Citrate pretreatment attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via regulating microRNA-142-3p/Rac1 aix

Xiang, Haiyan; Yang, Juesheng; Li, Jin; Yuan, Linhui; Lu, Fei; Liu, Chen; Tang, Yanhua

doi:10.1080/10799893.2020.1768548

Cited by 6 publications

(10 citation statements)

References 35 publications

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“…[21] miR-142-3p expression is suppressed in rat cardiomyocytes, and miR-142-3p overexpression inhibits H/R injuryinitiated apoptosis and autophagy and reduces LDH and MDA levels. [22] This is consistent with our findings. HIF1AN, an asparaginyl hydroxylase, has been reported to negatively regulate hypoxia-inducible factor-1 alpha (HIF-1α) stability and transcriptional activity by interacting with HIF-1α.…”

Section: Discussionsupporting

confidence: 94%

“…[ 21 ] miR‐142‐3p expression is suppressed in rat cardiomyocytes, and miR‐142‐3p overexpression inhibits H/R injury‐initiated apoptosis and autophagy and reduces LDH and MDA levels. [ 22 ] This is consistent with our findings. In addition, we have also demonstrated that PDG treatment can up‐regulate miR‐142‐3p expression in cardiomyocytes, decrease the levels of ROS, LDH, and CK‐MB, promote cell viability, and inhibit cardiomyocyte apoptosis, indicating that PDG may alleviate MIRI by promoting miR‐142‐3p expression.…”

Section: Discussionsupporting

confidence: 94%

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Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN

Yuan

Liang

Lin

et al. 2022

J Biochem & Molecular Tox

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This study is aimed to investigate the effect of pinoresinol diglucoside (PDG) in ameliorating myocardial ischemia-reperfusion injury (MIRI). Hypoxia/reperfusion (H/R)induced H9c2 cardiomyocytes were used to establish an in-vitro ischemia-reperfusion injury model of cardiomyocytes. Cells were treated with 1 μmol/L of PDG. Reactive oxygen species (ROS) level was detected by a 2′,7′-dichlorofluorescein-diacetate assay. The release of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) was examined by enzyme-linked immunosorbent assay. The viability and apoptosis of H9c2 cells were probed by MTT assay and flow cytometry. Besides this, Western blot and quantitative real-time PCR were used to detect microRNA-142-3p (miR-142-3p) and hypoxia-inducible factor 1 subunit alpha inhibitor (HIF1AN) expression levels. The binding sequence between miR-142-3p and HIF1AN 3′-untranslated region was validated by a dual-luciferase reporter gene assay. PDG treatment significantly reduced the level of ROS, LDH, and CK-MB, promoted viability, and inhibited the apoptosis of H9c2 cells. PDG treatment promoted miR-142-3p expression and inhibited HIF1AN expression in H9c2 cells. MiR-142-3p overexpression enhanced the effects of PDG on ROS, LDH, CK-MB levels, cell viability, and apoptosis in H9c2 cardiomyocytes, while overexpression of HIF1AN reversed the above effects. PDG ameliorates H/R-induced injury of cardiomyocytes by regulating miR-142-3p and HIF1AN.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 94%

Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN

Yuan

Liang

Lin

et al. 2022

J Biochem & Molecular Tox

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“…Upregulation of LAMP1 could form autolysosomes and accelerate ROS removal, thus inhibiting oxidative stress [ 29 ]. It is well known that excessive superoxide mediated oxidative stress and autophagy plays an important role in myocardial injury [ 30 ], suggesting that LAMP1 may be a key player in cardiomyocytes. Hence, whether CTRP3 and LAMP1 are related needs to be discussion.…”

