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Researchers find novel way to treat pulmonary arterial disease
By Yoon Min-sikPublished : Oct. 29, 2014 - 21:26
A group of scientists from Korea and the United States have managed to find a new way to treat blockages in the artery that connects the heart and the lungs, officials said Wednesday.
Professor Kim Jong-min from the department of biological science at Sookmyung University ― working with scientists from Yale University ― attempted to determine what caused pulmonary arterial hypertension, a disease characterized by increased pressure in the pulmonary artery. The disease, leading to a compromised capability to exercise and heart failure, results in shortness of breath, dizziness, fainting and leg swelling, along with other symptoms.
Scientists found that the activity of myocyte enhancer factor 2 proteins (MEF2) was significantly impaired in the patients’ pulmonary artery endothelial cells (PAECs). This is believed to have contributed to the abnormal proliferation of the PAECs and pulmonary artery smooth muscle cells, which play an important role in aggravating the disease.
The impaired activity of MEF2 was mediated through excess accumulation of two class IIa histone deacetylase proteins (HDACs) in the cell nuclei. Researchers said that treatment with HDAC IIa inhibitor (MC1568) led to improvements, such as decreasing the amount of muscle in the artery walls and also the number of vascular muscle proliferations.
The researchers said the results of their study show that augmenting MEF2 activity may have therapeutic value in treating the disease.
According to Kim’s team, conventional treatments focused on expanding the strangulated pulmonary vessel walls leading to increased hypertension. But such method could only alleviate the symptoms and did little to treat the disease itself.
“Our research is meaningful in that we presented a new paradigm of treatment to target microRNA pieces that prohibit the aberrant proliferation of the PAECs. After the MC1568 goes through tests for possible adverse effects, I think it (the study) will present a good opportunity for patients,” professor Kim said.
By Yoon Min-sik (minsikyoon@heraldcorp.com)
Professor Kim Jong-min from the department of biological science at Sookmyung University ― working with scientists from Yale University ― attempted to determine what caused pulmonary arterial hypertension, a disease characterized by increased pressure in the pulmonary artery. The disease, leading to a compromised capability to exercise and heart failure, results in shortness of breath, dizziness, fainting and leg swelling, along with other symptoms.
Scientists found that the activity of myocyte enhancer factor 2 proteins (MEF2) was significantly impaired in the patients’ pulmonary artery endothelial cells (PAECs). This is believed to have contributed to the abnormal proliferation of the PAECs and pulmonary artery smooth muscle cells, which play an important role in aggravating the disease.
The impaired activity of MEF2 was mediated through excess accumulation of two class IIa histone deacetylase proteins (HDACs) in the cell nuclei. Researchers said that treatment with HDAC IIa inhibitor (MC1568) led to improvements, such as decreasing the amount of muscle in the artery walls and also the number of vascular muscle proliferations.
The researchers said the results of their study show that augmenting MEF2 activity may have therapeutic value in treating the disease.
According to Kim’s team, conventional treatments focused on expanding the strangulated pulmonary vessel walls leading to increased hypertension. But such method could only alleviate the symptoms and did little to treat the disease itself.
“Our research is meaningful in that we presented a new paradigm of treatment to target microRNA pieces that prohibit the aberrant proliferation of the PAECs. After the MC1568 goes through tests for possible adverse effects, I think it (the study) will present a good opportunity for patients,” professor Kim said.
By Yoon Min-sik (minsikyoon@heraldcorp.com)
