CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis

The biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused b...

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Main Authors: Liting Kuang, Anshang Lu, Shaojuan Yao
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:Renal Failure
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Online Access:https://www.tandfonline.com/doi/10.1080/0886022X.2023.2236219
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author Liting Kuang
Anshang Lu
Shaojuan Yao
author_facet Liting Kuang
Anshang Lu
Shaojuan Yao
author_sort Liting Kuang
collection DOAJ
description The biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused by renal IR. Then, the circTLK1 expression level in HK-2 cells treated with OGD/R was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Functional experiments were performed with circTLK1 knockdown of HK-2 cells via Cell Counting Kit-8 (CCK8), flow cytometry (FCM), RT-qPCR, and western blotting. The circTLK1-miRNAs-mRNAs network was constructed following the ceRNA mechanism and visualized by Cytoscape software to investigate the mechanism of circTLK1 in AKI. RT-qPCR was performed to verify the relationship between circTLK1, miR-136-5p, and Bcl2. The level of miR-136-5p was knocked down to ensure its function in OGD/R-triggered apoptosis through experiments, including CCK8, FCM, RT-qPCR, and western blotting. CircTLK1 was downregulated in HK-2 cells subjected to OGD/R treatment and in mouse kidney tissues after renal IR, but the expression of miR-136-5p was the opposite. Interference with circTLK1 expression accelerated HK-2 cell apoptosis, which was overturned by miR-136-5p inhibitors. CircTLK1 targets miR-136-5p to upregulate Bcl2 expression and attenuate apoptosis in HK-2 cells. These data revealed the possible role of circTLK1 as a new biomarker for diagnosis as well as a target in AKI through the miR-136-5p/Bcl2 signaling axis.
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institution Kabale University
issn 0886-022X
1525-6049
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publishDate 2023-12-01
publisher Taylor & Francis Group
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series Renal Failure
spelling doaj-art-e7dd692663a242118bff8217471fa3062025-08-20T03:53:07ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492023-12-0145110.1080/0886022X.2023.2236219CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axisLiting Kuang0Anshang Lu1Shaojuan Yao2Department of Anaesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangdong, Guangzhou, ChinaDepartment of Research Projects, Guangzhou Cookgen Biotechnology Co., Ltd, Guangdong, Guangzhou, ChinaDepartment of Research Projects, Guangzhou Cookgen Biotechnology Co., Ltd, Guangdong, Guangzhou, ChinaThe biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused by renal IR. Then, the circTLK1 expression level in HK-2 cells treated with OGD/R was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Functional experiments were performed with circTLK1 knockdown of HK-2 cells via Cell Counting Kit-8 (CCK8), flow cytometry (FCM), RT-qPCR, and western blotting. The circTLK1-miRNAs-mRNAs network was constructed following the ceRNA mechanism and visualized by Cytoscape software to investigate the mechanism of circTLK1 in AKI. RT-qPCR was performed to verify the relationship between circTLK1, miR-136-5p, and Bcl2. The level of miR-136-5p was knocked down to ensure its function in OGD/R-triggered apoptosis through experiments, including CCK8, FCM, RT-qPCR, and western blotting. CircTLK1 was downregulated in HK-2 cells subjected to OGD/R treatment and in mouse kidney tissues after renal IR, but the expression of miR-136-5p was the opposite. Interference with circTLK1 expression accelerated HK-2 cell apoptosis, which was overturned by miR-136-5p inhibitors. CircTLK1 targets miR-136-5p to upregulate Bcl2 expression and attenuate apoptosis in HK-2 cells. These data revealed the possible role of circTLK1 as a new biomarker for diagnosis as well as a target in AKI through the miR-136-5p/Bcl2 signaling axis.https://www.tandfonline.com/doi/10.1080/0886022X.2023.2236219Acute kidney injury (AKI)ischemia/reperfusion (I/R)HK-2 cellscircTLK1miR-136-5papoptosis
spellingShingle Liting Kuang
Anshang Lu
Shaojuan Yao
CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
Renal Failure
Acute kidney injury (AKI)
ischemia/reperfusion (I/R)
HK-2 cells
circTLK1
miR-136-5p
apoptosis
title CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
title_full CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
title_fullStr CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
title_full_unstemmed CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
title_short CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis
title_sort circtlk1 alleviates oxygen glucose deprivation reperfusion induced apoptosis in hk 2 cells through mir 136 5p bcl2 signal axis
topic Acute kidney injury (AKI)
ischemia/reperfusion (I/R)
HK-2 cells
circTLK1
miR-136-5p
apoptosis
url https://www.tandfonline.com/doi/10.1080/0886022X.2023.2236219
work_keys_str_mv AT litingkuang circtlk1alleviatesoxygenglucosedeprivationreperfusioninducedapoptosisinhk2cellsthroughmir1365pbcl2signalaxis
AT anshanglu circtlk1alleviatesoxygenglucosedeprivationreperfusioninducedapoptosisinhk2cellsthroughmir1365pbcl2signalaxis
AT shaojuanyao circtlk1alleviatesoxygenglucosedeprivationreperfusioninducedapoptosisinhk2cellsthroughmir1365pbcl2signalaxis