The value of circulating exosomes-mediated lncRNA HOXA11-AS in the proliferation of vascular endothelial cell by up-regulating SOX4
WANG Ping1, MENG Liping1, LIU Longbin2, PENG Fang1
1.Department of Cardiology, Shaoxing People’s Hospital (Shaoxing Hospital of Zhejiang University), Shaoxing 312000, China;2.Department of Cardiology, Affiliated Hospital of Shaoxing College of Arts and Sciences (Shaoxing Municipal Hospital), Shaoxing 312000, China
WANG Ping,MENG Liping,LIU Longbin, et al. The value of circulating exosomes-mediated lncRNA HOXA11-AS in the proliferation of vascular endothelial cell by up-regulating SOX4[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(8): 639-645.
Abstract：Objective: To explore the effect of circulating exosomes on the proliferation ability of endothelialm cells and its possible mechanism. Methods: The plasma of patients with in-stent restenosis (ISR, n=199) and Non-ISR (n=32) was collected and the exosomes in the plasma were extracted. The exosomes were used to intervene the endothelial cell proliferation inhibition model induced by rapamycin. The cell proliferation ability of each group was measured by MTT method. The expression of PCNA and Ki67 in cells was measured by Western blot. The gene chip was used to detect the difference in non-coding RNA of the two groups of exosomes, and qRT-PCR was used to detect the expression of lnc HOXA11-AS. Results: Compared with the control group, the cell proliferation ability of the rapamycin group was weakened, and the expression of PCNA and Ki67 decreased (P<0.05); compared with the rapamycin group, the endothelial cell proliferation ability of the control group increased after exosomal intervention, and the expression of PCNA and Ki67 increased (P<0.05). The microarray results showed that the expression of lnc HOXA11-AS was reduced in ISR exosomes. pHOXA11-AS increased the proliferation of endothelial cells as well as the expression of PCNA, Ki67 and SOX4. Conclusion: Lnc HOXA11-AS in plasma exosomes may increase the proliferation ability of endothelial cells by up-regulating the expression of SOX4.
