Background
Hypertensive renal injury is one of the most lethal complications of hypertension. At present, renin-angiotensin-aldosterone system (RAAS) blockers are considered the best drugs for the treatment of renal injury in hypertension because of their nephroprotective effect of reducing proteinuria, but there are no specific drugs for this
Conclusions
The results of this study indicate that TrT has a reno-protective effect on AngII-induced hypertensive renal injury by miR-155-5p, which negatively regulates the expression of H2AC6. Our findings offer a new therapeutic strategy and have identified an effective candidate target for the treatment of hypertensive renal injury in clinical settings.
Methods
We investigated the underlying reno-protective mechanism of TrT on Angiotensin II (AngII)-induced hypertensive renal injury in glomerular endothelial cells by integrating the differential expression profiles of micro RNA (miRNA) and messenger RNA (mRNA) to construct a miRNA-mRNA interaction network associated with hypertensive kidney injury, followed by quantitative real-time polymerase chain reaction (qRT-PCR) for validation.
Results
Seventy-six differentially expressed mRNAs (DEmRNAs) and 1 differentially expressed miRNAs (DEmiRNAs) were identified in the control group and the AngII-induced hypertensive renal injury group, respectively. 110 DEmRNAs and 27 DEmiRNAs were identified in the TrT treatment group and the AngII-induced group, respectively. The core component of the miRNA-mRNA network was miR-155-5p. Our study showed that miR-155-5p expression levels were more decreased in the AngII-induced hypertensive renal injury group than the control group. TrT treatment also significantly upregulated miR-155-5p. Additionally, we found that miR-155-5p expression levels were negatively correlated with H2A clustered histone 6 (H2AC6). Conclusions: The results of this study indicate that TrT has a reno-protective effect on AngII-induced hypertensive renal injury by miR-155-5p, which negatively regulates the expression of H2AC6. Our findings offer a new therapeutic strategy and have identified an effective candidate target for the treatment of hypertensive renal injury in clinical settings.