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kazunori Nakagawa Last modified date：2024.04.15

Lecturer / Pathobiology
Department of Basic Medicine
Faculty of Medical Sciences


Graduate School
Department of Pathological Sciences
Graduate School of Medical Sciences
Undergraduate School
Department of Medicine
School of Medicine


Homepage
https://kyushu-u.elsevierpure.com/en/persons/kazunori-nakagawa
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http://www.med.kyushu-u.ac.jp/pathol1/
Official home page of Lab. .
Phone
092-642-6066
Fax
092-642-5965
Academic Degree
Ph.D(Kyushu University, JAPAN)
Field of Specialization
Vascular Pathobiology, Experimental Pathology
Outline Activities
The patho-physiological role of vascular remodeling in the development and progression of atherosclerosis, thrombosis and proliferative diabetic retinopathy, remains unclear. To elucidate the molecular basis of vascular remodeling and to establish the novel and effective therapy on the basis of scientific evidences, we study on the molecular mechanisms of pathological vascular remodeling, as following fields.
(1) Cellular and and spatial hierarchy of angiogenic factors in angiogenic diseases.:
(2) Pathology of atherogenesis, athero-thrombogenesis and intra-neointimal angiogenesis:
Research
Research Interests
  • Molecular biological studies on pathogenic remodeling of blood vessels
    keyword : atherosclerosis, lipid, d-amino acid, metabolomics
    2017.04～2026.03.
  • Molecular biological studies on pathogenic mechanism of thrombosis
    keyword : Tissue factor, DIC, extrinsic coagulation, atherosclerosis
    2002.04～2020.03.
  • Patho-physiological studies on cellular cross-talk signal system in vascular remodeling
    keyword : angiogenesis, endothelial cells, gene transfer, vascular remodeling.
    2002.04～2023.03.
  • Studies on regulation system by dephosphorylation in tumorigenesis
    keyword : dephosphorylation , phospatase, cell cycle
    2006.05～2008.05.
Academic Activities
Reports
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Papers
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1. Kazunori Nakagawa, Mitsuru Tanaka, Tae Hun Hahm, Huu-Nghi Nguyen, Toshiro Matsui, Yong-Xiang Chen, Yutaka Nakashima, Accumulation of Plasma-derived Lipids in the Lipid Core and Necrotic Core of Human Atheroma: Imaging Mass Spectrometry and Histopathological Analyses, Arteriosclerosis, Thrombosis, and Vascular Biology, doi: 10.1161/ATVBAHA.121.316154., 41, 11, e498-e511, Epub 2021 Sep 2., 2021.11.
2. Kazunori Nakagawa, Yutaka Nakashima, Pathologic intimal thickening in human atherosclerosis is formed by extracellular accumulation of plasma-derived lipids and dispersion of intimal smooth muscle cells, Atherosclerosis, 10.1016/j.atherosclerosis.2018.03.039, 274, 235-242, 2018.07, Background and aims: Pathologic intimal thickening (PIT) is an important stage of atherosclerosis that leads to atheroma. The present study aimed to clarify the pathogenesis of PIT in humans. Methods: Coronary arteries were obtained from 43 autopsy subjects aged 15–49 years. Non-atherosclerotic intima and atherosclerotic intimal lesions were classified into four groups, i.e. diffuse intimal thickening, fatty infiltration, fatty streak, and PIT, and the number and density of macrophages and smooth muscle cells (SMCs) were determined. Components of the lesions and proliferative and apoptotic activities of macrophages and SMCs were investigated by immunohistochemistry and TUNEL assay. Results: Extracellular lipids accumulated mildly in the fatty infiltration and fatty streak, and abundantly in the PIT to form the lipid pool. The extracellular lipids co-localized with apolipoprotein B and fibrinogen. Macrophage foam cells accumulated in the fatty streak and PIT, but no TUNEL-positive macrophages were detected in any lesion. No significant difference in the number of SMCs was found between the four groups, but the density of SMCs decreased in the fatty streak and PIT. The decrease correlated with an increase in the number of macrophages, and the accumulation of extracellular lipids in the lipid pool. Neither Ki-67-positive nor TUNEL-positive SMCs were detected in any lesion. Conclusions: In PIT in human atherosclerosis, the lipid pool is formed by infiltration and deposition of plasma-derived lipids. Intimal SMCs are dispersed in association with macrophage infiltration and lipid pool formation without undergoing significant proliferation or death..
3. Yamashita A, Yonemitsu Y, Okano S, Nakagawa K, Nakashima Y, Irisa T, Iwamoto Y, Nagai Y, Hasegawa M, Sueishi K, Fibroblast growth factor-2 determines severity of joint disease in adjuvant-induced arthritis in rats., J Immunol, 168, 1, 450-457, 168(1),pp450-457, 2002.01.
4. Masaki I, Yonemitsu Y, Komori K, Ueno H, Nakashima Y, Nakagawa K, Fukumura M, Kato A, Hasan M, Nagai Y, Sugimachi K, Alton EWFW, Hasegawa M, Sueishi K., Recombinant Sendai virus-mediated gene transfer to vasculature: a new class of efficient gene transfer vector to the vascular system., FASEB J, 15, 7, 1294-1296, 15(7): 1294-1296, 2001, 2001.01.
Presentations
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Membership in Academic Society
  • The Japanese Circulation Society
  • Japan Atherosclerosis Society
  • The Japanese Society on Thrombosis and Hemostasis.
  • The Japanese Vascular Biology end Medicine Organization
  • The Japanese Biochemical Society


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