| Full text | |
| Author(s): |
E.R. Parra
[1]
;
M.S. Pincelli
[1]
;
W.R. Teodoro
[2]
;
A.P.P. Velosa
[2]
;
V. Martins
[1]
;
M.P. Rangel
[1]
;
J.V. Barbas-Filho
[1]
;
V.L. Capelozzi
[1]
Total Authors: 8
|
| Affiliation: | [1] Univ Sao Paulo, Fac Med, Dept Patol, Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Med, Disciplina Reumatol, Sao Paulo - Brazil
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | Brazilian Journal of Medical and Biological Research; v. 47, n. 7, p. 567-575, 2014-06-04. |
| Abstract | |
Limitations on tissue proliferation capacity determined by telomerase/apoptosis balance have been implicated in pathogenesis of idiopathic pulmonary fibrosis. In addition, collagen V shows promise as an inductor of apoptosis. We evaluated the quantitative relationship between the telomerase/apoptosis index, collagen V synthesis, and epithelial/fibroblast replication in mice exposed to butylated hydroxytoluene (BHT) at high oxygen concentration. Two groups of mice were analyzed: 20 mice received BHT, and 10 control mice received corn oil. Telomerase expression, apoptosis, collagen I, III, and V fibers, and hydroxyproline were evaluated by immunohistochemistry, in situ detection of apoptosis, electron microscopy, immunofluorescence, and histomorphometry. Electron microscopy confirmed the presence of increased alveolar epithelial cells type 1 (AEC1) in apoptosis. Immunostaining showed increased nuclear expression of telomerase in AEC type 2 (AEC2) between normal and chronic scarring areas of usual interstitial pneumonia (UIP). Control lungs and normal areas from UIP lungs showed weak green birefringence of type I and III collagens in the alveolar wall and type V collagen in the basement membrane of alveolar capillaries. The increase in collagen V was greater than collagens I and III in scarring areas of UIP. A significant direct association was found between collagen V and AEC2 apoptosis. We concluded that telomerase, collagen V fiber density, and apoptosis evaluation in experimental UIP offers the potential to control reepithelization of alveolar septa and fibroblast proliferation. Strategies aimed at preventing high rates of collagen V synthesis, or local responses to high rates of cell apoptosis, may have a significant impact in pulmonary fibrosis. (AU) | |