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HB-EGF promotes angiogenesis in endothelial cells via PI3-kinase and MAPK signaling pathways.
Growth Factors. 2007 Aug; 25(4):253-63.GF

Abstract

OBJECTIVE

Heparin-binding EGF-like growth factor (HB-EGF) belongs to the epidermal growth factor (EGF) superfamily of ligands. It has been implicated as a regulator of angiogenesis. However, the mechanisms by which HB-EGF promotes angiogenesis are unknown. The goal of the present study was to define the pathways by which HB-EGF stimulates angiogenesis in endothelial cells.

METHODS

To characterize the angiogenic activity of HB-EGF, we treated human umbilical vein endothelial cells (HUVEC) with HB-EGF and analyzed the effects on cell proliferation, migration and tube formation. Side-by-side assays with EGF were used for comparison.

RESULTS

Both HB-EGF and EGF stimulated HUVEC migration in scratch assays and promoted vascular tube formation in 2D-angiogenesis assays, without inducing cell proliferation. HB-EGF- and EGF-induced HUVEC migration and capillary tube formation were dependent upon activation of PI3K, MAPK and eNOS. Importantly, HB-EGF-and EGF-induced tube formation was comparable to, but were independent of tube formation induced by VEGF.

CONCLUSIONS

We have demonstrated that HB-EGF and EGF induce angiogenesis via activation of PI3K, MAPK and eNOS in a VEGF-independent fashion. Thus, the role played by HB-EGF in stimulating physiologic processes such as wound healing in vivo may be dependent, in part, on its ability to promote angiogenesis.

Authors+Show Affiliations

Department of Pediatric Surgery, The Research Institute at Nationwide Children's Hospital, Center for Perinatal Research, Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, OH, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18092233

Citation

Mehta, Veela B., and Gail E. Besner. "HB-EGF Promotes Angiogenesis in Endothelial Cells Via PI3-kinase and MAPK Signaling Pathways." Growth Factors (Chur, Switzerland), vol. 25, no. 4, 2007, pp. 253-63.
Mehta VB, Besner GE. HB-EGF promotes angiogenesis in endothelial cells via PI3-kinase and MAPK signaling pathways. Growth Factors. 2007;25(4):253-63.
Mehta, V. B., & Besner, G. E. (2007). HB-EGF promotes angiogenesis in endothelial cells via PI3-kinase and MAPK signaling pathways. Growth Factors (Chur, Switzerland), 25(4), 253-63.
Mehta VB, Besner GE. HB-EGF Promotes Angiogenesis in Endothelial Cells Via PI3-kinase and MAPK Signaling Pathways. Growth Factors. 2007;25(4):253-63. PubMed PMID: 18092233.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HB-EGF promotes angiogenesis in endothelial cells via PI3-kinase and MAPK signaling pathways. AU - Mehta,Veela B, AU - Besner,Gail E, PY - 2007/12/20/pubmed PY - 2008/3/28/medline PY - 2007/12/20/entrez SP - 253 EP - 63 JF - Growth factors (Chur, Switzerland) JO - Growth Factors VL - 25 IS - 4 N2 - OBJECTIVE: Heparin-binding EGF-like growth factor (HB-EGF) belongs to the epidermal growth factor (EGF) superfamily of ligands. It has been implicated as a regulator of angiogenesis. However, the mechanisms by which HB-EGF promotes angiogenesis are unknown. The goal of the present study was to define the pathways by which HB-EGF stimulates angiogenesis in endothelial cells. METHODS: To characterize the angiogenic activity of HB-EGF, we treated human umbilical vein endothelial cells (HUVEC) with HB-EGF and analyzed the effects on cell proliferation, migration and tube formation. Side-by-side assays with EGF were used for comparison. RESULTS: Both HB-EGF and EGF stimulated HUVEC migration in scratch assays and promoted vascular tube formation in 2D-angiogenesis assays, without inducing cell proliferation. HB-EGF- and EGF-induced HUVEC migration and capillary tube formation were dependent upon activation of PI3K, MAPK and eNOS. Importantly, HB-EGF-and EGF-induced tube formation was comparable to, but were independent of tube formation induced by VEGF. CONCLUSIONS: We have demonstrated that HB-EGF and EGF induce angiogenesis via activation of PI3K, MAPK and eNOS in a VEGF-independent fashion. Thus, the role played by HB-EGF in stimulating physiologic processes such as wound healing in vivo may be dependent, in part, on its ability to promote angiogenesis. SN - 0897-7194 UR - https://www.unboundmedicine.com/medline/citation/18092233/HB_EGF_promotes_angiogenesis_in_endothelial_cells_via_PI3_kinase_and_MAPK_signaling_pathways_ L2 - http://www.tandfonline.com/doi/full/10.1080/08977190701773070 DB - PRIME DP - Unbound Medicine ER -