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Repositorio Institucional de la Universidad de Murcia

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  1. Home
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Browsing by Subject "eNOS"

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    eNOS and iNOS trigger apoptosis in the brains of sheep and goats naturally infected with the border disease virus
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Cagdas Dince, Gungor; Kul, Oguz
    In this study, apoptotic and anti-apoptotic mechanisms and if present, which pathway to trigger the apoptosis in the brains of Border Disease Virus (BDV) infected lambs (n=10) and goat kids (n=5) were investigated. Briefly, apoptotic (caspase 3, caspase 9) and anti-apoptotic markers (Bcl-2), cytokine response (TNF-α, INF-γ), reactive gliosis and myelin loss were examined. eNOS, iNOS, caspase 9, caspase 3 and GFAP expressions were higher in BDV infected tissues compared to control animals (6 kids and 6 lambs) (p<0.05). Double immunoperoxidase test revelaed that TUNEL positive apoptotic cells showed significant association with increased eNOS-iNOS and iNOS-BDV expressions. However, no significant differences were found for TNFR1, TNF-α and INF-γ expressions in BD (p>0.05). There was a positive correlation between the intensity of myelin loss, GFAP activity and severity of infection. Inconclusion, as a novel finding, it is established that eNOS and iNOS overexpressions are coassociated with apoptosis in BDV infected neurons and neuroglia. The results also strongly suggested that BDV infected apoptotic cells mainly prefer the intrinsic pathway that might be most likely related to increased nitric oxide levels.
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    Preliminary analysis of the association of TRPV1 to the formation of Marfan syndrome aneurysms
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Soto, María Elena; Soria Castro, Elizabeth; Guarner Lans, Verónica; Martínez Guzmán, Andrés; Morales Marín, Cesar Amilcar; Martínez Zavala, Karla Susana; Pérez Torres, Israel
    Marfan syndrome (MS) is an autosomal dominant disorder of connective tissue that is caused by mutations in the fibrillin-1 (FBN-1) gene that cause degeneration of the artery. It is accompanied by endothelial dysfunction. The potential transient receptor of the vanilloid subfamily 1 (TRPV1) ion channel plays an important role in endothelial vascular functioning. Here we determine the association of the presence TRPV1 in aortic aneurysm with dilation and dissection of the artery in MS patients. Histological sections of aortic aneurysm tissue obtained by the surgical procedure of Bentall and De Bono or David, were processed by immunohistochemistry with antibodies against ICAM, VCAM, iNOS, eNOS, TRPV1 and TNF- α and the immunolabelling area was determined. We also measured the NO 3- /NO 2- ratio in the aortic tissue. C-reactive protein and HDL in plasma were quantified. A significant increase in iNOS, TRPV1, VCAM (p≤0.05), NO 3- /NO 2- ratio (p=0.002) and a significant decrease in eNOS (p=0.04) and HDL in plasma (p=0.02) in the MS vs. the C group were found. Conclusion: TRPV1 is over-expressed in aortic tissue from MS patients and can be associated with increases in iNOS, VCAM and a decrease in eNOS. These changes might contribute to the progression and rupture of the thoracic aneurysm.

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