Vasoconstriction is commonly regarded as the cause of pulmonary arterial hypertension (PAH), but another cause that cannot be ignored is artery wall remodeling marked by the thickening of tunica intima, media, and adventitia. Several parameters' expressions indicating PAH include basic fibroblast growth factor-2 (bFGF-2), transforming growth factor-1 (TGF-1), matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-1 (TIMP-1), and type 1 collagen. This study aims to verify the progressive increase in the expression of bFGF-2, TGF-β1, TIMP-1, and type 1 collagen, the decrease of MMP-2 expression, as well as the MMP-2:TIMP-1 ratio in the tunica adventitia of pulmonary arteries. The samples of paraffin blocks in rat models' lung tissue of pulmonary arterial hypertension were made in a particular time span. The immunohistochemical method was employed to examine the expressions of bFGF-2, TGF-β1, MMP-2, TIMP-1, and type 1 collagen. The data analysis was carried out using the Pearson and Spearman statistical test. After 28-day observation, the number of cells expressing bFGF-2, TGF-β1, TIMP-1, progressively increased and had a strong, positive and significant correlation with the time reaching p-value of 0.005, 0.000, and 0.000 respectively. Meanwhile, MMP-2 and MMP-2:TIMP-1 ratio had a weak negative and insignificant correlation with the time. In tunica adventitia of pulmonary arteries on rat models of pulmonary arterial hypertension induced with monocrotaline, it is proven that there is a progressive increase in the expression of bFGF-2, TGF-β1, TIMP-1, and type 1 collagen. In addition, MMP-2 expression suggests a progressive decrease, while the MMP-2:TIMP-1 ratio also decreases.
|Number of pages||6|
|Journal||Journal of International Dental and Medical Research|
|Publication status||Published - 2020|
- Pulmonary arterial hypertension
- Tunica adventitia