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Stony Brook Researchers' discovery of "Anti-Pulmonary Hypertension" gene in mice may impact treatment


Dr. Sami Said, Lead Researcher, Says Study Provides Clue to Mechanisms of Disease

A team of Stony Brook University Medical Center researchers has identified the Vasoactive Intestinal Peptide (VIP) gene as an "anti-pulmonary hypertension" gene. This finding helps clarify what mechanisms lead to the disease known as idiopathic pulmonary arterial hypertension (PAH) and could have major implications for treatment. PAH is a complex and potentially fatal lung disorder in which the blood pressure in the pulmonary artery rises far above normal levels causing heart failure. The discovery may also help with the treatment of more common forms of pulmonary hypertension. Their findings were reported in the March 13 issue of Circulation, the Journal of the American Heart Association.

The Study, "Moderate Pulmonary Arterial Hypertension in Male Mice Lacking the Vasoactive Intestinal Peptide Gene," shows that mice without the VIP gene develop PAH. But when the mice are given VIP-replacement therapy, they have significantly fewer signs of disease, such as reduced right ventricle hypertrophy and less thickened pulmonary arteries. In contrast, non-treated mice with the knockout VIP gene had progressive disease and decreased survival.

"The ability of the VIP to ameliorate the pulmonary arterial hypertension pathology in these mice provides a solid rationale for its therapeutic potential in chronic human disease," says Sami I. Said, M.D., Distinguished S.U.N.Y. Professor and lead investigator. "Because arterial lesions in the model resemble those of clinical pulmonary arterial hypertension and are expressed secondary to the loss of a single gene, the study is useful in exploring mechanisms of pathogenesis of the disease, especially the interactions between different genetic pathways," explains Dr. Said, who discovered VIP 37 years ago.

Dr. Said added that his interdisciplinary investigative team continues to research the significance of the VIP gene in the development of pulmonary hypertension and other chronic diseases. Team members include Sayyed Hamidi, M.D.; Richard Z. Lin, M.D.;Tarek Abdel-Razek, Ph.D.; Kathleen G. Dickman, Ph.D.; Anthony M. Szema, M.D., and and Smadar Kort, M.D.

In 2006, the team reported in the American Journal of Physiology, Lung Cellular and Molecular Physiology that VIP gene-deficient mice expressed two major features of asthma, namely airway hyperresponsiveness and airway inflammation.

Dr. Szema, Assistant Professor of Medicine at Stony Brook and primary author of the VIP/asthma study, says that, "overall these studies support the concept that VIP gene deficiency may be related not only to inflammation but also to pulmonary vascular pathology."

Idiopathic PAH is rare and its cause unknown. PAH is more commonly associated with other diseases, particularly those of the lungs and heart. According to the American Heart Association (AHA), there are an estimated 500 to 1,000 new cases of PAH diagnosed each year in the United States, most often affecting younger women.

The AHA says that diagnosing and treating PAH is complex and that studies have been difficult because a good animal model of the disease has not been available. Dr. Said points out that his experimental model of PAH suggests that the VIP gene may be part of the complex process that causes PAH in humans.

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