Pulmonary hypertension is a highly fatal disease. Thin flexible pulmonary vessels thicken and vascular dysfunction leads to death. Scientists believe that a protein of high expression in lethal disease is the culprit, but it is also a potentially effective new therapeutic target. Vascular biologist Fulton and Dr. Scott Barman at pharmacology and toxicology department of MCG are the main researchers in this study. They wanted to better understand the role of protein galectin -3 (gal-3) in causing pulmonary vascular chronic and unhealthy remodeling and to find a way to stop it by the use of recombinant proteins.
In disease models of human and animals, MCG scientists found in the media-specific increase gal-3 expression of arterial smooth muscle-rich intermediate layer usually helps to enhance blood vessel strength and toughness. They have shown that at least when culturing in vitro, improving gal-3 levels can increase unnatural proliferation and survival of human smooth muscle cells, while gal-3 cell viability decreased when silencing the expression.
Gal-3 is also related to and cancer, renal fibrosis and liver fibrosis. "Gal-3 also has excessive and unhealthy expression patterns in these diseases," Barman said. A key goal of their research is not only to prevent over expression of new gal 3 in pulmonary hypertension, but also to figure out the reason why smooth muscle cells make it excessive. They also wanted to determine epigenetic mechanism which constitutes persistent cell function changes, explaining cellular erratic behavior in many diseases.
When they were studying the cause of the problem, they were also concerned about whether gal-3 inhibitor GR-MD-02 which had been always studied could continue to be effective in reversing or preventing the disease. Barman and Fulton collaborated with Chief Medical Officer Dr. Peter g. Traber of Atlanta Galectin Therapeutics Ltd to further study the gal-3 inhibitor which was developed by the company and they are testing patients with hepatic fibrosis.
Although the inhibitors would not directly reduce gal-3 level, but they can prevent its effects. The ongoing studies will help to better determine the optimal dose, and the dose they used had shown results in early major diseases reversals. After treatment, the smooth muscle cell grew normally, blood vessel relaxed or smooth and cavity expanded. The new study will include more severe disease models that reflect the situation in many patients the diagnosis phase more closely. Flarebio provides superior recombinant proteins like recombinant COLEC12.
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