RT Journal Article
SR Electronic
T1 Overexpression of angiotensin II type 1 receptor (AGTR1) and lymphatic vasculature rarefaction is present in scleroderma with pulmonary compromised
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P3643
VO 40
IS Suppl 56
A1 Aline Domingos Pinto Ruppert
A1 Vera Capelozzi
A1 Edwin Roger Parra
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/P3643.abstract
AB Background: The aim of this study was to evaluate the activity of angiotensin II type 1 and 2 receptors and lymphatic vessels in lungs of patients with systemic sclerosis comparing to normal lung tissue (NLT).Methods: Lung specimens were obtained from 23 females patients with scleroderma. NLT were obtained from 10 individuals who's died suddenly of non-pulmonary causes. Immunohistochemistry and histomorphometry were used to evaluate the amount of AGTR-1 and AGTR-2 pulmonary expression. We also studied the lymphatic (D2-40) expression and the percent of area occupied by these lymphatics in lung specimens. Pulmonary fibrosis was obtained from high-resolution computed tomography (HRCT) score.Results: We observed higher amount of AGTR-1 and AGTR-2 expression in the pulmonary parenchyma of patients with scleroderma when compared with NLT (p>0.01). The density of lymphatic vessels was markedly reduced in pulmonary scleroderma when compared with NLT (p=0.02) group. Similar situation was observed when we compared the area occupied by these lymphatics (p=0.001) group. Patients with several fibrosis showed a increased expression of AGTR-1 and increased area occupied by lymphatic than minimal fibrosis (p<0.05) patients.Conclusions: Our data showed that the AGTR-1 and AGTR-2 and lymphatic system are very affected in pulmonary SSc. AGTR-1 showed higher expression in more pulmonary fibrosis HRCT score. Rarefaction of lymphatic vasculature was correlated with degree of pulmonary fibrosis and pulmonary function test. The role of AGTR-1 and lymphatics are probably essential in evaluation and progression of Systemic Sclerosis.Financial Support: FAPESP.