Downregulated microRNA‑133a induces HUVECs injury: Potential role of the (pro) renin receptor in angiotensin II‑dependent hypertension
The renin‑angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II‑dependent hypertension. We aimed to explore the roles of Ang II and miR‑133a in the mechanism underlying hypertension. Human umbilical v...
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Published in | Molecular medicine reports Vol. 20; no. 3; pp. 2796 - 2804 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Spandidos Publications UK Ltd
01.09.2019
D.A. Spandidos |
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Abstract | The renin‑angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II‑dependent hypertension. We aimed to explore the roles of Ang II and miR‑133a in the mechanism underlying hypertension. Human umbilical vein endothelial cells (HUVECs) were identified by immunofluorescence staining. Cell viability and miR‑133a expression under the inhibition of Ang II of various concentrations were determined by an MTT assay and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), respectively. The effects of HUVECs transfected with miR‑133a mimic or inhibitor on Ang II‑induced apoptosis were measured using flow cytometry. The potential targeting of miR‑133a to the 3' untranslated region of (pro) renin receptor (PRR) was assessed using TargetScan and a dual‑luciferase assay. The effects of PRR interference using small interfering (si)RNA on PRR expression and the rate of apoptosis were determined by RT‑qPCR, western blotting and flow cytometry, respectively. Ang II at a concentration of 10‑5 M significantly inhibited the cell viability (P<0.05) and miR‑133a expression (P<0.01); Downregulation of miR‑133a suppressed cell viability. HUVECs transfected with miR‑133a mimic reduced the rate of Ang II‑induced apoptosis from 21.99 to 12.38%, but miR‑133a inhibitor promoted Ang II‑induced apoptosis (apoptosis rate, 28.9%). PRR was predicted to be a target gene of miR‑133a. Transfection with siPRR decreased the apoptotic rate in Ang II + negative control and Ang II + miR‑133a inhibitor group to 11.39 and 12.94%, respectively. Our findings also suggested that Ang II promoted PRR expression to enhance the apoptotic rate of HUVECs via the suppression of miR‑133a. Furthermore, siPRR efficiently decreased the Ang II‑induced apoptosis. |
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AbstractList | The renin-angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II-dependent hypertension. We aimed to explore the roles of Ang II and miR-133a in the mechanism underlying hypertension. Human umbilical vein endothelial cells (HUVECs) were identified by immunofluorescence staining. Cell viability and miR-133a expression under the inhibition of Ang II of various concentrations were determined by an MTT assay and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), respectively. The effects of HUVECs transfected with miR-133a mimic or inhibitor on Ang II-induced apoptosis were measured using flow cytometry. The potential targeting of miR-133a to the 3′ untranslated region of (pro) renin receptor (PRR) was assessed using TargetScan and a dual-luciferase assay. The effects of PRR interference using small interfering (si)RNA on PRR expression and the rate of apoptosis were determined by RT-qPCR, western blotting and flow cytometry, respectively. Ang II at a concentration of 10
−5
M significantly inhibited the cell viability (P<0.05) and miR-133a expression (P<0.01); Downregulation of miR-133a suppressed cell viability. HUVECs transfected with miR-133a mimic reduced the rate of Ang II-induced apoptosis from 21.99 to 12.38%, but miR-133a inhibitor promoted Ang II-induced apoptosis (apoptosis rate, 28.9%). PRR was predicted to be a target gene of miR-133a. Transfection with siPRR decreased the apoptotic rate in Ang II + negative control and Ang II + miR-133a inhibitor group to 11.39 and 12.94%, respectively. Our findings also suggested that Ang II promoted PRR expression to enhance the apoptotic rate of HUVECs via the suppression of miR-133a. Furthermore, siPRR efficiently decreased the Ang II-induced apoptosis. The renin‑angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II‑dependent hypertension. We aimed to explore the roles of Ang II and miR‑133a in the mechanism underlying hypertension. Human umbilical vein endothelial cells (HUVECs) were identified by immunofluorescence staining. Cell viability and miR‑133a expression under the inhibition of Ang II of various concentrations were determined by an MTT assay and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), respectively. The effects of HUVECs transfected with miR‑133a mimic or inhibitor on Ang II‑induced apoptosis were measured using flow cytometry. The potential targeting of miR‑133a to the 3' untranslated region of (pro) renin receptor (PRR) was assessed using TargetScan and a dual‑luciferase assay. The effects of PRR interference using small interfering (si)RNA on PRR expression and the rate of apoptosis were determined by RT‑qPCR, western blotting and flow cytometry, respectively. Ang II at a concentration of 10‑5 M significantly inhibited the cell viability (P<0.05) and miR‑133a expression (P<0.01); Downregulation of miR‑133a suppressed cell viability. HUVECs transfected with miR‑133a mimic reduced the rate of Ang II‑induced apoptosis from 21.99 to 12.38%, but miR‑133a inhibitor promoted Ang II‑induced apoptosis (apoptosis rate, 28.9%). PRR was predicted to be a target gene of miR‑133a. Transfection with siPRR decreased the apoptotic rate in Ang II + negative control and Ang II + miR‑133a inhibitor group to 11.39 and 12.94%, respectively. Our findings also suggested that Ang II promoted PRR