Endothelial Nitric Oxide Synthase-Deficient Mice: A Model of Spontaneous Cerebral Small-Vessel Disease.

Szczegóły
Abstrakt

Tytuł:: Endothelial Nitric Oxide Synthase-Deficient Mice: A Model of Spontaneous Cerebral Small-Vessel Disease.
Autorzy:: Liao FF; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee. Electronic address: .
Lin G; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee; Department of Histology and Embryology, Basic Medical University, China Medical University, Shenyang, China.
Chen X; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee; Department of Neurology, Fujian Provincial Hospital, Provincial Clinical College of Fujian Medical University, Fuzhou, China.
Chen L; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee; Department of Cell Biology and Genetics, The School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Zheng W; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee; Department of Histology and Embryology, Basic Medical University, China Medical University, Shenyang, China.
Raghow R; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee.
Zhou FM; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee.
Shih AY; Center for Developmental Biology and Regenerative Medicine, Seattle Children's Research Institute, Seattle, Washington.
Tan XL; Department of Pharmacology, Addiction Science, Toxicology, University of Tennessee Health Science Center, College of Medicine, Memphis, Tennessee; Department of Neurology, Nanhai Hospital of Southern Medical University, Foshan, China.
Źródło:: The American journal of pathology [Am J Pathol] 2021 Nov; Vol. 191 (11), pp. 1932-1945. Date of Electronic Publication: 2021 Mar 10.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
Język:: English
Imprint Name(s):: Publication: 2011-: New York : Elsevier
Original Publication: Philadelphia [etc.] American Assn. of Pathologists [etc.]
MeSH Terms:: Disease Models, Animal*
Bone Morphogenetic Protein 4/*metabolism
Cerebral Small Vessel Diseases/*metabolism
Cerebral Small Vessel Diseases/*physiopathology
Nitric Oxide Synthase Type III/*deficiency
Animals ; Cerebral Small Vessel Diseases/pathology ; Mice
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Grant Information:: R01 NS097671 United States NS NINDS NIH HHS; RF1 AG058467 United States AG NIA NIH HHS; R21 NS091593 United States NS NINDS NIH HHS; R21 AG041934 United States AG NIA NIH HHS; R01 NS097775 United States NS NINDS NIH HHS; R21 NS106138 United States NS NINDS NIH HHS; R21 AG063031 United States AG NIA NIH HHS; R21 AG069375 United States AG NIA NIH HHS; RF1 NS120327 United States NS NINDS NIH HHS
Substance Nomenclature:: 0 (Bmp4 protein, mouse)
0 (Bone Morphogenetic Protein 4)
EC 1.14.13.39 (Nitric Oxide Synthase Type III)
Entry Date(s):: Date Created: 20210312 Date Completed: 20211105 Latest Revision: 20231108
Update Code:: 20240104
PubMed Central ID:: PMC8647425
DOI:: 10.1016/j.ajpath.2021.02.022
PMID:: 33711310
: Czasopismo naukowe

Age-related cerebral small-vessel disease (CSVD) is a major cause of stroke and dementia. Despite a widespread acceptance of small-vessel arteriopathy, lacunar infarction, diffuse white matter injury, and cognitive impairment as four cardinal features of CSVD, a unifying pathologic mechanism of CSVD remains elusive. Herein, we introduce partial endothelial nitric oxide synthase (eNOS)-deficient mice as a model of age-dependent, spontaneous CSVD. These mice developed cerebral hypoperfusion and blood-brain barrier leakage at a young age, which progressively worsened with advanced age. Their brains exhibited elevated oxidative stress, astrogliosis, cerebral amyloid angiopathy, microbleeds, microinfarction, and white matter pathology. Partial eNOS-deficient mice developed gait disturbances at middle age, and hippocampus-dependent memory deficits at older ages. These mice also showed enhanced expression of bone morphogenetic protein 4 (BMP4) in brain pericytes before myelin loss and white matter pathology. Because BMP4 signaling not only promotes astrogliogenesis but also blocks oligodendrocyte differentiation, we posit that paracrine actions of BMP4, localized within the neurovascular unit, promote white matter disorganization and neurodegeneration. These observations point to BMP4 signaling pathway in the aging brain vasculature as a potential therapeutic target. Finally, because studies in partial eNOS-deficient mice corroborated recent clinical evidence that blood-brain barrier disruption is a primary cause of white matter pathology, the mechanism of impaired nitric oxide signaling-mediated CSVD warrants further investigation.
(Copyright © 2021 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

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