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MicroRNA-322-5p Protects Against Myocardial Infarction through Targeting BTG2

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Abstract Objective: A large cohort of studies have addressed the therapeutic importance of microRNA (miR) in the treatment of myocardial infarction (MI). The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2).Methods: In a rat model of MI miR-322-5p and BTG2 expression was estimated. Adenovirus that altered miR-322-5p or BTG2 expression was injected into MI rats. After that, cardiac function, inflammation, myocardial injury, pathological condition, apoptosis, and the NF-κB pathway-related genes in the myocardial tissue of MI rats after targeted treatment were evaluated. The targeting relationship between miR-322-5p and BTG2 was assessed.Results: miR-322-5p was lowly expressed and BTG2 was highly expressed in the myocardial tissue of MI rats. Restored miR-322-5p improved cardiac function, relived inflammation and myocardial injury, suppressed pathological condition and apoptosis and inactivated NF-κB pathway in MI rats. BTG2 expression was negatively mediated by miR-322-5p. Overexpressed BTG2 rescued miR-322-5p-induced cardioprotection on MI rats.Conclusion: It is evident that miR-322-5p protects against MI through suppressing BTG2 expression.
Title: MicroRNA-322-5p Protects Against Myocardial Infarction through Targeting BTG2
Description:
Abstract Objective: A large cohort of studies have addressed the therapeutic importance of microRNA (miR) in the treatment of myocardial infarction (MI).
The current paper gives prominence to the role of miR-322-5p in MI by regulating B-cell translocation gene 2 (BTG2).
Methods: In a rat model of MI miR-322-5p and BTG2 expression was estimated.
Adenovirus that altered miR-322-5p or BTG2 expression was injected into MI rats.
After that, cardiac function, inflammation, myocardial injury, pathological condition, apoptosis, and the NF-κB pathway-related genes in the myocardial tissue of MI rats after targeted treatment were evaluated.
The targeting relationship between miR-322-5p and BTG2 was assessed.
Results: miR-322-5p was lowly expressed and BTG2 was highly expressed in the myocardial tissue of MI rats.
Restored miR-322-5p improved cardiac function, relived inflammation and myocardial injury, suppressed pathological condition and apoptosis and inactivated NF-κB pathway in MI rats.
BTG2 expression was negatively mediated by miR-322-5p.
Overexpressed BTG2 rescued miR-322-5p-induced cardioprotection on MI rats.
Conclusion: It is evident that miR-322-5p protects against MI through suppressing BTG2 expression.

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