AO was supported by Programa Intensificación Actividad Investigadora (ISCIII) and MSDN by Sara Borrell. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedĭata Availability: All relevant data are within the paper and its Supporting Information files.įunding: This work was supported by Fondo de Investigaciones Sanitarias ( ) grants PS12/01770, FIS PI13/00047, ISCIII-RETIC REDinREN RD12/0021, Comunidad de Madrid S2010/BMD-2378, and CYTED IBERERC. Received: JAccepted: AugPublished: August 31, 2015Ĭopyright: © 2015 Bozic et al. PLoS ONE 10(8):Įditor: Michael Bader, Max-Delbrück Center for Molecular Medicine (MDC), GERMANY (2015) Impaired Vitamin D Signaling in Endothelial Cell Leads to an Enhanced Leukocyte-Endothelium Interplay: Implications for Atherosclerosis Development. The results reveal an important role for basal levels of endothelial VDR in limiting endothelial cell inflammation and atherosclerosis.Ĭitation: Bozic M, Álvarez Á, de Pablo C, Sanchez-Niño M-D, Ortiz A, Dolcet X, et al. Our data demonstrate that lack of VDR signaling in endothelial cells leads to a state of endothelial activation with increased leukocyte-endothelial cell interactions that may contribute to the more severe plaque accumulation observed in apoE -/-VDR -/- mice. apoE -/-VDR -/-mice showed higher aortic expression of VCAM-1, ICAM-1 and IL-6 when compared to apoE -/-VDR +/+ mice. In vivo, deletion of VDR led to significantly larger aortic arch and aortic root lesions in apoE -/- mice, with higher macrophage content. Inhibition of NF-κB activation with super-repressor IκBα blunted all signs of endothelial cell activation caused by downregulation of VDR in endothelial cells. shVDR cells showed decreased IκBα levels and accumulation of p65 in the nucleus compared to shRNA controls.
Knockdown of VDR in endothelial cells (shVDR) led to endothelial cell activation, characterized by upregulation of VCAM-1, ICAM-1 and IL-6, decreased peripheral blood mononuclear cell (PBMC) rolling velocity and increased PBMC rolling flux and adhesion to the endothelium. Our aim was to assess the role of basal levels of vitamin D receptor (VDR) on the early leukocyte recruitment and related endothelial cell-adhesion-molecule expression, as essential prerequisites for the onset of atherosclerosis.
Vitamin D has cardioprotective actions, while its deficiency is a risk factor for the progression of cardiovascular damage. It's probably also not a bad idea to book a vacation to a sunnier climate.Endothelial cell activation leading to leukocyte recruitment and adhesion plays an essential role in the initiation and progression of atherosclerosis. Again, as with any supplement, if you’re unsure about exactly how much you should be taking, it’s never a bad idea to check with your doctor. “Since vitamin D is a fat-soluble vitamin, too high a dosage can result in harmful side effects such as fatigue, loss of appetite, dehydration, vomiting, confusion, and high blood pressure,” Gans warns. Just be sure not to take more than 10,000 IU per day. If you are deficient, Gans says, your doctor may recommend a a higher dosage. “But to really benefit from the supplement, it would warrant being tested to find out if a deficiency is present.” If you want to check your vitamin D levels, make an appointment with your doctor, who can order a blood test to determine where you stand. “There is potentially no harm in taking the recommended dosage of 600 IU daily,” Gans says, citing the Institute of Medicine’s recommendation for healthy individuals. So how much vitamin D should I consider taking?
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