Role of matrix metalloproteinases and apoptosis markers in pathogenesis of bronchopulmonary dysplasia in children born with low weight

Abstract

Bronchopulmonary dysplasia involves abnormal development of lung tissue. It most often affects premature babies, who are born with underdeveloped lungs. "Dysplasia" means abnormal changes in the structure or organization of a group of cells. The cell changes in BPD take place in the smaller airways and lung alveoli, making breathing difficult and causing problems with lung function. 32 early aged children involved in survey. All children were divided into 2 groups. Group 1 was classified as a classic BPD with 24 children (surfactant received), the 2nd group of 8 children with new form of BPD. All surveyed babies consist of 4 from 1 group were born prematurely (less than 32 weeks ). 20 babies without BPD consisted comparative group. The levels of apoptosis markers (Cytochrome-S, ammakon-V) during both classical and new forms of BPD are increasingly related to the pathological process severity and have the same orientation; indicates the general nature of autoregulatory mechanisms in the latter apoptosis process. Increased concentrations of MMP-2, MMP-9 and MMTS in the background of MMP-1 in the initial stage of BPD formation causes the structural changes in the extracellular matrix, pathological remodeling of the lungs and the development of fibrous tissue.