LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis
Abstract Objective: To investigate the involvement of HOX transcript antisense RNA (HOTAIR) in the injury of renal tubular epithelial cells induced by high glucose. Results: In high glucose‐induced HK‐2 cells, the expression of HOTAIR was upregulated, resulting in suppressed cell proliferation. Mean...
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Format: | Article |
Language: | English |
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Wiley
2023-12-01
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Series: | Aging Medicine |
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Online Access: | https://doi.org/10.1002/agm2.12266 |
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author | Qiong Jiang Ting Yang Yan Zou Mingjie He Qingchun Li Xiaohui Chen Aimin Zhong |
author_facet | Qiong Jiang Ting Yang Yan Zou Mingjie He Qingchun Li Xiaohui Chen Aimin Zhong |
author_sort | Qiong Jiang |
collection | DOAJ |
description | Abstract Objective: To investigate the involvement of HOX transcript antisense RNA (HOTAIR) in the injury of renal tubular epithelial cells induced by high glucose. Results: In high glucose‐induced HK‐2 cells, the expression of HOTAIR was upregulated, resulting in suppressed cell proliferation. Meanwhile, HOTAIR upregulates the expression of pro‐apoptotic proteins Bax and cleaved caspase‐3, while downregulating the expression of the anti‐apoptotic protein Bcl‐2. Luciferase reporter assays revealed that HOTAIR could target miR‐126‐5p. Additionally, it was found that the PI3K/Akt signaling pathway serves as a downstream target of miR‐126‐5p. Knockdown of HOTAIR relieved apoptosis, whereas further inhibition of miR‐126‐5p led to apoptosis in HK‐2 cells. Conclusions: HOTAIR plays a regulatory role in mediating high glucose‐induced injuries in HK‐2 cells, specifically affecting apoptosis and cell viability, via the miR‐126‐5p/PI3K/Akt signaling pathway. |
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issn | 2475-0360 |
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last_indexed | 2024-03-08T13:32:24Z |
publishDate | 2023-12-01 |
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series | Aging Medicine |
spelling | doaj.art-5e95e1bda1ed4ce89d934e6a07e452f32024-01-17T07:41:07ZengWileyAging Medicine2475-03602023-12-016442743410.1002/agm2.12266LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axisQiong Jiang0Ting Yang1Yan Zou2Mingjie He3Qingchun Li4Xiaohui Chen5Aimin Zhong6Jiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaJiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang ChinaAbstract Objective: To investigate the involvement of HOX transcript antisense RNA (HOTAIR) in the injury of renal tubular epithelial cells induced by high glucose. Results: In high glucose‐induced HK‐2 cells, the expression of HOTAIR was upregulated, resulting in suppressed cell proliferation. Meanwhile, HOTAIR upregulates the expression of pro‐apoptotic proteins Bax and cleaved caspase‐3, while downregulating the expression of the anti‐apoptotic protein Bcl‐2. Luciferase reporter assays revealed that HOTAIR could target miR‐126‐5p. Additionally, it was found that the PI3K/Akt signaling pathway serves as a downstream target of miR‐126‐5p. Knockdown of HOTAIR relieved apoptosis, whereas further inhibition of miR‐126‐5p led to apoptosis in HK‐2 cells. Conclusions: HOTAIR plays a regulatory role in mediating high glucose‐induced injuries in HK‐2 cells, specifically affecting apoptosis and cell viability, via the miR‐126‐5p/PI3K/Akt signaling pathway.https://doi.org/10.1002/agm2.12266diabetic nephropathy (DN)HOX transcript antisense RNA (HOTAIR)miR‐126‐5p |
spellingShingle | Qiong Jiang Ting Yang Yan Zou Mingjie He Qingchun Li Xiaohui Chen Aimin Zhong LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis Aging Medicine diabetic nephropathy (DN) HOX transcript antisense RNA (HOTAIR) miR‐126‐5p |
title | LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis |
title_full | LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis |
title_fullStr | LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis |
title_full_unstemmed | LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis |
title_short | LncRNA HOX transcript antisense RNA mediates hyperglycemic‐induced injury in the renal tubular epithelial cell via the miR‐126‐5pAkt axis |
title_sort | lncrna hox transcript antisense rna mediates hyperglycemic induced injury in the renal tubular epithelial cell via the mir 126 5pakt axis |
topic | diabetic nephropathy (DN) HOX transcript antisense RNA (HOTAIR) miR‐126‐5p |
url | https://doi.org/10.1002/agm2.12266 |
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