About: CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice

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About: CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice
Creator	Ghosh, Mallika Subramani, Jaganathan Liang, Brannen Schacke, Wolfgang Agosto, Mariela Cronin, Chunxia Shen, Jian-Bing Wang, Ruibo Zhou, Si-Yuan Yang, Shapiro, Linda Liang, Bruce Mcaulliffe, Beata Pereira, Flavia Tie, Hong
Source	PMC
abstract	AIMS: To determine the role of CD13 as an adhesion molecule in trafficking of inflammatory cells to the site of injury in vivo and its function in wound healing following myocardial infarction induced by permanent coronary artery occlusion. METHODS AND RESULTS: Seven days post-permanent ligation, hearts from CD13 knockout (CD13(KO)) mice showed significant reductions in cardiac function, suggesting impaired healing in the absence of CD13. Mechanistically, CD13(KO) infarcts showed an increase in small, endothelial-lined luminal structures, but no increase in perfusion, arguing against an angiogenic defect in the absence of CD13. Cardiac myocytes of CD13(KO) mice showed normal basal contractile function, eliminating myocyte dysfunction as a mechanism of adverse remodelling. Conversely, immunohistochemical and flow cytometric analysis of CD13(KO) infarcts demonstrated a dramatic 65% reduction in infiltrating haematopoietic cells, including monocytes, macrophages, dendritic, and T cells, suggesting a critical role for CD13 adhesion in inflammatory trafficking. Accordingly, CD13(KO) infarcts also contained fewer myofibroblasts, consistent with attenuation of fibroblast differentiation resulting from the reduced inflammation, leading to adverse remodelling. CONCLUSION: In the ischaemic heart, while compensatory mechanisms apparently relieve potential angiogenic defects, CD13 is essential for proper trafficking of the inflammatory cells necessary to prime and sustain the reparative response, thus promoting optimal post-infarction healing.
has issue date	2013-06-12(xsd:dateTime)
bibo:doi	10.1093/cvr/cvt155
bibo:pmid	23761403
has license	bronze-oa
sha1sum (hex)	7822013922e0bfb03c045d7f54b83df4c450fbbe
schema:url	https://doi.org/10.1093/cvr/cvt155
resource representing a document's title	CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice
has PubMed Central identifier	PMC3778957
has PubMed identifier	23761403
schema:publication	Cardiovascular Research
resource representing a document's body	covid:7822013922e0bfb03c045d7f54b83df4c450fbbe#body_text
is schema:about of	named entity 'WOUND HEALING' named entity 'ROLE' named entity 'INFLAMMATORY CELLS' named entity 'ESSENTIAL' named entity 'INFLAMMATORY' named entity 'PERMANENT' named entity 'TRAFFICKING' named entity 'CD13' named entity 'MICE' named entity 'INDUCED' named entity 'DETERMINE' named entity 'FOLLOWING' named entity 'CORONARY ARTERY OCCLUSION' named entity 'INFARCT' named entity 'MYOCARDIAL INFARCTION' named entity 'CORONARY ARTERY OCCLUSION' named entity 'FOLLOWING' named entity 'ADHESION MOLECULE' named entity 'SITE OF' named entity 'FUNCTION' named entity 'CD13' named entity 'ITS' named entity 'TRAFFICKING' named entity 'INJURY' named entity 'HEALING' named entity 'IN VIVO' named entity 'PERMANENT' covid:arg/7822013922e0bfb03c045d7f54b83df4c450fbbe named entity 'permanent' named entity 'mice' named entity 'wound healing' named entity 'adhesion' named entity 'angiogenic' named entity 'confounding effects' named entity 'CD13' named entity 'CD13' named entity 'Flow cytometry' named entity 'CD13' named entity 'CD13' named entity 'endothelial' named entity 'infarcted tissue' named entity 'Gr-1' named entity 'left ventricular' named entity 'blood vessels' named entity 'transgenic mice' named entity 'macrophages' named entity 'CD13' named entity 'cell types' named entity 'wound healing' named entity 'CD13' named entity 'CD13' named entity 'cell surface' named entity 'infarcts' named entity 'monocytes' named entity 'tissue repair' named entity 'xylazine' named entity 'myocardial ischaemia' named entity 'endothelial cell' named entity 'Fluorescence' named entity 'CD45+' named entity 'CD13' named entity 'Lung' named entity 'Gr-1' named entity 'time-point' named entity 'phenotype' named entity 'CD13' named entity 'cardiac output'

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