{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T21:16:02Z","timestamp":1773350162718,"version":"3.50.1"},"reference-count":44,"publisher":"Hindawi Limited","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>Collateral growth, arteriogenesis, represents a proliferative mechanism involving endothelial cells, smooth muscle cells, and monocytes\/macrophages. Here we investigated the role of Density-Enhanced Phosphatase-1 (DEP-1) in arteriogenesis<jats:italic>in vivo<\/jats:italic>, a protein-tyrosine-phosphatase that has controversially been discussed with regard to vascular cell biology. Wild-type C57BL\/6 mice subjected to permanent left common carotid artery occlusion (CCAO) developed a significant diameter increase in distinct arteries of the<jats:italic>circle of Willis<\/jats:italic>, especially in the anterior cerebral artery. Analyzing the impact of loss of DEP-1 function, induction of collateralization was quantified after CCAO and hindlimb femoral artery ligation comparing wild-type and DEP-1<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Both cerebral collateralization assessed by latex perfusion and peripheral vessel growth in the femoral artery determined by microsphere perfusion and micro-CT analysis were not altered in DEP-1<jats:sup>\u2212\/\u2212<\/jats:sup>compared to wild-type mice. Cerebrovascular reserve capacity, however, was significantly impaired in DEP-1<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Cerebrovascular transcriptional analysis of proarteriogenic growth factors and receptors showed specifically reduced transcripts of PDGF-B. SiRNA knockdown of DEP-1 in endothelial cells<jats:italic>in vitro<\/jats:italic>also resulted in significant PDGF-B downregulation, providing further evidence for DEP-1 in PDGF-B gene regulation. In summary, our data support the notion of DEP-1 as positive functional regulator in vascular cerebral arteriogenesis, involving differential PDGF-B gene expression.<\/jats:p>","DOI":"10.1155\/2013\/802149","type":"journal-article","created":{"date-parts":[[2013,8,6]],"date-time":"2013-08-06T21:01:39Z","timestamp":1375822899000},"page":"1-9","source":"Crossref","is-referenced-by-count":7,"title":["Knockout of Density-Enhanced Phosphatase-1 Impairs Cerebrovascular Reserve Capacity in an Arteriogenesis Model in Mice"],"prefix":"10.1155","volume":"2013","author":[{"given":"Daniel","family":"Hackbusch","sequence":"first","affiliation":[{"name":"Center for Cardiovascular Research (CCR), Institute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Charit\u00e9-University Medicine Berlin, Hessische Stra\u00dfe 3-4, 10115 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andr\u00e9","family":"D\u00fclsner","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiology and Angiology, Richard Thoma Laboratories for Arteriogenesis, Center for Cardiovascular Research, Charit\u00e9-University Medicine Berlin, Hessische Stra\u00dfe 3-4, 10115 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nora","family":"Gatzke","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiology and Angiology, Richard Thoma Laboratories for Arteriogenesis, Center for Cardiovascular Research, Charit\u00e9-University Medicine Berlin, Hessische Stra\u00dfe 3-4, 10115 Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janine","family":"Kr\u00fcger","sequence":"additional","affiliation":[{"name":"Center for Cardiovascular Research (CCR), Institute of Laboratory Medicine, Clinical Chemistry and 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