CXCL16 induces angiogenesis in autocrine signaling pathway involving hypoxia-inducible factor 1α in human umbilical vein endothelial cells | Zendy

Xiaowen Yu | Zendy; Renping Zhao | Zendy; Sensen Lin | Zendy; Xianshu Bai | Zendy; Luyong Zhang | Zendy; Shengtao Yuan | Zendy; Li Sun | Zendy

Open Access

CXCL16 induces angiogenesis in autocrine signaling pathway involving hypoxia-inducible factor 1α in human umbilical vein endothelial cells

Author(s) -

Xiaowen Yu,

Renping Zhao,

Sensen Lin,

Xianshu Bai,

Luyong Zhang,

Shengtao Yuan,

Li Sun

Publication year - 2015

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2015.4520

Subject(s) - angiogenesis , autocrine signalling , cxcl16 , mapk/erk pathway , protein kinase b , human umbilical vein endothelial cell , microbiology and biotechnology , biology , cancer research , vascular endothelial growth factor , umbilical vein , cxcl14 , vascular endothelial growth factor a , p38 mitogen activated protein kinases , signal transduction , chemistry , chemokine , immunology , receptor , chemokine receptor , biochemistry , inflammation , vegf receptors , in vitro

Chemokine (C-X-C motif) ligand 16 (CXCL16) is a new angiogenic factor inducing angiogenesis via extracellular signal-regulated kinases pathway. To further understand the molecular mechanism underlying CXCL16‑induced angiogenesis, we explored involvement of other relevant pathways in CXCL16-induced angiogenesis. In the present study, we investigated the mechanisms underlying CXCL16-induced angiogenesis in human umbilical vein endothelial cells (HUVECs). CXCL16 promoted HUVEC proliferation, tube formation and migration. Enzyme-linked immunosorbent assay revealed that CXCL16 induced vascular endothelial growth factor secretion from HUVECs. Western blot analysis showed that CXCL16 increased the level of hypoxia‑inducible factor 1α, p-extracellular signal-regulated kinases (ERK), p-p38 and p-Akt dose- and time-dependently. ERK-, p38- and Akt-selective inhibitors significantly suppressed HUVEC proliferation, migration, tube formation and hypoxia-inducible factor 1α (HIF-1α) expression induced by CXCL16. Furthermore, CXCL16 peptides induced CXCL16 secretion via ERK, p38 and Akt pathways, which was suppressed by HIF-1α-selective inhibitor PX12. Our data suggest that CXCL16 induces angiogenesis in autocrine manner via ERK, Akt, p38 pathways and HIF-1α modulation.

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