Jean-Francois Jasmin, PhD

Can Membrane Protein Prevent Development of Pulmonary Hypertension?

Pulmonary arterial hypertension (PAH) is a disease of high blood pressure in the arteries of the lungs. PAH is progressive and lifethreatening because the pressure in a patient’s pulmonary arteries rises to dangerously high levels, putting a strain on the heart. None of the current drugs cure or halt the progression of this disease.

Caveolin-1, or Cav-1, is a membrane protein that has recently been shown to be involved in the regulation of pulmonary arterial hypertension. Decreases in Caveolin-1 expression have been reported in patients with severe pulmonary arterial hypertension.

Dr. Jasmin used an American Lung Association Biomedical Research Grant to study whether a Caveolin- 1-mimetic peptide can reverse the development of pulmonary arterial hypertension in an animal model. He treated hypertensive rodents at various stages of the disease with a Cav-1-mimetic peptide to see at which point the treatment might decrease pressure in the arteries and improve survival.

He found that administering Cav-1 not only reduced the development of PAH and the enlarged right heart ventricle that accompanies it, but also improved survival in rats. “The results could have a direct impact on the management of human PAH”, Dr. Jasmin says.

He plans to continue investigating the mechanisms underlying the development of pulmonary hypertension. “This Biomedical Research Grant definitely jump-started my pulmonary hypertension research program and I am thankful to the American Lung Association for this opportunity,” he added.

Publications:
de Almeida CJ, Witkiewicz AK, Jasmin JF, Tanowitz HB, Sotgia F, Frank PG, Lisanti MP. Caveolin-2-deficient mice show increased sensitivity to endotoxemia. Cell Cycle. 2011 Jul 1;10(13):2151-61.

Jasmin JF, Rengo G, Lymperopoulos A, Gupta R, Eaton GJ, Quann K, Gonzales DM, Mercier I, Koch WJ, Lisanti MP. Caveolin-1 deficiency exacerbates cardiac dysfunction and reduces survival in mice with myocardial infarction. Am J Physiol Heart Circ Physiol. 2011 Apr;300(4):H1274-81.