Growth hormone-releasing hormone antagonists counteract interferon-γ - induced barrier dysfunction in bovine and human endothelial cells.

GHRH regulates the secretion of GH from the anterior pituitary gland. An emerging body of evidence suggests that the activities of that neuropeptide are not limited to the GH/IGF-I axis, but they expand towards the mediation of inflammatory processes. GHRHAnt were developed to oppose the activities of GHRH in malignancies, and have been associated with strong anti-inflammatory and anti-oxidative effects in a diverse variety of tissues, including the lungs. In the present study we report that GHRHAnt oppose interferon-γ - induced paracellular hyperpermeability and reactive oxygen species generation in bovine and human pulmonary endothelial cells; and suppress interferon-γ - triggered STAT3, cofilin and ERK1/2 activation. Our observations substantiate previous findings on the protective effects of GHRHAnt in endothelial inflammation and barrier break-down.