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首页> 外文期刊>Cell biology international. >Inhibition of microRNA‐143‐3p attenuates myocardial hypertrophy by inhibiting inflammatory response
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Inhibition of microRNA‐143‐3p attenuates myocardial hypertrophy by inhibiting inflammatory response

机译：通过抑制炎症反应，抑制microRNA-143-3P衰减心肌肥厚

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Abstract MicroRNA‐143‐3p (miR‐143‐3p) is involved in the initiation of inflammatory response and the progression of cardiovascular diseases. Myocardial hypertrophy is a common symptom in numerous cardiovascular diseases. In the current study, we attempted to demonstrate the role of miR‐143‐3p in the development of myocardial hypertrophy by focusing on its association with inflammation. Myocardial hypertrophy was induced by transverse aortic constriction (TAC) method in vivo and by H 2 O 2 administration in vitro. The expression status of miR‐143‐3p and downstream effectors were detected in animal heart tissues and H9c2 cells. Furthermore, the effect of miR‐143‐3p inhibition on H 2 O 2 ‐induced changes in ERK5/PPARδ/NF‐κB axis was assessed. TAC induced oxidative stress and inflammation in rat heart tissues, which was associated with the increased expressions of miR‐143‐3p and p‐ERK5. However, the up‐regulated expression of miR‐143‐3p had no effect on the expression of ERK5, which was a direct target of miR‐143‐3p. The results of in vitro assays showed that H 2 O 2 administration increased the levels of miR‐143‐3p and p‐EKR5 and induced the activation of NF‐κB pathway. After the inhibition of miR‐143‐3p, the activation of EKR5 and NF‐κB pathway was suppressed, whereas the expression of PPARδ was up‐regulated. The current study demonstrated that miR‐143‐3p is crucial to the initiation of inflammatory response induced by myocardial hypertrophy. The activation of ERK5 following miR‐143‐3p up‐regulation appears to be a complementary response to induce the subsequent anti‐inflammatory signaling transduction, which needed further exploration.
机译：摘要MicroRNA-143-3P（MIR-143-3P）参与炎症反应的启动和心血管疾病的进展。心肌肥大是许多心血管疾病的常见症状。在目前的研究中，我们试图通过重点关注其与炎症的关联来展示MIR-143-3P在心肌肥厚中的作用。体内体内的横向主动脉收缩（TAC）法诱导了心肌肥大，并在体外通过H 2 O 2施用。在动物心脏组织和H9C2细胞中检测到miR-143-3p和下游效应器的表达状态。此外，评估miR-143-3p抑制对H 2 O 2-in诱导的ERK5 /PPARδ/ NF-κB轴的影响的影响。 TAC诱导大鼠心脏组织中的氧化应激和炎症，其与MIR-143-3P和P-ERK5的表达增加有关。然而，miR-143-3p的上调表达对ERK5的表达没有影响，这是miR-143-3p的直接靶标。体外测定的结果表明，H 2 O 2给药增加了MiR-143-3P和P-EKR5的水平，并诱导了NF-κB途径的活化。在抑制miR-143-3p之后，抑制了EKR5和NF-κB途径的激活，而PPARδ的表达上调。目前的研究表明，miR-143-3p对心肌肥大引起的炎症反应的开始至关重要。 MiR-143-3P上调后ERK5的激活似乎是诱导后续抗炎信号传递转导的互补响应，这需要进一步探索。

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