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CRACK Scanitto Pro V3.17 Final Loader – [SH] !FULL! ↗️

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]\]. Consistent with this, our preliminary data also indicated that the expression of miR‐31 was increased in the PASMCs of the PAH rats and was inversely correlated with the mRNA expression of UCP2, a hallmark of mitochondrial uncoupling \[[20](#sct312784-bib-0020){ref-type=”ref”}, [21](#sct312784-bib-0021){ref-type=”ref”}, [22](#sct312784-bib-0022){ref-type=”ref”}\]. Our findings are consistent with the previous studies which showed that repressing miR‐31 in cancer stem cell increased their mitochondrial uncoupling, causing a severe reduction in stem cell self‐renewal and tumorigenesis \[[11](#sct312784-bib-0011){ref-type=”ref”}, [12](#sct312784-bib-0012){ref-type=”ref”}, [23](#sct312784-bib-0023){ref-type=”ref”}\].

Our data indicate that the effects of miR‐31 on promoting proliferation and reducing apoptosis could be attenuated by increasing UCP2 in PAH rat PASMCs. However, how UCP2 is involved in the cellular effects of miR‐31 in PAH is still not fully understood. In terms of how these two molecules are connected, we found that the expression of miR‐31 was decreased while UCP2 was increased after overexpressing miR‐31 in PASMCs, which could lead to mitochondrial uncoupling. Further experiments indicated that inhibiting UCP2 in PASMCs could recover the proliferation and apoptosis phenotypes which were induced by miR‐31 overexpression in PAH rat PASMCs. These data confirmed our hypothesis that miR‐31‐mediated mitochondrial uncoupling could be involved in the proliferation and apoptosis of PAH PASMCs.

Our data indicated that the overexpression of UCP2 rescued the mitochondrial uncoupling effect of miR‐31 on P
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