HYPOXIA-INDUCIBLE FACTOR-1 ALPHA AND VASCULAR ENDOTHELIAL GROWTH FACTOR IN THE CAROTID ATHEROMA ARE EXPRESSED MORE IN SYMPTOMATIC CASES THAN IN ASYMPTOMATIC CASES

  • OSAWA TOMOSHI
    Departments of Neurosurgery, Nagoya City University Medical School
  • MASE MITSUHITO
    Departments of Neurosurgery, Nagoya City University Medical School
  • TANIKAWA MOTOKI
    Departments of Neurosurgery, Nagoya City University Medical School
  • FUJITA MASATAKA
    Departments of Neurophysiology, Nagoya City University Medical School
  • KATANO HIROYUKI
    Departments of Neurosurgery, Nagoya City University Medical School
  • AOYAMA KIMINORI
    Departments of Neurosurgery, Nagoya City University Medical School
  • OHNO TAKAYUKI
    Departments of Neurosurgery, Nagoya City University Medical School
  • SAKURAI KEITA
    Departments of Radiology, Nagoya City University Medical School
  • SASAKI SHIGERU
    Departments of Radiology, Nagoya City University Medical School
  • YAMADA KAZUO
    Departments of Neurosurgery, Nagoya City University Medical School

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Objects: We studied the expression of hypoxia-inducible factor-1 alpha (HIF1-alpha) and vascular endothelial growth factor (VEGF) in the carotid plaques, because they are involved in the tissue neovascularization and the resulting symptomatic transformation of asymptomatic carotid stenosis. We also explored the relation of tissue expression of HIF1-alpha and VEGH to preoperative MRI plaque imaging. Methods: We undertook immunohistochemical staining of endarterectomy tissues of 13 patients for HIF1-alpha and VEGF. We also undertook double immunostaining for macrophages of smooth muscle cells and HIF1-alpha or VEGF in order to identify the source cells of HIF1-alpha and VEGF. Immunostaining results and histological grading of atherosclerosis as defined by American Heart Association (AHA) were compared to preoperative profiles of the patients including plaque imaging on MRI. Results: Both HIF1-alpha and VEGF were expressed in the carotid plaques and the sources of those hypoxia-related proteins were macrophages and smooth muscle cells. Plaques from symptomatic patients expressed HIF1-alpha and VEGF more strongly than those from asymptomatic patients. The degree of carotid stenosis and plaque intensity on MRI had no correlation with the plaques obtained from the symptomatic or asymptomatic group. However, high-intensity carotid plaques had a significantly more advanced histological grading of atherosclerosis as defined by AHA. Conclusion: Symptomatic carotid plaques express more HIF1-alpha and VEGF. This may have a role in neovascularization and plaque hemorrhage, causing symptomatic transformation of asymptomatic plaques.

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