Linked Life Data

21875910

Source:http://linkedlifedata.com/resource/pubmed/id/21875910

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2011-9-20
pubmed:abstractText
BACKGROUND: Angiotensin II (ATII), a potent vasoconstrictor, causes hypertension, promotes infiltration of myelomonocytic cells into the vessel wall, and stimulates both vascular and inflammatory cell NADPH oxidases. The predominant source of reactive oxygen species, eg, vascular (endothelial, smooth muscle, adventitial) versus phagocytic NADPH oxidase, and the role of myelomonocytic cells in mediating arterial hypertension have not been defined yet. METHODS AND RESULTS: Angiotensin II (1 mg · kg(-1) · d(-1) for 7 days) increased the number of both CD11b(+)Gr-1(low)F4/80(+) macrophages and CD11b(+)Gr-1(high)F4/80(-) neutrophils in mouse aorta (verified by flow cytometry). Selective ablation of lysozyme M-positive (LysM(+)) myelomonocytic cells by low-dose diphtheria toxin in mice with inducible expression of the diphtheria toxin receptor (LysM(iDTR) mice) reduced the number of monocytes in the circulation and limited ATII-induced infiltration of these cells into the vascular wall, whereas the number of neutrophils was not reduced. Depletion of LysM(+) cells attenuated ATII-induced blood pressure increase (measured by radiotelemetry) and vascular endothelial and smooth muscle dysfunction (assessed by aortic ring relaxation studies) and reduced vascular superoxide formation (measured by chemiluminescence, cytochrome c assay, and oxidative fluorescence microtopography) and the expression of NADPH oxidase subunits gp91(phox) and p67(phox) (assessed by Western blot and mRNA reverse-transcription polymerase chain reaction). Adoptive transfer of wild-type CD11b(+)Gr-1(+) monocytes into depleted LysM(iDTR) mice reestablished ATII-induced vascular dysfunction, oxidative stress, and arterial hypertension, whereas transfer of CD11b(+)Gr-1(+) neutrophils or monocytes from gp91(phox) or ATII receptor type 1 knockout mice did not. CONCLUSIONS- Infiltrating monocytes with a proinflammatory phenotype and macrophages rather than neutrophils appear to be essential for ATII-induced vascular dysfunction and arterial hypertension.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1524-4539
pubmed:author
pubmed:issnType
Electronic
pubmed:day
20
pubmed:volume
124
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1370-81
pubmed:meshHeading
pubmed-meshheading:21875910-Angiotensin II, pubmed-meshheading:21875910-Animals, pubmed-meshheading:21875910-Antigens, CD11b, pubmed-meshheading:21875910-Endothelium, Vascular, pubmed-meshheading:21875910-Gene Expression, pubmed-meshheading:21875910-Hypertension, pubmed-meshheading:21875910-Macrophages, pubmed-meshheading:21875910-Male, pubmed-meshheading:21875910-Mice, pubmed-meshheading:21875910-Mice, Inbred C57BL, pubmed-meshheading:21875910-Mice, Transgenic, pubmed-meshheading:21875910-Monocytes, pubmed-meshheading:21875910-Muramidase, pubmed-meshheading:21875910-Muscle, Smooth, Vascular, pubmed-meshheading:21875910-Neutrophils, pubmed-meshheading:21875910-Nitric Oxide, pubmed-meshheading:21875910-Oxidative Stress, pubmed-meshheading:21875910-Reactive Oxygen Species, pubmed-meshheading:21875910-Receptors, Chemokine, pubmed-meshheading:21875910-Respiratory Burst, pubmed-meshheading:21875910-Vasculitis, pubmed-meshheading:21875910-Vasoconstrictor Agents
pubmed:year
2011
pubmed:articleTitle
Lysozyme M-positive monocytes mediate angiotensin II-induced arterial hypertension and vascular dysfunction.
pubmed:affiliation
2(nd) Medical Clinic, University Medical Center Mainz, Germany. wenzelp@uni-mainz.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't