INVESTIGADORES
RABINOVICH Gabriel Adrian
artículos
Título:
CELL TYPE-SPECIFIC REGULATION OF GALECTIN-3 EXPRESSION BY GLUCOCORTICOIDS IN LUNG CLARA CELLS AND MACROPHAGES
Autor/es:
CRISTINA MALDONADO; VICTORIA SUNDBLAD; MARIANA SALATINO; JORGE ELIAS; LUCIANA N. GARCIA; CAROLINA LEIMBRUGER; DIEGO O. CROCI; GABRIEL A. RABINOVICH
Revista:
HISTOLOGY AND HISTOPATHOLOGY
Editorial:
F HERNANDEZ
Referencias:
Lugar: MADRID; Año: 2011 vol. 26 p. 747 - 759
ISSN:
0213-3911
Resumen:
Abstract
Bronchiolar Clara cells are integral components of lung homeostasis, predominantly
distributed in distal airways. In addition to the 16 kDa Clara cell protein, a major secretory
product with anti-inflammatory effects, rat Clara cells express the glycan-binding protein
galectin-3 and secrete it into the airways. Given the essential role of galectin-3 in the
control of inflammation and the well-established function of glucocorticoids (GCs) in lung
physiology, here we investigated whether galectin-3 is a target of the regulatory effects of
GCs. Adult male rats were subjected to bilateral adrenalectomy and the lungs were
processed for light and transmission electron microscopy, immunoelectron microscopy and
Western blot analysis. Profound changes in bronchiolar Clara cells and macrophage
morphology could be observed by electron microscopy after adrenalectomy. While specific
galectin-3 staining was detected in the nucleus and cytoplasm of Clara cells and
macrophages from control animals, cytoplasmic galectin-3 expression was dramatically
reduced after adrenalectomy in both cell-types. This effect was cell-specific as it did not
affect expression of this lectin in ciliated cells. After dexamethasone treatment, galectin-3
expression increased significantly in the nucleus and cytoplasm of macrophages and Clara
cells. Western blot analysis showed a clear decrease in galectin-3 expression in ADX
animals, which was recovered after a 7-day treatment with dexamethasone. In peritoneal
macrophages, galectin-3 expression was also dependent on the effects of GCs both in vivoin vivo
and in vitro. Our results identify a cell type-specific control of galectin-3 synthesis by GCs
in lung bronchiolar Clara cells and interstitial macrophages, which may provide an
alternative mechanisms by which GCs contribute to modulate the inflammatory response.
in lung bronchiolar Clara cells and interstitial macrophages, which may provide an
alternative mechanisms by which GCs contribute to modulate the inflammatory response.
in lung bronchiolar Clara cells and interstitial macrophages, which may provide an
alternative mechanisms by which GCs contribute to modulate the inflammatory response.
in vitro. Our results identify a cell type-specific control of galectin-3 synthesis by GCs
in lung bronchiolar Clara cells and interstitial macrophages, which may provide an
alternative mechanisms by which GCs contribute to modulate the inflammatory response.