Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells
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Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells

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Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells

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dc.contributor.author Novella del Campo, Susana
dc.contributor.author Laguna-Fernández, Andrés
dc.contributor.author Lázaro-Franco, Macarena
dc.contributor.author Sobrino, Agua
dc.contributor.author Bueno Betí, Carlos
dc.contributor.author Tarín, Juan José
dc.contributor.author Monsalve, Elena
dc.contributor.author Sanchís, Juan
dc.contributor.author Hermenegildo Caudevilla, Carlos
dc.date.accessioned 2014-02-07T11:59:19Z
dc.date.available 2014-02-07T11:59:19Z
dc.date.issued 2013
dc.identifier.uri http://dx.doi.org/10.1016/j.mce.2012.08.020
dc.identifier.uri http://hdl.handle.net/10550/32815
dc.description.abstract Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the alterations induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, or the specific ERα antagonist MPP. ADMA concentration was measured by HPLC and concentration of NO by amperometry. Protein expression and DDAH activity were measured by immunoblotting and an enzymatic method, respectively. oxLDL, but not to nLDL, increased ADMA concentration with a concomitant decrease of DDAH activity. oxLDL reduced eNOS protein and NO production. Estradiol alone had no effects on DDAH/ADMA/NO pathway, but increased the attenuated endothelial NO production induced by oxLDL by restoring the DDAH activity. ICI 182780 and MPP completely abolished these effects of estradiol on oxLDL-exposed cells. In conclusion, estradiol restores DDAH activity ADMA levels and NO production impaired by oxLDL in HUAEC acting through ERα.
dc.relation.ispartof Molecular and Cellular Endocrinology, 2013, vol. 365, num. 1, p. 111-6
dc.rights.uri info:eu-repo/semantics/openAccess
dc.source Novella del Campo, Susana Laguna-Fernández, Andrés Lázaro-Franco, Macarena Sobrino, Agua Bueno Betí, Carlos Tarín, Juan José Monsalve, Elena Sanchís, Juan Hermenegildo Caudevilla, Carlos 2013 Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells. Molecular and Cellular Endocrinology 365 1 111 6
dc.subject Endoteli vascular
dc.subject Artèries
dc.title Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-treated human arterial endothelial cells
dc.type info:eu-repo/semantics/article
dc.date.updated 2014-02-07T11:59:19Z
dc.identifier.idgrec 081274

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