The expression of CD36 in vessels with blood-brain barrier impairment in a stroke-prone hypertensive model

被引:18
|
作者
Ueno, M. [1 ]
Nakagawa, T. [4 ]
Nagai, Y. [4 ]
Nishi, N. [4 ]
Kusaka, T. [5 ]
Kanenishi, K. [2 ]
Onodera, M. [1 ]
Hosomi, N. [6 ]
Huang, C. [7 ]
Yokomise, H. [3 ]
Tomimoto, H. [8 ]
Sakamoto, H. [1 ]
机构
[1] Kagawa Univ, Fac Med, Dept Pathol & Host Def, Miki, Kagawa 7610793, Japan
[2] Kagawa Univ, Fac Med, Dept Perinatol & Gynecol, Miki, Kagawa 7610793, Japan
[3] Kagawa Univ, Fac Med, Dept Gen Thorac Surg, Miki, Kagawa 7610793, Japan
[4] Kagawa Univ, Fac Med, Life Sci Res Ctr, Miki, Kagawa 7610793, Japan
[5] Kagawa Univ, Fac Med, Maternal & Perinatal Ctr, Miki, Kagawa 7610793, Japan
[6] Hiroshima Univ, Grad Sch Biomed Sci, Dept Clin Neurosci & Therapeut, Hiroshima, Japan
[7] Kyoto Univ, Fac Med, Dept Thorac Surg, Kyoto, Japan
[8] Mie Univ, Grad Sch Med, Dept Neurol, Tsu, Mie 514, Japan
关键词
blood-brain barrier; CD36; hypertension; SHRSP; LOW-DENSITY-LIPOPROTEIN; B SCAVENGER RECEPTOR; AMYLOID-BETA; LDL RECEPTOR; OXIDANT STRESS; PROTEIN; RATS; HIPPOCAMPUS; PEPTIDE; OVEREXPRESSION;
D O I
10.1111/j.1365-2990.2011.01172.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Aims: The class B scavenger receptor CD36, the receptor for oxidized low-density lipoprotein, mediates free radical production and brain injury in cerebral ischaemia. Free radical production is known to be involved in the remodelling of the cerebral vasculature of stroke-prone spontaneously hypertensive rats (SHRSP). Accordingly, we examined whether the expression of CD36 is increased in the vasculature with blood-brain barrier (BBB) impairment and collagen deposition of SHRSP. Methods: The gene and protein expression of CD36 was examined in the vessels of the hippocampus of SHRSP with BBB impairment and those of Wistar Kyoto rats without the impairment, by real-time RT-PCR, Western blotting and immunohistochemical techniques. Results: The gene and protein expression of CD36 was increased in the hippocampus of SHRSP compared with that of Wistar Kyoto rats. Confocal microscopic examination revealed CD36 immunoreactivity in perivascular microglial cells immunopositive for ED1. Immunoelectron microscopic examination revealed that the immunosignals for CD36 were located mainly in the cytoplasm of perivascular cells in vessels showing increased vascular permeability and a few in the cytoplasmic membranes of endothelial cells. Conclusions: These findings indicate that the expression of CD36 was increased in vessels with BBB impairment in the hippocampus of SHRSP and was mainly seen in the cytoplasm of perivascular microglial cells, suggesting a role of CD36 in cerebrovascular injury.
