Thromb Haemost 2000; 83(06): 949-955
DOI: 10.1055/s-0037-1613948
Commentary
Schattauer GmbH

Expression of Vascular Endothelial Growth Factor in Human Umbilical Vein Endothelial Cells Stimulated with Interleukin-1α

An Autocrine Regulation of Angiogenesis and Inflammatory Reactions
Tadaatsu Imaizumi
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Hiroyuki Itaya
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Satoki Nasu
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Hidemi Yoshida
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Yuki Matsubara
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Koji Fujimoto
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
,
Tomoh Matsumiya
1   Department of Dentistry and Oral Surgery, Hirosaki University School of Medicine, Hirosaki, Japan
,
Hiroto Kimura
1   Department of Dentistry and Oral Surgery, Hirosaki University School of Medicine, Hirosaki, Japan
,
Kei Satoh
2   From the Department of Pathological Physiology, Institute of Neurological Diseases, Hirosaki, Japan
› Author Affiliations
Further Information

Publication History

Received 22 March 1999

Accepted after resubmission 28 January 2000

Publication Date:
14 December 2017 (online)

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Summary

Vascular endothelial growth factor (VEGF) is a specific mitogen for endothelial cells. We studied the production of VEGF by human umbilical vein endothelial cells (HUVEC) and smooth muscle cells (SMC) in response to the stimulation with interleukin-1α (IL-1α). HUVEC expressed VEGF mRNA in response to IL-1α in doseand time-dependent manners. In HUVEC VEGF protein was detected only in cell lysates whereas in SMC most of the VEGF protein was detected in the conditioned medium. Immunofluorescent staining also confirmed the cell-associated VEGF in HUVEC. IL-1α also induced the expression of mRNA for IL-1α itself in HUVEC. Cycloheximide treatment of HUVEC slightly inhibited the IL-1α-induced expression of VEGF mRNA, and IL-1α may mediate, at least in part, VEGF expression in response to IL-1α. The growth of HUVEC stimulated with IL-1α was inhibited by a neutralizing antibody against VEGF. We conclude that IL-1α and VEGF may play an important role in autocrine growth regulation of HUVEC.