4.7 Article

Endothelin 1, its endothelin type A receptor, connective tissue growth factor, platelet-derived growth factor, and adrenomedullin expression in lungs of pulmonary hypertensive and nonhypertensive chickens

Journal

POULTRY SCIENCE
Volume 86, Issue 5, Pages 909-916

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/ps/86.5.909

Keywords

pulmonary hypertension; endothelin 1; connective tissue growth factor; platelet-derived growth factor; adrenomedullin

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Twenty-four 1-d-old broilers were distributed in 2 groups, pulmonary hypertensive broilers (PHB) and pulmonary nonhypertensive broilers (NPHB), to estimate possible differences between them in the expression of endothelin I (ET-1) and its type A receptor, connective tissue growth factor, platelet-derived growth factor, and adrenomedullin expression in the lungs. For this purpose, total RNA extraction and real-time PCR analysis were used. Endothelin I mRNA levels in the lungs of PHB were significantly higher than the corresponding level in NPHB (P < 0.001). In contrast, the opposite was true for ET-1 type A receptor mRNA levels (P < 0.001). Connective tissue growth factor mRNA levels in the lungs of PHB were significantly higher than in the lungs of NPHB (P < 0.01). However, no differences were encountered between the 2 groups of broilers in platelet-derived growth factor mRNA expression (P > 0.05). Adrenomedullin mRNA levels in the lungs of PHB were significantly higher than in NPHB (P < 0.01). It has been demonstrated for the first time that ET-1, connective tissue growth factor, and adrenomedullin are upregulated in the lungs of PHB. Furthermore, it is suggested that these peptides may play a major role in pulmonary hypertension pathophysiology. Present data might provide clues for future research directions such as genetic selection and therapeutic intervention to revert the process of pulmonary vasoconstriction and vascular remodeling. Major research goals could be to find endothelium-derived factors that probably trigger endothelial dysfunction, as well as possible interactions with already identified molecules which also intervene in the pulmonary response to hypoxia.

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