Section: Discussionmentioning

confidence: 99%

CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway

Song

Zhang

Wan

et al. 2022

Aging

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Background: C1q/tumor necrosis factor-related protein 3 (CTRP3) has been reported to be a crucial regulator in myocardial infarction. Nevertheless, the potential molecular mechanism of CTRP3 in ischemia/reperfusion (I/R) injury remains largely unclear. Methods: The cell model of myocardial I/R injury was established by oxygen-glucose deprivation/reoxygenation (OGD/R) of rat cardiomyocyte H9C2. Expression of CTRP3 and lysosomal-associated membrane protein 1 (LAMP1) was detected in H9C2 cells treated with oxygen-glucose deprivation/reoxygenation (OGD/R). H9C2 cells were transfected with overexpression plasmids of CTRP3 (pcDNA-CTRP3) and LAMP1 (pcDNA-LAMP1), or CTRP3 small interfering RNA (si-CTRP3) or/and pcDNA-LAMP1, and cell proliferation, apoptosis and oxidative stress were testified. Co-IP assay was performed to validate the relationship among CTRP3, LAMP1 and JIP2. The role of CTRP3 and LAMP1 in JIP2/JNK pathway was evaluated with Western blot assay. Furthermore, in vivo myocardial I/R injury model was constructed to investigate the effect of CTRP3. Results: Overexpression of CTRP3 and LAMP1 both significantly promoted cell proliferation, inhibited apoptosis and the production of reactive oxygen species (ROS), malondialdehyde (MAD) and cardiac troponin (cTn-I), while silencing CTRP3 exerted the opposite effects, and LAMP1 overexpression reversed the effect of silencing CTRP3 on the aspects above. CTRP3 interacted with LAMP1, and both CTRP3 and LAMP1 bound with JIP2. SP600125 (JNK inhibitor) could restore the effects of CTRP3 or LAMP1 overexpression on the expression of JIP2 and phosphorylated-JNK (p-JNK), proliferation and apoptosis. Moreover, overexpression of CTRP3 improved cardiac I/R injury in vivo . Conclusion: CTRP3 alleviates cardiac I/R injury by elevating LAMP1 and activating JIP2/JNK signaling pathway, which may serve as a potential therapeutic target for I/R injury.

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“…miR‐142‐3p inhibits the expression of HMGB1, which partially suppressed hypoxia/reoxygenation (H/R)‐induced cardiomyocyte apoptosis and fibrosis 26 . Xiang et al also found that the pretreatment of citrate alleviates H/R‐induced cardiomyocyte injury by affecting miR‐142‐3p/Rac1 pathway 27 . Zhao et al's study suggested that miR‐142‐3p serves as a protecting role in the damage myocardial ischemia–reperfusion (MI/R) by mediating TLR4/NFkB pathway 28 .…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA TUG1 attenuates cerebral ischemia/reperfusion injury through regulating miR‐142‐3p

Zhang

Wang

et al. 2021

BioFactors

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Cerebral ischemia-reperfusion injury (CI/RI) is one of the most common diseases of the central nervous system. At present, there is no specific treatment for CI/RI. It is necessary to explore the mechanism of CI/RI and find new ways to prevent and treat CI/RI. An oxygen and glucose deprivation/recovery (OGD/R) model was established to evaluate the effects of mouse astrocytes (MA-C) cell viability and apoptosis of stepwise exposure to oxygen and glucose deprivation followed by their replenishment. This assessment included using taurine upregulated gene 1-small interfering RNAs (TUG1-siRNA) transfection to determine the effects of TUG1 knockdown on MA-C survival and apoptosis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate TUG1 and miR-142-3p expression levels. The luciferase gene reporter assay was performed to validate that miR-142-3p is a TUG1 target.Accordingly, the effects of miR-142-3p knockdown on TUG1-induced MA-C apoptosis were determined using flow cytometry. Methyl thiazolyl tetrazolium (MTT) method was used to detect cell growth viability. Western blotting analysis was performed to detect the expression levels of apoptosis-related proteins.TUG1 was upregulated, while miR-142-3p was downregulated in the OGD/R model of MA-C cells. Inhibiting the expression of TUG1 could protect MA-C cells and reverse the decrease in growth viability and increasing apoptosis of MA-C cells caused by OGD/R stimulation. On the other hand, the inhibition of miR-142-3p offset the effect of TUG1 knockdown on cell viability and apoptosis. Inhibition of OGD/R-induced increases in TUG1 expression that in turn reduces miR-142-3p upregulation may suppress reperfusion-induced losses in cell viability.

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Citrate pretreatment attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via regulating microRNA-142-3p/Rac1 aix

Cited by 6 publications

References 35 publications

Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN

Pinoresinol diglucoside ameliorates H/R‐induced injury of cardiomyocytes by regulating miR‐142‐3p and HIF1AN

CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway

Knockdown of lncRNA TUG1 attenuates cerebral ischemia/reperfusion injury through regulating miR‐142‐3p

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