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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#_4 http://www.w3.org/ns/prov#value Arterial remodeling in response to pathological insult is a complex process that depends in part on the balance between vascular cell apoptosis and proliferation. Studies in experimental models suggest that HO-1 mediates neointimal formation while limiting lumen stenosing, indicating a differential effect on vascular endothelial (EC) and smooth muscle cells (SMC). We investigated the effect of HO-1 expression on cell cycle progression in EC and SMC. The addition of SnMP (10 microM), an inhibitor of HO activity, to EC or SMC for 24h, resulted in significant abnormalities in DNA distribution and cell cycle progression compared to cells treated with the HO-1 inducers, heme (10 microM) or SnCl(2) (10 microM). SnMP increased G(1) phase and decreased S and G(2)/M phases in EC while heme or SnCl(2) decreased G(1) phase, but increased S and G(2)/M phases (p<0.05). Opposite effects were obtained in SMC. SnMP decreased G(1) phase and increased S and G(2)/M phases while heme or SnCl(2) increased G(1) phase but decreased S and G(2)/M phases (p<0.05). Our data demonstrate that HO-1 regulates the cell cycle in a cell-specific manner; it increases EC but decreases SMC cycle progression. The mechanisms underlying the HO-1 cell-specific effect on cell cycle progression within the vascular wall are yet to be explored. Nevertheless, these findings suggest that cell-specific targeting of HO-1 expression may provide a novel therapeutic strategy for the treatment of cardiovascular diseases. http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#_4 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/12207883 http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#_5 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/12207883 http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#_4 http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo#pubinfo http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo http://purl.org/dc/terms/created 2014-07-03T14:31:53.467+02:00 http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RA70H6JsN3Pgr7ehSuC1WO6GQWOrfhGwuid57k7T-9bLo http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234