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Regulation of endothelial cell and endothelial progenitor cell survival and vasculogenesis by integrin-linked kinase.
Arterioscler Thromb Vasc Biol. 2005 Jun; 25(6):1154-60.AT

Abstract

OBJECTIVE

New vessel formation is a dynamic process of attachment, detachment, and reattachment of endothelial cells (ECs) and endothelial progenitor cells (EPCs) with each other and with the extracellular matrix (ECM). Integrin-linked kinase (ILK) plays a pivotal role in ECM-mediated signaling. Therefore, we investigated the role of ILK in ECs and EPCs during neovascularization.

METHODS AND RESULTS

In human umbilical cord vein ECs and EPCs, endogenous ILK expression, along with subsequent cell survival signals phospho-Akt and phospho-glycogen synthase kinase 3beta, was reduced after anchorage or nutrient deprivation. Even brief anchorage deprivation resulted in retarded capillary tube formation by ECs. Adenoviral ILK gene transfer in ECs and EPCs reversed the decrease in cell survival signals after anchorage or nutrient deprivation, leading to enhanced survival, reduced apoptosis, and significantly accelerated the functional recovery after reattachment. And ILK overexpressing EPCs significantly improved blood flow recovery and prevented limb loss in nude mice hindlimb ischemia model. Furthermore, the efficacy of systemic delivery was equivalent to local injection of ILK-EPCs.

CONCLUSIONS

ILK overexpression protects ECs and EPCs from anchorage- or nutrient-deprived stress and enhances neovascularization, suggesting that ILK is an optimal target gene for genetically modified cell-based therapy. Neovascularization is a dynamic process of detachment and reattachment of ECs and EPCs. Endogenous ILK expression was decreased in various stress conditions, and the gene transfer of ILK protected ECs and EPCs from temporary anchorage or nutrient deprivation. Furthermore, ILK gene transfer in EPCs significantly enhanced neovascularization in vivo.

Authors+Show Affiliations

Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15802621

Citation

Cho, Hyun-Jai, et al. "Regulation of Endothelial Cell and Endothelial Progenitor Cell Survival and Vasculogenesis By Integrin-linked Kinase." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 25, no. 6, 2005, pp. 1154-60.
Cho HJ, Youn SW, Cheon SI, et al. Regulation of endothelial cell and endothelial progenitor cell survival and vasculogenesis by integrin-linked kinase. Arterioscler Thromb Vasc Biol. 2005;25(6):1154-60.
Cho, H. J., Youn, S. W., Cheon, S. I., Kim, T. Y., Hur, J., Zhang, S. Y., Lee, S. P., Park, K. W., Lee, M. M., Choi, Y. S., Park, Y. B., & Kim, H. S. (2005). Regulation of endothelial cell and endothelial progenitor cell survival and vasculogenesis by integrin-linked kinase. Arteriosclerosis, Thrombosis, and Vascular Biology, 25(6), 1154-60.
Cho HJ, et al. Regulation of Endothelial Cell and Endothelial Progenitor Cell Survival and Vasculogenesis By Integrin-linked Kinase. Arterioscler Thromb Vasc Biol. 2005;25(6):1154-60. PubMed PMID: 15802621.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of endothelial cell and endothelial progenitor cell survival and vasculogenesis by integrin-linked kinase. AU - Cho,Hyun-Jai, AU - Youn,Seock-Won, AU - Cheon,Soo-In, AU - Kim,Tae-Youn, AU - Hur,Jin, AU - Zhang,Shu-Ying, AU - Lee,Seung Pyo, AU - Park,Kyung-Woo, AU - Lee,Myoung-Mook, AU - Choi,Yun-Shik, AU - Park,Young-Bae, AU - Kim,Hyo-Soo, Y1 - 2005/03/31/ PY - 2005/4/2/pubmed PY - 2005/12/22/medline PY - 2005/4/2/entrez SP - 1154 EP - 60 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 25 IS - 6 N2 - OBJECTIVE: New vessel formation is a dynamic process of attachment, detachment, and reattachment of endothelial cells (ECs) and endothelial progenitor cells (EPCs) with each other and with the extracellular matrix (ECM). Integrin-linked kinase (ILK) plays a pivotal role in ECM-mediated signaling. Therefore, we investigated the role of ILK in ECs and EPCs during neovascularization. METHODS AND RESULTS: In human umbilical cord vein ECs and EPCs, endogenous ILK expression, along with subsequent cell survival signals phospho-Akt and phospho-glycogen synthase kinase 3beta, was reduced after anchorage or nutrient deprivation. Even brief anchorage deprivation resulted in retarded capillary tube formation by ECs. Adenoviral ILK gene transfer in ECs and EPCs reversed the decrease in cell survival signals after anchorage or nutrient deprivation, leading to enhanced survival, reduced apoptosis, and significantly accelerated the functional recovery after reattachment. And ILK overexpressing EPCs significantly improved blood flow recovery and prevented limb loss in nude mice hindlimb ischemia model. Furthermore, the efficacy of systemic delivery was equivalent to local injection of ILK-EPCs. CONCLUSIONS: ILK overexpression protects ECs and EPCs from anchorage- or nutrient-deprived stress and enhances neovascularization, suggesting that ILK is an optimal target gene for genetically modified cell-based therapy. Neovascularization is a dynamic process of detachment and reattachment of ECs and EPCs. Endogenous ILK expression was decreased in various stress conditions, and the gene transfer of ILK protected ECs and EPCs from temporary anchorage or nutrient deprivation. Furthermore, ILK gene transfer in EPCs significantly enhanced neovascularization in vivo. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/15802621/Regulation_of_endothelial_cell_and_endothelial_progenitor_cell_survival_and_vasculogenesis_by_integrin_linked_kinase_ L2 - https://www.ahajournals.org/doi/10.1161/01.ATV.0000164312.20008.93?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -