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Long noncoding RNA TDRG1 aggravates doxorubicin‐induced cardiomyopathy by binding with miR‐873‐5p to upregulate PRKAR2
Doxorubicin‐induced cardiomyopathy (DCM) is a life‐threatening event. The long noncoding RNAs (lncRNAs) have been reported with close associations with DCM, which may provide novel insight into pathophysiological mechanisms of DCM. DCM rat model and cell models were established using doxorubicin. Echocardiography analyses were performed to assess cardiac function. We found that testis developmental‐related gene 1 (TDRG1) expression was upregulated in DCM rats and in doxorubicin‐treated human umbilical vein endothelial cells (HUVECs). TDRG1 knockdown enhanced cell viability, promoted tube formation, and inhibited apoptosis of doxorubicin‐treated HUVECs. Additionally, knockdown of TDRG1 alleviated cardiac injury in DCM rats. Mechanistically, miR‐873‐5p was identified to bind with TDRG1. In addition, protein kinase cAMP‐dependent type II regulatory subunit alpha (PRKAR2) was confirmed to bind with miR‐873‐5p as a target mRNA. MiR‐873‐5p negatively regulated PRKAR2 mRNA and protein levels. At last, rescue assays indicated that the overexpression of PRKAR2 restored the effect of TDRG1 knockdown on doxorubicin‐treated HUVEC angiogenesis and apoptosis. To conclude, TDRG1 aggravates DCM progression by binding with miR‐873‐5p to upregulate PRKAR2. This work suggested the potential of TDRG1 as a target for DCM treatment.
Long noncoding RNA TDRG1 aggravates doxorubicin‐induced cardiomyopathy by binding with miR‐873‐5p to upregulate PRKAR2
Doxorubicin‐induced cardiomyopathy (DCM) is a life‐threatening event. The long noncoding RNAs (lncRNAs) have been reported with close associations with DCM, which may provide novel insight into pathophysiological mechanisms of DCM. DCM rat model and cell models were established using doxorubicin. Echocardiography analyses were performed to assess cardiac function. We found that testis developmental‐related gene 1 (TDRG1) expression was upregulated in DCM rats and in doxorubicin‐treated human umbilical vein endothelial cells (HUVECs). TDRG1 knockdown enhanced cell viability, promoted tube formation, and inhibited apoptosis of doxorubicin‐treated HUVECs. Additionally, knockdown of TDRG1 alleviated cardiac injury in DCM rats. Mechanistically, miR‐873‐5p was identified to bind with TDRG1. In addition, protein kinase cAMP‐dependent type II regulatory subunit alpha (PRKAR2) was confirmed to bind with miR‐873‐5p as a target mRNA. MiR‐873‐5p negatively regulated PRKAR2 mRNA and protein levels. At last, rescue assays indicated that the overexpression of PRKAR2 restored the effect of TDRG1 knockdown on doxorubicin‐treated HUVEC angiogenesis and apoptosis. To conclude, TDRG1 aggravates DCM progression by binding with miR‐873‐5p to upregulate PRKAR2. This work suggested the potential of TDRG1 as a target for DCM treatment.
Long noncoding RNA TDRG1 aggravates doxorubicin‐induced cardiomyopathy by binding with miR‐873‐5p to upregulate PRKAR2
Liu, Yihang (author) / Tan, Linlin (author) / Zhang, Ming (author) / Yang, Chuang (author)
Environmental Toxicology ; 37 ; 2072-2083
2022-08-01
12 pages
Article (Journal)
Electronic Resource
English
Protective effect of Co-enzyme Q10 On doxorubicin-induced cardiomyopathy of rat hearts
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