ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjec...

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Published inJournal of biochemical and molecular toxicology Vol. 38; no. 4; pp. e23710 - n/a
Main Authors Li, Jiarong, Wang, Zhirong, Tan, Huayi, Tang, Mi
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.04.2024
Subjects
Adenine
AlkB Homolog 5, RNA Demethylase - genetics
AlkB Homolog 5, RNA Demethylase - metabolism
ALKBH5
Animals
Cell viability
Chromosome 5
Demethylation
Echocardiography
Flow cytometry
Heart function
Immunofluorescence
Immunohistochemistry
Immunoprecipitation
Injury prevention
Ischemia
Maturation
MI/RI
MicroRNAs - metabolism
Molecular modelling
Myocardial ischemia
Myocardial Reperfusion Injury - genetics
Myocardial Reperfusion Injury - metabolism
N6-methyladenosine
pri‐miR‐199a‐5p
Pyroptosis
Rats
Reperfusion
TNF Receptor-Associated Factor 3 - genetics
TNF Receptor-Associated Factor 3 - metabolism
TRAF3
Tumor necrosis factor receptors
Western blotting
pyroptosis
ALKBH5
MI/RI
TRAF3
pri‐miR‐199a‐5p
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Abstract Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT‐qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme‐linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit‐8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri‐miR‐199a‐5p m6A modification was detected by Me‐RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R‐induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri‐miR‐199a‐5p m6A methylation to block miR‐199a‐5p maturation and inhibit its expression. TNF receptor‐associated Factor 3 (TRAF3) is a downstream gene of miR‐199a‐5p. Furthermore, in H/R‐induced H9C2 cells, the miR‐199a‐5p inhibitor‐mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression‐mediated promotion of pyroptosis was offset by miR‐199a‐5p upregulation. ALKBH5 silencing inhibited pri‐miR‐199a‐5p expression and enhanced pri‐miR‐199a‐5p m6A modification to promote miR‐199a‐5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression. In this study, alkB homolog 5 (ALKBH5) enhanced the m6A demethylation of pri‐miR‐199a‐5p to block the maturation of miR‐199a‐5p and decrease miR‐199a‐5p expression. In addition, miR‐199a‐5p negatively regulated TNF receptor‐associated Factor 3 (TRAF3) expression through interacting with TRAF3. Furthermore, ALKBH5 silencing resulted in suppression of pyroptosis in myocardial ischemia‒reperfusion injury (MI/RI) through regulating miR‐199a‐5p/TRAF3 axis.
AbstractList Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT‐qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme‐linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit‐8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri‐miR‐199a‐5p m6A modification was detected by Me‐RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R‐induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri‐miR‐199a‐5p m6A methylation to block miR‐199a‐5p maturation and inhibit its expression. TNF receptor‐associated Factor 3 (TRAF3) is a downstream gene of miR‐199a‐5p. Furthermore, in H/R‐induced H9C2 cells, the miR‐199a‐5p inhibitor‐mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression‐mediated promotion of pyroptosis was offset by miR‐199a‐5p upregulation. ALKBH5 silencing inhibited pri‐miR‐199a‐5p expression and enhanced pri‐miR‐199a‐5p m6A modification to promote miR‐199a‐5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression.
Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT‐qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme‐linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit‐8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri‐miR‐199a‐5p m6A modification was detected by Me‐RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R‐induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri‐miR‐199a‐5p m6A methylation to block miR‐199a‐5p maturation and inhibit its expression. TNF receptor‐associated Factor 3 (TRAF3) is a downstream gene of miR‐199a‐5p. Furthermore, in H/R‐induced H9C2 cells, the miR‐199a‐5p inhibitor‐mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression‐mediated promotion of pyroptosis was offset by miR‐199a‐5p upregulation. ALKBH5 silencing inhibited pri‐miR‐199a‐5p expression and enhanced pri‐miR‐199a‐5p m6A modification to promote miR‐199a‐5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression. In this study, alkB homolog 5 (ALKBH5) enhanced the m6A demethylation of pri‐miR‐199a‐5p to block the maturation of miR‐199a‐5p and decrease miR‐199a‐5p expression. In addition, miR‐199a‐5p negatively regulated TNF receptor‐associated Factor 3 (TRAF3) expression through interacting with TRAF3. Furthermore, ALKBH5 silencing resulted in suppression of pyroptosis in myocardial ischemia‒reperfusion injury (MI/RI) through regulating miR‐199a‐5p/TRAF3 axis.
Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT-qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit-8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri-miR-199a-5p m6A modification was detected by Me-RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R-induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri-miR-199a-5p m6A methylation to block miR-199a-5p maturation and inhibit its expression. TNF receptor-associated Factor 3 (TRAF3) is a downstream gene of miR-199a-5p. Furthermore, in H/R-induced H9C2 cells, the miR-199a-5p inhibitor-mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression-mediated promotion of pyroptosis was offset by miR-199a-5p upregulation. ALKBH5 silencing inhibited pri-miR-199a-5p expression and enhanced pri-miR-199a-5p m6A modification to promote miR-199a-5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression.Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT-qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit-8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri-miR-199a-5p m6A modification was detected by Me-RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R-induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri-miR-199a-5p m6A methylation to block miR-199a-5p maturation and inhibit its expression. TNF receptor-associated Factor 3 (TRAF3) is a downstream gene of miR-199a-5p. Furthermore, in H/R-induced H9C2 cells, the miR-199a-5p inhibitor-mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression-mediated promotion of pyroptosis was offset by miR-199a-5p upregulation. ALKBH5 silencing inhibited pri-miR-199a-5p expression and enhanced pri-miR-199a-5p m6A modification to promote miR-199a-5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression.
Author Tang, Mi
Li, Jiarong
Wang, Zhirong
Tan, Huayi
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  fullname: Wang, Zhirong
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  surname: Tang
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MI/RI
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Snippet Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However,...
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SubjectTerms Adenine
AlkB Homolog 5, RNA Demethylase - genetics
AlkB Homolog 5, RNA Demethylase - metabolism
ALKBH5
Animals
Cell viability
Chromosome 5
Demethylation
Echocardiography
Flow cytometry
Heart function
Immunofluorescence
Immunohistochemistry
Immunoprecipitation
Injury prevention
Ischemia
Maturation
MI/RI
MicroRNAs - metabolism
Molecular modelling
Myocardial ischemia
Myocardial Reperfusion Injury - genetics
Myocardial Reperfusion Injury - metabolism
N6-methyladenosine
pri‐miR‐199a‐5p
Pyroptosis
Rats
Reperfusion
TNF Receptor-Associated Factor 3 - genetics
TNF Receptor-Associated Factor 3 - metabolism
TRAF3
Tumor necrosis factor receptors
Western blotting
Title ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjbt.23710
https://www.ncbi.nlm.nih.gov/pubmed/38605440
https://www.proquest.com/docview/3039083804
https://www.proquest.com/docview/3038426994
Volume 38
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