引用
收藏
页码:727 / 737
页数:11
相关论文
共 50 条
  • [1] The expression of LDL receptor in vessels with blood-brain barrier impairment in a stroke-prone hypertensive model
    Ueno, Masaki
    Wu, Bin
    Nakagawa, Toshitaka
    Nagai, Yukiko
    Onodera, Masayuki
    Huang, Cheng-long
    Kusaka, Takashi
    Kanenishi, Kenji
    Sakamoto, Haruhiko
    HISTOCHEMISTRY AND CELL BIOLOGY, 2010, 133 (06) : 669 - 676
  • [2] The expression of matrix metalloproteinase-13 is increased in vessels with blood-brain barrier impairment in a stroke-prone hypertensive model
    Ueno, Masaki
    Wu, Bin
    Nishiyama, Akira
    Huang, Cheng-long
    Hosomi, Naohisa
    Kusaka, Takashi
    Nakagawa, Toshitaka
    Onodera, Masayuki
    Kido, Mizue
    Sakamoto, Haruhiko
    HYPERTENSION RESEARCH, 2009, 32 (05) : 332 - 338
  • [3] The expression of P-glycoprotein is increased in vessels with blood-brain barrier impairment in a stroke-prone hypertensive model
    Ueno, M.
    Nakagawa, T.
    Huang, C. -I.
    Ueki, M.
    Kusaka, T.
    Hosomi, N.
    Kanenishi, K.
    Onodera, M.
    Wu, B.
    Sakamoto, H.
    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2009, 35 (02) : 147 - 155
  • [4] The expression of LDL receptor in vessels with blood–brain barrier impairment in a stroke-prone hypertensive model
    Masaki Ueno
    Bin Wu
    Toshitaka Nakagawa
    Yukiko Nagai
    Masayuki Onodera
    Cheng-long Huang
    Takashi Kusaka
    Kenji Kanenishi
    Haruhiko Sakamoto
    Histochemistry and Cell Biology, 2010, 133 : 669 - 676
  • [5] The expression of matrix metalloproteinase-13 is increased in vessels with blood–brain barrier impairment in a stroke-prone hypertensive model
    Masaki Ueno
    Bin Wu
    Akira Nishiyama
    Cheng-long Huang
    Naohisa Hosomi
    Takashi Kusaka
    Toshitaka Nakagawa
    Masayuki Onodera
    Mizue Kido
    Haruhiko Sakamoto
    Hypertension Research, 2009, 32 : 332 - 338
  • [6] The expression of osteopontin is increased in vessels with blood-brain barrier impairment
    Iwanaga, Y.
    Ueno, M.
    Ueki, M.
    Huang, C. -L.
    Tomita, S.
    Okamoto, Y.
    Ogawa, T.
    Ueda, N.
    Maekawa, N.
    Sakamoto, H.
    NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2008, 34 (02) : 145 - 154
  • [7] Defective Function of the Blood-Brain Barrier in a Stroke-Prone Spontaneously Hypertensive Rat: Evaluation in an In Vitro Cell Culture Model
    Nakagawa, Shinsuke
    Ohara, Hiroki
    Niwa, Masami
    Yamagata, Kazuo
    Nabika, Toru
    CELLULAR AND MOLECULAR NEUROBIOLOGY, 2022, 42 (01) : 243 - 253
  • [8] Faulty induction of blood-brain barrier functions by astrocytes isolated from stroke-prone spontaneously hypertensive rats
    Yamagata, K
    Tagami, M
    Nara, Y
    Fujino, H
    Kubota, A
    Numano, F
    Kato, T
    Yamori, Y
    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 1997, 24 (9-10) : 686 - 691
  • [9] Hydrogen improves neurological function through attenuation of blood-brain barrier disruption in spontaneously hypertensive stroke-prone rats
    Takeuchi, Satoru
    Nagatani, Kimihiro
    Otani, Naoki
    Nawashiro, Hiroshi
    Sugawara, Takashi
    Wada, Kojiro
    Mori, Kentaro
    BMC NEUROSCIENCE, 2015, 16
  • [10] Structural alterations of tight junctions are associated with loss of polarity in stroke-prone spontaneously hypertensive rat blood-brain barrier endothelial cells
    Lippoldt, A
    Kniesel, U
    Liebner, S
    Kalbacher, H
    Kirsch, T
    Wolburg, H
    Haller, H
    BRAIN RESEARCH, 2000, 885 (02) : 251 - 261