Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia.

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Abstract Text:

The extracellular matrix (ECM) is an important regulator of angiogenesis and vascular remodeling. We showed previously that angiogenic capillaries in the developing CNS express high levels of fibronectin and its receptor alpha5beta1 integrin, and that this expression is developmentally downregulated. As cerebral hypoxia leads to an angiogenic response, we sought to determine whether angiogenic vessels in the adult CNS re-express fibronectin and the alpha5beta1 integrin. Ten-week old mice were subject to hypobaric hypoxia for 0, 4, 7 and 14 days, and fibronectin/integrin expression examined. Fibronectin and the alpha5 integrin subunit were strongly upregulated on capillaries in the hypoxic CNS, with the effect maximal at the earliest time point examined (4 days). Immunofluorescent studies demonstrated that the alpha5 integrin was expressed by angiogenic endothelial cells. In light of the defined angiogenic role for fibronectin in other systems, this work suggests that induction of fibronectin-alpha5beta1 integrin expression may be an important molecular switch driving angiogenesis in the hypoxic CNS.

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Publishing Authors By Initials

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Molecular and cellular neurosciences

VOLUME: 38

Page Numbers: 43-52

Journal Abbreviation: Mol. Cell. Neurosci.

ISSN: 1095-9327

DAY: 13

MONTH: 02

YEAR: 2008

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9100095

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia.

AFFILIATION: Department of Molecular and Experimental Medicine, MEM-132, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Mol Cell Neurosci

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia Related Publications

• Fibronectin- and vitronectin-induced microglial activation and matrix metalloproteinase-9 expression is mediated by integrins alpha5beta1 and alphavbeta5.
• Increased expression of fibronectin and the alpha5beta1 integrin in angiogenic cerebral blood vessels of mice subject to hypobaric hypoxia.
• Neuroradiologic evaluation of patients with acute stroke treated with recombinant tissue plasminogen activator. The rt-PA Acute Stroke Study Group.
• Responses of endothelial cell and astrocyte matrix-integrin receptors to ischemia mimic those observed in the neurovascular unit.
• The rapid decrease in astrocyte-associated dystroglycan expression by focal cerebral ischemia is protease-dependent.
• [Not Available.]