Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-28
pubmed:abstractText
Orchestration of the rapid formation and reorganization of new tissue observed in wound healing involves not only cells and polypeptides but also the extracellular matrix (ECM) microenvironment. The ability of heparan sulfate (HS) to interact with major components of the ECM suggests a key role for HS in maintaining the structural integrity of the ECM. Heparanase, an endoglycosidase-degrading HS in the ECM and cell surface, is involved in the enzymatic machinery that enables cellular invasion and release of HS-bound polypeptides residing in the ECM. Bioavailabilty and activation of multitude mediators capable of promoting cell migration, proliferation, and neovascularization are of particular importance in the complex setting of wound healing. We provide evidence that heparanase is normally expressed in skin and in the wound granulation tissue. Heparanase stimulated keratinocyte cell migration and wound closure in vitro. Topical application of recombinant heparanase significantly accelerated wound healing in a flap/punch model and markedly improved flap survival. These heparanase effects were associated with enhanced wound epithelialization and blood vessel maturation. Similarly, a marked elevation in wound angiogenesis, evaluated by MRI analysis and histological analyses, was observed in heparanase-overexpressing transgenic mice. This effect was blocked by a novel, newly developed, heparanase-inhibiting glycol-split fragment of heparin. These results clearly indicate that elevation of heparanase levels in healing wounds markedly accelerates tissue repair and skin survival that are mediated primarily by an enhanced angiogenic response.-Zcharia, E., Zilka, R., Yaar, A., Yacoby-Zeevi, O., Zetser, A., Metzger, S., Sarid, R., Naggi, A., Casu, B., Ilan, N., Vlodavsky, I., Abramovitch, R. Heparanase accelerates wound angiogenesis and wound healing in mouse and rat models.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
211-21
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15677344-Animals, pubmed-meshheading:15677344-Antibodies, pubmed-meshheading:15677344-Blood Vessels, pubmed-meshheading:15677344-CHO Cells, pubmed-meshheading:15677344-Cell Line, pubmed-meshheading:15677344-Cricetinae, pubmed-meshheading:15677344-Cricetulus, pubmed-meshheading:15677344-Disease Models, Animal, pubmed-meshheading:15677344-Endothelium, Vascular, pubmed-meshheading:15677344-Enzyme Inhibitors, pubmed-meshheading:15677344-Epithelium, pubmed-meshheading:15677344-Exudates and Transudates, pubmed-meshheading:15677344-Glucuronidase, pubmed-meshheading:15677344-Male, pubmed-meshheading:15677344-Mice, pubmed-meshheading:15677344-Mice, Transgenic, pubmed-meshheading:15677344-Neovascularization, Physiologic, pubmed-meshheading:15677344-Rats, pubmed-meshheading:15677344-Rats, Sprague-Dawley, pubmed-meshheading:15677344-Skin, pubmed-meshheading:15677344-Transfection, pubmed-meshheading:15677344-Wound Healing, pubmed-meshheading:15677344-Wounds and Injuries
pubmed:year
2005
pubmed:articleTitle
Heparanase accelerates wound angiogenesis and wound healing in mouse and rat models.
pubmed:affiliation
Department of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural