Endothelial disfunction by increased nitric oxide synthase isoforms, endothelin 1 and apoptosis varied in lungs from patients with SSc and had impact on pulmonary function tests | Health & Environmental Research Online (HERO)

Health & Environmental Research Online (HERO)

Print Feedback Export to File

This record has one attached file:

Citation
Tags

HERO ID

2262178

Reference Type

Journal Article

Subtype

Abstract

Title

Endothelial disfunction by increased nitric oxide synthase isoforms, endothelin 1 and apoptosis varied in lungs from patients with SSc and had impact on pulmonary function tests

Author(s)

Aguiar, ACJ; Souza, HSP; E Silva, LO; Fernezlian, SDM; Capelozzi, VL; Parra, ER

Year

2010

Is Peer Reviewed?

Yes

Journal

American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970

Volume

181

Page Numbers

A2772

Language

English

DOI

10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A2772

Web of Science Id

WOS:000208771001685

Relationship(s)

is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans

Abstract

Background: Endothelial dysfunction shows promise as a primary event in the etiology of systemic sclerosis (SSc). Endothelial nitric oxide synthase isoforms (NOS1 and NOS2), endothelin 1 and apoptosis pulmonary expression were evaluated in 23 surgical lung biopsies from patients with SSc without pulmonary hypertension.

Material and methods: Immunohistochemistry, in situ detection of cell death (TUNEL), and morphometry were used to evaluate the amount of NOS1, NOS2, endothelin 1 and apoptosis expressed by endothelial, epithelial and myofibroblasts. The impact of these markers was tested on pulmonary function tests.

Results: A significant and progressive augment of NOS1, NOS2 and endothelin 1 was found in vascular compared to septal walls. Equally significant was the vascular apoptosis found in vessels from areas of activity and remodeling. A significant association was found between DCO/VA, vascular apoptosis and endothelial NOS2 expression (p<0.05).

Conclusions: Endothelial NOS1, NOS2, endothelin 1 and vascular apoptosis expression varied in lungs from patients with SSc and had impact on pulmonary function tests, suggesting that strategies aimed at preventing high expression of different nitric oxide synthase isoforms and endothelin, or local responses to high vascular apoptosis, may have a greater impact in SSc treatment. Further studies are needed to determine whether this relationship is causal or consequential.

Conference Name

American Thoracic Society 2010 International Conference

Conference Location

New Orleans, LA

Conference Dates

May 14-19, 2010