Our study explored the effects of
lncRNA UCA1 on the proliferation and apoptosis in hypoxic human pulmonary artery smooth muscle cells (HPASMCs) and highlighted the endogenous relationship between UCA1, ING5, and
hnRNP I in cell proliferation.
Hypoxia-induced HPASMCs were used to simulate
pulmonary arterial hypertension in vitro. Microarray assay was adopted to screen the dysregulated expressed lncRNAs in HPASMCs to find out the target gene of our study. And RT-qPCR was performed to detect the expression of
lncRNA UCA1 under
hypoxia and normoxia. After transfection, the relationship between UCA1 and cell proliferation in HPASMCs under
hypoxia were determined by cell proliferation assay and relative expression of
PCNA. Next, ELISA assays were conducted to measure the
protein levels of
PCNA and ING5. What's more, flow cytometry was employed to measure the apoptosis rate in differentially UCA1-expressed HPASMCs. RIP assays were conducted to further clarify the endogenous relationship between UCA1 and ING5 in hypoxic HPASMCs. Finally, the effects of ING5 to HPASMCs were detected after transfection of ING5 and UCA1 to figure out the role of ING5 in HPASMCs.
Hypoxia was revealed to induce proliferation and inhibited apoptosis in HPASMCs. Besides, UCA1 was confirmed to be highly expressed under
hypoxia compared with normoxia. UCA1 boosted cell proliferation under
hypoxia in HPASMCs. However, the apoptosis was suppressed in the hypoxic HPASMCs transfected with pcDNA3.1-UCA1. Further, mechanism studies found that UCA1 competed with ING5 for
hnRNP I, so that upregulating UCA1 inhibited the
protein levels of ING5. And finally we found that ING5 restrained cell viability, but promoted cell apoptosis in hypoxic HPASMCs, which was reversed by UCA1 over-expression. In summary, our findings manifested that UCA1 promoted proliferation and restrained apoptosis by competing with ING5 for
hnRNP I in HPASMCs induced by
hypoxia, indicating their potential roles for the cure of hypoxic
pulmonary hypertension.