High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells
There are seven endoplasmic reticulum (ER)-resident selenoproteins in human body and they can regulate the inflammation, oxidative stress, and ER stress. We established transforming growth factor-β1 (TGF-β1) or high glucose (HG) induced human mesangial cells (HMCs) fibronectin expression model in vi...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2019-01-01
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| Series: | Renal Failure |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/0886022X.2019.1641413 |
| _version_ | 1818646802761515008 |
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| author | Fumeng Huang Yuanxu Guo Li Wang Lanmei Jing Zhao Chen Shemin Lu Rongguo Fu Lifang Tian |
| author_facet | Fumeng Huang Yuanxu Guo Li Wang Lanmei Jing Zhao Chen Shemin Lu Rongguo Fu Lifang Tian |
| author_sort | Fumeng Huang |
| collection | DOAJ |
| description | There are seven endoplasmic reticulum (ER)-resident selenoproteins in human body and they can regulate the inflammation, oxidative stress, and ER stress. We established transforming growth factor-β1 (TGF-β1) or high glucose (HG) induced human mesangial cells (HMCs) fibronectin expression model in vitro. Next, the expression changes of seven ER-resident selenoproteins were detected under HG conditions and we found selenoprotein S (SELENOS), selenoprotein N (SELENON) were significantly down-regulated but selenoprotein M was significantly up-regulated in transcription level. Furthermore, we found that TGF-β1 and HG down-regulated the expression of SELENOS and SELENON in a time- and dose-dependent manner, respectively. Finally, SELENOS was knocked down by siRNA and we found that knocking down SELENOS decreased TGF-β1 induced fibronectin expression. Our research indicates the potential value of ER-resident selenoproteins on renal fibrosis. |
| first_indexed | 2024-12-17T00:52:26Z |
| format | Article |
| id | doaj.art-958810331eed4a4eb83100d2b3289f52 |
| institution | Directory Open Access Journal |
| issn | 0886-022X 1525-6049 |
| language | English |
| last_indexed | 2024-12-17T00:52:26Z |
| publishDate | 2019-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Renal Failure |
| spelling | doaj.art-958810331eed4a4eb83100d2b3289f522022-12-21T22:09:44ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492019-01-0141176276910.1080/0886022X.2019.16414131641413High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cellsFumeng Huang0Yuanxu Guo1Li Wang2Lanmei Jing3Zhao Chen4Shemin Lu5Rongguo Fu6Lifang Tian7The Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’an Jiaotong University College of MedicineThe Second Affiliated Hospital of Xi’an Jiaotong UniversityThe Second Affiliated Hospital of Xi’an Jiaotong UniversityThe Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’an Jiaotong University College of MedicineThe Second Affiliated Hospital of Xi’an Jiaotong UniversityThe Second Affiliated Hospital of Xi’an Jiaotong UniversityThere are seven endoplasmic reticulum (ER)-resident selenoproteins in human body and they can regulate the inflammation, oxidative stress, and ER stress. We established transforming growth factor-β1 (TGF-β1) or high glucose (HG) induced human mesangial cells (HMCs) fibronectin expression model in vitro. Next, the expression changes of seven ER-resident selenoproteins were detected under HG conditions and we found selenoprotein S (SELENOS), selenoprotein N (SELENON) were significantly down-regulated but selenoprotein M was significantly up-regulated in transcription level. Furthermore, we found that TGF-β1 and HG down-regulated the expression of SELENOS and SELENON in a time- and dose-dependent manner, respectively. Finally, SELENOS was knocked down by siRNA and we found that knocking down SELENOS decreased TGF-β1 induced fibronectin expression. Our research indicates the potential value of ER-resident selenoproteins on renal fibrosis.http://dx.doi.org/10.1080/0886022X.2019.1641413endoplasmic reticulumselenoprotein sselenoprotein nhmcsglucosetgf-β1 |
| spellingShingle | Fumeng Huang Yuanxu Guo Li Wang Lanmei Jing Zhao Chen Shemin Lu Rongguo Fu Lifang Tian High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells Renal Failure endoplasmic reticulum selenoprotein s selenoprotein n hmcs glucose tgf-β1 |
| title | High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells |
| title_full | High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells |
| title_fullStr | High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells |
| title_full_unstemmed | High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells |
| title_short | High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells |
| title_sort | high glucose and tgf β1 reduce expression of endoplasmic reticulum resident selenoprotein s and selenoprotein n in human mesangial cells |
| topic | endoplasmic reticulum selenoprotein s selenoprotein n hmcs glucose tgf-β1 |
| url | http://dx.doi.org/10.1080/0886022X.2019.1641413 |
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