Vascular cell components of the medullary arteries in Binswanger's disease brains

A morphometric and immunoelectron microscopic study

Jin Xi Lin, Hidekazu Tomimoto, Ichiro Akiguchi, Akinori Matsuo, Hideaki Wakita, Hiroshi Shibasaki, Herbert Budka

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Background and Purpose - It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods - A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results - The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 μm (P<0.0001), there was no corresponding increase in the arteries of >100 μm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. Conclusions - The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.

Original languageEnglish
Pages (from-to)1838-1842
Number of pages5
JournalStroke
Volume31
Issue number8
DOIs
Publication statusPublished - 01-01-2000

Fingerprint

Vascular Dementia
Cellular Structures
Blood Vessels
Arteries
Brain
Arterioles
Collagen Type I
Smooth Muscle
Actins
Collagen
Adventitia
Immunoelectron Microscopy
Sclerosis
Basement Membrane
Smooth Muscle Myocytes
Endothelial Cells
Immunohistochemistry
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialised Nursing

Cite this

Lin, Jin Xi ; Tomimoto, Hidekazu ; Akiguchi, Ichiro ; Matsuo, Akinori ; Wakita, Hideaki ; Shibasaki, Hiroshi ; Budka, Herbert. / Vascular cell components of the medullary arteries in Binswanger's disease brains : A morphometric and immunoelectron microscopic study. In: Stroke. 2000 ; Vol. 31, No. 8. pp. 1838-1842.
@article{9ed8a1b4ac00439f83f63ef1e6867a67,
title = "Vascular cell components of the medullary arteries in Binswanger's disease brains: A morphometric and immunoelectron microscopic study",
abstract = "Background and Purpose - It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods - A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results - The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 μm (P<0.0001), there was no corresponding increase in the arteries of >100 μm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. Conclusions - The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.",
author = "Lin, {Jin Xi} and Hidekazu Tomimoto and Ichiro Akiguchi and Akinori Matsuo and Hideaki Wakita and Hiroshi Shibasaki and Herbert Budka",
year = "2000",
month = "1",
day = "1",
doi = "10.1161/01.STR.31.8.1838",
language = "English",
volume = "31",
pages = "1838--1842",
journal = "Stroke",
issn = "0039-2499",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

Vascular cell components of the medullary arteries in Binswanger's disease brains : A morphometric and immunoelectron microscopic study. / Lin, Jin Xi; Tomimoto, Hidekazu; Akiguchi, Ichiro; Matsuo, Akinori; Wakita, Hideaki; Shibasaki, Hiroshi; Budka, Herbert.

In: Stroke, Vol. 31, No. 8, 01.01.2000, p. 1838-1842.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Vascular cell components of the medullary arteries in Binswanger's disease brains

T2 - A morphometric and immunoelectron microscopic study

AU - Lin, Jin Xi

AU - Tomimoto, Hidekazu

AU - Akiguchi, Ichiro

AU - Matsuo, Akinori

AU - Wakita, Hideaki

AU - Shibasaki, Hiroshi

AU - Budka, Herbert

PY - 2000/1/1

Y1 - 2000/1/1

N2 - Background and Purpose - It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods - A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results - The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 μm (P<0.0001), there was no corresponding increase in the arteries of >100 μm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. Conclusions - The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.

AB - Background and Purpose - It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods - A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results - The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 μm (P<0.0001), there was no corresponding increase in the arteries of >100 μm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. Conclusions - The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.

UR - http://www.scopus.com/inward/record.url?scp=0033853722&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033853722&partnerID=8YFLogxK

U2 - 10.1161/01.STR.31.8.1838

DO - 10.1161/01.STR.31.8.1838

M3 - Article

VL - 31

SP - 1838

EP - 1842

JO - Stroke

JF - Stroke

SN - 0039-2499

IS - 8

ER -