Preliminary analysis of the association of TRPV1 to the formation of Marfan syndrome aneurysms

• María Elena Soto ^[1] ; Elizabeth Soria-Castro ^[1] ; Verónica Guarner-Lans ^[1] ; Andrés Martínez Guzmán ^[1] ; Cesar Amilcar Morales Marín ^[1] ; Karla Susana Martínez Zavala ^[1] ; Israel Pérez-Torres ^[1]
  1. [1] y “Ignacio Chávez”, Tlalpan, México City, México
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 34, Nº. 12, 2019, págs. 1329-1343
• Idioma: inglés
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• Resumen

  • 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 TNFα and the immunolabelling area was determined. We also measured the NO3 - /NO2 - ratio in the aortic tissue.

    C-reactive protein and HDL in plasma were quantified.

    A significant increase in iNOS, TRPV1, VCAM (p≤0.05), NO3 - /NO2 - 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