Background: Long non-coding RNA (lncRNA) hypoxia
inducible factor 1-antisense RNA 1
(HIF1A-AS1) serves
critical roles in cardiovascular diseases (CVDs). Vascular endothelial cells
(VECs) are vulnerable to stimuli. Our previous study revealed that knockdown of
HIF1A-AS1 reduces palmitic acid-induced apoptosis and promotes the
proliferation of human VECs (HUVECs);
however, the underlying mechanism remains unclear.
Material and Methods: Cell Counting Kit-8, flow
cytometry, transwell invasion, and wound healing were applied to detect the
function of HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing
(RNA-seq) were conducted to uncover its underlying mechanism. Quantitative
Polymerase Chain Reaction (qPCR) was implemented to assess the accuracy of
miRNA-seq. A co-expression network was generated to determine the relationship
between differentially expressed miRNAs (DEmiRNAs) and differentially expressed
genes (DEGs). Results: Knockdown of HIF1A-AS1 promoted the
proliferation, migration, and invasion but reduced the apoptosis of HUVECs, and
the overexpression of this lncRNA had the opposite effect. Numerous DEmiRNAs and
DEGs were identified, which might contribute to this phenomenon. Multiple target
genes of DEmiRNAs were associated with cell proliferation and apoptosis, and
overlapped with DEGs identified from RNA-seq. Finally, the network manifested
that lncRNA HIF1A-AS1 moderated the function of HUVECs by not only
regulating the expression of some genes directly but also by influencing a few
miRNAs to indirectly mediate the expression of mRNAs. Conclusions: The
results suggested that HIF1A-AS1 might regulate HUVEC
function by not only regulating the expression of some genes directly but also by
influencing some miRNAs to indirectly mediate the expression level of mRNA.