Jian and Xia discovered that the microRNA miR-1226-3p promoted the endothelial nitric oxide synthase (eNOS) expression of pulmonary arterial endothelial cells and protected rat models from injury caused by pulmonary arterial hypertension (PAH), according to a new study published in BioMed Research International.
Scientists have observed pathological changes in patients with PAH, such as pulmonary vasoconstriction and inflammation. The key question is how medical intervention can be introduced effectively to mitigate PAH injury.
One method is to increase arterial pressure by inducing nitric oxide deficiency in endothelial cells, which is controlled by eNOS in human pulmonary arterial endothelial cells (HPAECs).
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Profilin 1 (Pfn1) has also gained scientific interest due to its abundance in stable atherosclerotic plaques extracted from infarct-related arteries in patients with acute myocardial infarction. Overexpression of Pfn1 has been associated with decreased levels of eNOS in rat PAECS (rPAECS) in rat model studies.
In addition, scientists have also been studying the role of microRNA expression in disease regulation. MicroRNAs have been discovered to be involved in the dysfunction of HPAECs, and miR-1226-3p has been discovered to be downregulated in the serum of patients with PAH. Jian and Xia thus decided to conduct a study to further investigate its role in PAH regulation.
Read more about PAH etiology
First, PAH-like conditions were introduced in rat models through the injection of monocrotaline at 60 mg/kg. The PAH rat models were then divided into 3 groups:
- A PAH and miR-NC group (miR-NC was the negative control microRNA)
- A PAH and miR-1226-3p group
- A PAH and saline group.
After 21 days, the rats were anesthetized and measured for their hemodynamics.
“The results showed that miR-1226-3p was significantly downregulated in the lungs of the PAH rats. Besides, overexpressed miR-1226-3p increased the expression level of eNOS in rPAECs,” Jian and Xia wrote.
The increased expression of eNOS in rPAECs alleviated the symptoms of PAH in PAH-induced rat models. miR-12226-3p inhibited the expression of Pfn1, which also contributed to an increased expression of eNOS in rPAECs. This demonstrated that miR-1226-3p has a protective effect in PAH.
Reference
Jian J, Xia L. miR-1226-3p promotes eNOS expression of pulmonary arterial endothelial cells to mitigate hypertension in rats via targeting Profilin-1. BioMed Res Int. Published online November 3, 2021. doi:10.1155/2021/1724722
