d-glucose increased l-arginine transport and nitric oxide synthesis through an autocrine mechanism involving TGF-β1 and TGF-β receptor II (TβRII) in human umbilical vein endothelium

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dc.catalogadorpau
dc.contributor.authorVásquez, Rodrigo
dc.contributor.authorFarías Jofré, Marcelo Enrique
dc.contributor.authorSan Martín, Rody
dc.contributor.authorCasanello Toledo, Paola Cecilia
dc.contributor.authorSobrevía Luarte, Luis Alberto
dc.date.accessioned2023-05-18T19:49:48Z
dc.date.available2023-05-18T19:49:48Z
dc.date.issued2006
dc.description.abstractHigh D-glucose increases L-arginine transport, nitric oxide (NO) synthesis, and release of Transforming Growth Factor β1 (TGF-β1) in human umbilical vein endothelium (HUVEC). Changes in cell proliferation in response to D-glucose have been explained by a TGF-β1 autocrine mechanism in this cell type. However, the involvement of TGF-β1 and TGF-β1 receptor II (TβRII) on D-glucose effect on endothelial L-arginine/NO pathway has not been reported. L-[3H]Arginine transport (100 μM, 2 μCi/ml) and endothelial NO synthase (eNOS) activity [L-[3H]citrulline formation from L-[3H]arginine, 4 μCi/ml, 30 min, ± NG-nitro-L-arginine methyl ester (L-NAME), 100 μM] were determined in primary cultures of HUVEC exposed (6 h) to 5 mM (normal) or 25 mM (high) D-glucose, in absence or presence of TGF-β1 (2 ng/ml). Supernatant TGF-β1 level was measured by ELISA. HUVEC were infected (2% sera for 12 h) with an adenovirus expressing a negative dominant truncated TβRII (AdTβRIIt). Expression of TβRIIt was determined by Western blot. High D-glucose and TGF-β1 [half maximal effect (Ks): 0.28 ng/ml] increased L-arginine transport, effects that were significantly (P< 0.005) reduced in AdTβRIIt infected cells. L-Arginine transport was not further increased in non-infected infected cells co-incubated with high D-glucose and TGF-β1. However, L-arginine transport in AdTβRIIt infected cells co-incubated with these molecules was reduced. High D-glucose and TGF-β1 increased L-citrulline formation only in non-infected cells. High D-glucose also increased supernatant TGF-β1 level. We propose that stimulation of endothelial L-arginine/NO pathway by high D-glucose could result from a mechanism involving activation of TβRII by TGF-β1 as a consequence of increased release of this growth factor in HUVEC. Supported by FONDECYT 1030781 & 1030607 (Chile). R.V. holds a DIPUC-School of Medicine PhD (Chile) fellowship. M.F. holds CONICYT and School of Medicine–PhD (Chile) fellowships
dc.format.extent2 páginas
dc.fuente.origenORCID
dc.identifier.doi10.1016/j.vph.2006.08.362
dc.identifier.issn1537-1891
dc.identifier.urihttps://www.sciencedirect.com/science/article/abs/pii/S153718910600526X?via%3Dihub
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/67125
dc.information.autorucEscuela de Medicina ; Farías Jofré, Marcelo Enrique ; 0000-0003-0473-2295 ; 12286
dc.information.autorucEscuela de Medicina ; San Martín, Rody ; 0000-0002-0750-3714 ; 1003218
dc.information.autorucEscuela de Medicina ; Casanello Toledo, Paola Cecilia ; 0000-0002-2355-1476 ; 146772
dc.information.autorucEscuela de Medicina ; Sobrevía Luarte, Luis Alberto ; 0000-0001-5802-2243 ; 1002656
dc.issue.numero3
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.finale138
dc.pagina.inicioe137
dc.relation.ispartofInternational Vascular Biology Meeting (14° ; 2006 ; Noordwijkerhout, The Netherlands)
dc.revistaVascular Pharmacology
dc.rightsacceso restringido
dc.titled-glucose increased l-arginine transport and nitric oxide synthesis through an autocrine mechanism involving TGF-β1 and TGF-β receptor II (TβRII) in human umbilical vein endothelium
dc.typecomunicación de congreso
dc.volumen45
sipa.codpersvinculados12286
sipa.codpersvinculados1003218
sipa.codpersvinculados146772
sipa.codpersvinculados1002656
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