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...

Full description

Bibliographic Details
Main Authors: Qiong Jiang, Ting Yang, Yan Zou, Mingjie He, Qingchun Li, Xiaohui Chen, Aimin Zhong
Format: Article
Language:English
Published: Wiley 2023-12-01
Series:Aging Medicine
Subjects:
Online Access:https://doi.org/10.1002/agm2.12266
_version_ 1797353530858668032
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.
first_indexed 2024-03-08T13:32:24Z
format Article
id doaj.art-5e95e1bda1ed4ce89d934e6a07e452f3
institution Directory Open Access Journal
issn 2475-0360
language English
last_indexed 2024-03-08T13:32:24Z
publishDate 2023-12-01
publisher Wiley
record_format Article
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
work_keys_str_mv AT qiongjiang lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT tingyang lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT yanzou lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT mingjiehe lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT qingchunli lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT xiaohuichen lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis
AT aiminzhong lncrnahoxtranscriptantisensernamediateshyperglycemicinducedinjuryintherenaltubularepithelialcellviathemir1265paktaxis