dc.contributor.author |
Qi, Xuewen |
|
dc.contributor.author |
Liu, Haifeng |
|
dc.contributor.author |
Mao, Limei |
|
dc.contributor.author |
Sun, Peng |
|
dc.contributor.author |
Kong, Degui |
|
dc.date.accessioned |
2022-11-03T10:09:09Z |
|
dc.date.available |
2022-11-03T10:09:09Z |
|
dc.date.issued |
2017-03 |
|
dc.identifier.citation |
Qi, X., Liu, H., Mao, L., Sun, P., & Kong, D. (2017). Combination of exendin-4 and DPP-4 silencing promoted angiogenesis of human coronary artery endothelial cells via activation of PI3K/Akt pathway. Pakistan journal of pharmaceutical Sciences, 30. |
en_US |
dc.identifier.issn |
1011-601X |
|
dc.identifier.uri |
http://142.54.178.187:9060/xmlui/handle/123456789/13909 |
|
dc.description.abstract |
This study was aimed to explore the combined effects of Exendin-4 with dipeptidyl peptidase-IV (DPP-4)
silencing on vascular endothelial growth factor (VEGF)-induced cell proliferation and angiogenesis in Human Coronary Artery Endothelial Cells (HCAECs), as well as the underlying molecular mechanisms which were involved in this process. HCAECs were treated by exendin-4, small interfering RNA (siRNA) targeting DPP-4 (DPP-4-siRNA) or exendin-4 plus DPP-4-siRNA, respectively. Cell migration, proliferation and angiogenesis in vitro were assessed by scratch-wound assay, MTT, tran swell assay, and matrigel tube formation, respectively. Cell apoptosis was investigated by TUNEL assay. Expression of apoptosis and PI3K/Akt related proteins were assessed by Western blotting. Incubation of HCAECs with exendin-4 and silencing of DPP-4 both caused an increase in cell proliferation, migration and tube formation, while a significant decrease in apoptosis (all p<0.05). Furthermore, the combination of the exendin-4 and silencing of DPP-4 had additional effects on HCAECs. Protein levels of p-Akt and p-PI3K were markedly increased by exendin-4 incubation, silencing of DPP-4 in HCAECs. These results suggest that combination of exendin-4 and silencing of DPP-4 had additional promoted effects on angiogenesis of HCAECs via activation of PI3K/Akt pathway. Our study indicated an alternative therapeutic strategy for atherosclerotic neovascularization. |
en_US |
dc.language.iso |
en_US |
en_US |
dc.publisher |
Faculty of Pharmacy & Pharmaceutical Sciences |
en_US |
dc.subject |
Exendin |
en_US |
dc.subject |
Dipeptidyl peptidase-IV |
en_US |
dc.subject |
angiogenesis |
en_US |
dc.subject |
HCAEC |
en_US |
dc.subject |
PI3K/Akt |
en_US |
dc.title |
Combination of exendin-4 and DPP-4 silencing promoted angiogenesis of human coronary artery endothelial cells via activation of PI3K/Akt pathway |
en_US |
dc.type |
Article |
en_US |