pathway and Col-1 triggering in NRK-52E cultures. This study revealed that miR-29c inhibited TGF-β1 expression in NRK-52E cell cultures. Overexpression of miR-29c significantly inhibits NRK-52E culture proliferation mediated by TGF-β1. miR-29c inhibited the expression of Col-1 and decreased PI3K/Akt phosphorylation. These findings revealed a novel mechanism by which miR29c inhibits the proliferation of renal interstitial fibrotic cultures by downregulating the PI3k-Akt pathway, which is controlled by TGF-β1.http://dx.doi.org/10.1155/2022/6382323 |
| spellingShingle | Weifeng Feng Huijun Xie Jiong Li Xianxin Yan Shiping Zhu Shengyun Sun miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway Applied Bionics and Biomechanics |
| title | miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway |
| title_full | miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway |
| title_fullStr | miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway |
| title_full_unstemmed | miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway |
| title_short | miR-29c Inhibits Renal Interstitial Fibrotic Proliferative Properties through PI3K-AKT Pathway |
| title_sort | mir 29c inhibits renal interstitial fibrotic proliferative properties through pi3k akt pathway |
| url | http://dx.doi.org/10.1155/2022/6382323 |
| work_keys_str_mv | AT weifengfeng mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway AT huijunxie mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway AT jiongli mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway AT xianxinyan mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway AT shipingzhu mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway AT shengyunsun mir29cinhibitsrenalinterstitialfibroticproliferativepropertiesthroughpi3kaktpathway |