expression to enhance the apoptotic rate of HUVECs via the suppression of miR‑133a. Furthermore, siPRR efficiently decreased the Ang II‑induced apoptosis. The renin-angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin (Ang) II-dependent hypertension. We aimed to explore the roles of Ang II and miR-133a in the mechanism underlying hypertension. Human umbilical vein endothelial cells (HUVECs) were identified by immunofluorescence staining. Cell viability and miR-133a expression under the inhibition of Ang II of various concentrations were determined by an MTT assay and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), respectively. The effects of HUVECs transfected with miR-133a mimic or inhibitor on Ang II-induced apoptosis were measured using flow cytometry. The potential targeting of miR-133a to the 3′ untranslated region of (pro) renin receptor (PRR) was assessed using TargetScan and a dual-luciferase assay. The effects of PRR interference using small interfering (si)RNA on PRR expression and the rate of apoptosis were determined by RT-qPCR, western blotting and flow cytometry, respectively. Ang II at a concentration of 10−5 M significantly inhibited the cell viability (P<0.05) and miR-133a expression (P<0.01); Downregulation of miR-133a suppressed cell viability. HUVECs transfected with miR-133a mimic reduced the rate of Ang II-induced apoptosis from 21.99 to 12.38%, but miR-133a inhibitor promoted Ang II-induced apoptosis (apoptosis rate, 28.9%). PRR was predicted to be a target gene of miR-133a. Transfection with siPRR decreased the apoptotic rate in Ang II + negative control and Ang II + miR-133a inhibitor group to 11.39 and 12.94%, respectively. Our findings also suggested that Ang II promoted PRR expression to enhance the apoptotic rate of HUVECs via the suppression of miR-133a. Furthermore, siPRR efficiently decreased the Ang II-induced apoptosis. |
Author | Teng, Jiwei Liu, Bing Zhang, Dapeng Liu, Junmeng Wei, Huali Lan, Ming |
AuthorAffiliation | 3 Heart Center and Beijing Key Laboratory of Hypertension Disease, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100028, P.R. China 2 Department of Gynecology and Obstetrics, China Meitan General Hospital, Capital Medical University, Beijing 100028, P.R. China 4 Department of Cardiovascular Medicine, The Second Affiliated Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China 1 Department of Cardiology, Beijing Hospital, National Center of Gerontology of China, Beijing 100730, P.R. China |
AuthorAffiliation_xml | – name: 2 Department of Gynecology and Obstetrics, China Meitan General Hospital, Capital Medical University, Beijing 100028, P.R. China – name: 1 Department of Cardiology, Beijing Hospital, National Center of Gerontology of China, Beijing 100730, P.R. China – name: 4 Department of Cardiovascular Medicine, The Second Affiliated Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China – name: 3 Heart Center and Beijing Key Laboratory of Hypertension Disease, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100028, P.R. China |
Author_xml | – sequence: 1 givenname: Bing surname: Liu fullname: Liu, Bing organization: Department of Cardiology, Beijing Hospital, National Center of Gerontology of China, Beijing 100730, P.R. China – sequence: 2 givenname: Ming surname: Lan fullname: Lan, Ming organization: Department of Cardiology, Beijing Hospital, National Center of Gerontology of China, Beijing 100730, P.R. China – sequence: 3 givenname: Huali surname: Wei fullname: Wei, Huali organization: Department of Gynecology and Obstetrics, China Meitan General Hospital, Beijing 100028, P.R. China – sequence: 4 givenname: Dapeng surname: Zhang fullname: Zhang, Dapeng organization: Heart Center and Beijing Key Laboratory of Hypertension Disease, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100028, P.R. China – sequence: 5 givenname: Junmeng surname: Liu fullname: Liu, Junmeng organization: Department of Cardiology, Beijing Hospital, National Center of Gerontology of China, Beijing 100730, P.R. China – sequence: 6 givenname: Jiwei surname: Teng fullname: Teng, Jiwei organization: Department of Cardiovascular Medicine, The Second Affiliated Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31524252$$D View this record in MEDLINE/PubMed |
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Copyright | Copyright Spandidos Publications UK Ltd. 2019 Copyright: © Liu et al. 2019 |
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Snippet | The renin‑angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin... The renin-angiotensin system (RAS) serves an essential role in hypertension. MicroRNAs (miRs) have been reported to be important regulators in angiotensin... |
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SubjectTerms | 3' Untranslated Regions Angiotensin Angiotensin II Angiotensin II - metabolism Angiotensin II - pharmacology Apoptosis Biomarkers Blood pressure Cell Survival - drug effects Cell viability Endothelial cells Flow cytometry Fluorescent Antibody Technique Gene Expression Regulation - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Hypertension Hypertension - etiology Hypertension - metabolism Hypertension - physiopathology Immunofluorescence Investigations Medical prognosis MicroRNAs MicroRNAs - genetics miRNA Permeability Polymerase chain reaction Proteins Receptors, Cell Surface - metabolism Renin Renin-Angiotensin System Reverse transcription RNA Interference siRNA Transfection Umbilical vein Vacuolar Proton-Translocating ATPases - metabolism Western blotting |
Title | Downregulated microRNA‑133a induces HUVECs injury: Potential role of the (pro) renin receptor in angiotensin II‑dependent hypertension |
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