dc.creatorPARRA, Edwin Roger
dc.creatorAGUIAR JR., Armando Costa
dc.creatorTEODORO, Walcy Rosolia
dc.creatorSOUZA, Romy de
dc.creatorYOSHINARI, Natalino Hajime
dc.creatorCAPELOZZI, Vera Luiza
dc.date.accessioned2012-10-19T17:52:29Z
dc.date.accessioned2018-07-04T15:09:33Z
dc.date.available2012-10-19T17:52:29Z
dc.date.available2018-07-04T15:09:33Z
dc.date.created2012-10-19T17:52:29Z
dc.date.issued2009
dc.identifierCLINICAL RESPIRATORY JOURNAL, v.3, n.3, p.135-142, 2009
dc.identifier1752-6981
dc.identifierhttp://producao.usp.br/handle/BDPI/22629
dc.identifier10.1111/j.1752-699X.2008.00118.x
dc.identifierhttp://dx.doi.org/10.1111/j.1752-699X.2008.00118.x
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1619360
dc.description.abstractBackground: Systemic sclerosis (SSc) is a multisystem disorder characterized by inflammation, fibrosis and vascular damage. The aim of this study was to evaluate the interactions between basement membrane disruption, endothelial injury and collagen V deposition on the vascular wall, as well as their association with pulmonary function tests in patients with SSc. Method: The endothelial apoptosis was assessed by TUNEL and electron microscopy, and quantified through the point-counting technique. To evaluate basement membrane integrity, laminin immunostaining and electron microscopy were used. Immunofluorescence and morphometric analysis were used to determine the amount of collagen V in the vascular walls in 23 open lung biopsies of patients with SSc without pulmonary hypertension. Normal lung tissue was obtained from five individuals who had died of traumatic injuries. Results: The apoptosis index in SSc was higher in the endothelial cells (13.83 +/- 6.83) when compared with the control (2.51 +/- 2.06) group (P < 0.001) and confirmed by electron microscopy. We observed an important disruption of the basement membrane on the vascular wall shown by discontinuous laminin immunostaining and electron microscopy. An increase in collagen V on the vascular wall of the SSc group was observed (45.28 +/- 13.21), when compared with control group (22.90 +/- 4.13, P < 0.001), and this difference was statistically significant. An inverse correlation was found between vital capacity, forced vital capacity, forced expiratory volume in 1 s, vascular collagen V and endothelial apoptosis (P < 0.05). Conclusions: We conclude that the endothelial apoptosis and vascular collagen V interaction reinforce the vascular pathway in the SSc pathogenesis. Further studies are needed to determine whether this relationship is causal or consequential. Please cite this paper as: Parra ER, Aguiar AC Jr, Teodoro WR, de Souza R, Yoshinari NH and Capelozzi VL. Collagen V and vascular injury promote lung architectural changes in systemic sclerosis. The Clinical Respiratory Journal 2009; 3: 135-142.
dc.languageeng
dc.publisherWILEY-BLACKWELL PUBLISHING, INC
dc.relationClinical Respiratory Journal
dc.rightsCopyright WILEY-BLACKWELL PUBLISHING, INC
dc.rightsclosedAccess
dc.subjectcollagen V
dc.subjectelectron microscopy endothelial apoptosis
dc.subjectpulmonary function tests
dc.subjectsystemic sclerosis
dc.titleCollagen V and vascular injury promote lung architectural changes in systemic sclerosis
dc.typeArtículos de revistas


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