Linked Life Data

19464844

Source:http://linkedlifedata.com/resource/pubmed/id/19464844

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2009-11-2
pubmed:abstractText
Angiotensin II (Ang II) is a bioactive peptide that plays important roles in blood pressure regulation and salt-water homeostasis. Recently, Ang II was reported to function in the promotion of angiogenesis. Since the wound healing process is highly dependent upon angiogenesis, we employed Ang II receptor knockout mice (AT1a(-/-)) to investigate whether or not Ang II facilitates angiogenesis and wound healing via AT1a receptor signaling. In comparison to wild-type (WT) mice, wound healing and wound-induced angiogenesis were significantly suppressed in AT1a(-/-) mice, and these mice exhibited reduced expression of CD31 in wound granulation tissues. In comparison to vehicle-treated mice, wound healing was delayed significantly in mice treated with an AT1-R antagonist and this delay was accompanied by the reduced expression of vascular endothelial growth factor in wound granulation tissues. These findings suggest that Ang II-AT1a signaling plays a crucial role in wound healing and wound-induced angiogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1950-6007
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
627-34
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice.
pubmed:affiliation
Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't