Expression of leptin receptor (Ob-R) in human atherosclerotic lesions

potential role in intimal neovascularization.

seokmin kang, H. M. Kwon, B. K. Hong, D. Kim, I. J. Kim, E. Y. Choi, Yangsoo Jang, H. S. Kim, M. S. Kim, H. C. Kwon

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Neovascularization of the adventitial vasa vasorum with extension into the intima of atherosclerotic lesions is frequently observed, but its pathophysiological significance is still subject to debate. Recently, leptin, the product of the Ob gene, was identified. Leptin, via activation of the endothelial receptor (Ob-R), generates a growth signal involving a tyrosine kinase-dependent intracellular pathway and promotes angiogenic processes. We hypothesized that a high concentration of leptin within vasa vasorum and plaque itself, may influence inflammatory and vascular neovascularization coupling with functional upregulation of the vascular endothelial growth factor (VEGF). Microscopic computerized tomography was utilized for the spatial distribution of vasa vasorum and intimal neovascularization from atherosclerotic human coronary arteries. Atherosclerotic coronary arteries showed a dense plexus of microvessels in the adventitia and plaque itself. Microscopic analysis from human atherosclerotic aortas revealed an increase in the intimal thickness with neovascularization. The immunoreactivity for Ob-R, VEGF and matrix metalloproteinase (MMP) increased in atherosclerotic plaque, predominantly in the endothelial lining of the intimal neovessel and macrophages/foam cells. Our observation of a prominent colocalization between Ob-R, VEGF and MMP supports this hypothesis and these factors participate in the neovascularization of atherosclerotic lesions. The present study is the first report on vascular tissue and it opens a promising perspective concerning future investigations of leptin-dependent modulation of atherogenesis and vascular neovascularization under pathophysiolgical conditions.

Original languageEnglish
Pages (from-to)68-75
Number of pages8
JournalYonsei medical journal
Volume41
Issue number1
DOIs
Publication statusPublished - 2000 Jan 1

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Tunica Intima
Leptin Receptors
Leptin
Vasa Vasorum
Vascular Endothelial Growth Factor A
Blood Vessels
Adventitia
Matrix Metalloproteinases
Coronary Vessels
Foam Cells
Atherosclerotic Plaques
Microvessels
Protein-Tyrosine Kinases
Aorta
Atherosclerosis
Up-Regulation
Macrophages
Tomography
Observation
Growth

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

kang, seokmin ; Kwon, H. M. ; Hong, B. K. ; Kim, D. ; Kim, I. J. ; Choi, E. Y. ; Jang, Yangsoo ; Kim, H. S. ; Kim, M. S. ; Kwon, H. C. / Expression of leptin receptor (Ob-R) in human atherosclerotic lesions : potential role in intimal neovascularization. In: Yonsei medical journal. 2000 ; Vol. 41, No. 1. pp. 68-75.
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Expression of leptin receptor (Ob-R) in human atherosclerotic lesions : potential role in intimal neovascularization. / kang, seokmin; Kwon, H. M.; Hong, B. K.; Kim, D.; Kim, I. J.; Choi, E. Y.; Jang, Yangsoo; Kim, H. S.; Kim, M. S.; Kwon, H. C.

In: Yonsei medical journal, Vol. 41, No. 1, 01.01.2000, p. 68-75.

Research output: Contribution to journalArticle

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T1 - Expression of leptin receptor (Ob-R) in human atherosclerotic lesions

T2 - potential role in intimal neovascularization.

AU - kang, seokmin

AU - Kwon, H. M.

AU - Hong, B. K.

AU - Kim, D.

AU - Kim, I. J.

AU - Choi, E. Y.

AU - Jang, Yangsoo

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AU - Kwon, H. C.

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N2 - Neovascularization of the adventitial vasa vasorum with extension into the intima of atherosclerotic lesions is frequently observed, but its pathophysiological significance is still subject to debate. Recently, leptin, the product of the Ob gene, was identified. Leptin, via activation of the endothelial receptor (Ob-R), generates a growth signal involving a tyrosine kinase-dependent intracellular pathway and promotes angiogenic processes. We hypothesized that a high concentration of leptin within vasa vasorum and plaque itself, may influence inflammatory and vascular neovascularization coupling with functional upregulation of the vascular endothelial growth factor (VEGF). Microscopic computerized tomography was utilized for the spatial distribution of vasa vasorum and intimal neovascularization from atherosclerotic human coronary arteries. Atherosclerotic coronary arteries showed a dense plexus of microvessels in the adventitia and plaque itself. Microscopic analysis from human atherosclerotic aortas revealed an increase in the intimal thickness with neovascularization. The immunoreactivity for Ob-R, VEGF and matrix metalloproteinase (MMP) increased in atherosclerotic plaque, predominantly in the endothelial lining of the intimal neovessel and macrophages/foam cells. Our observation of a prominent colocalization between Ob-R, VEGF and MMP supports this hypothesis and these factors participate in the neovascularization of atherosclerotic lesions. The present study is the first report on vascular tissue and it opens a promising perspective concerning future investigations of leptin-dependent modulation of atherogenesis and vascular neovascularization under pathophysiolgical conditions.

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