Localization and potential role of matrix metalloproteinase-1 and tissue inhibitors of metalloproteinase-1 and-2 in different phases of bronchopulmonary dysplasia

被引:23
作者
Dik, WA
De Krijger, RR
Bonekamp, L
Naber, BAE
Zimmermann, LJI
Versnel, MA
机构
[1] Erasmus Univ, Dept Immunol, Sophia Childrens Hosp, Div Neonatol, NL-3000 DR Rotterdam, Netherlands
[2] Erasmus Univ, Dept Pathol, Sophia Childrens Hosp, Div Neonatol, NL-3000 DR Rotterdam, Netherlands
[3] Erasmus Univ, Dept Pediat, Sophia Childrens Hosp, Div Neonatol, NL-3000 DR Rotterdam, Netherlands
[4] Univ Hosp Rotterdam Dijkzigt, Rotterdam, Netherlands
关键词
D O I
10.1203/00006450-200112000-00022
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Bronchopulmonary dysplasia (BPD) can evolve in prematurely born infants who require mechanical ventilation because of hyaline membrane disease (HMD). The development of BPD can be divided in an acute, a regenerative, a transitional and a chronic phase. During these different phases, extensive remodeling of the lung parenchyma with re-epithelialization of the alveoli and formation of fibrosis occurs. Matrix metalloproteinase-1 (MMP-1) is an enzyme that is involved in re-epithelialization processes, and dysregulation of MMP-1 activity contributes to fibrosis. Localization of MMP-1 and its inhibitors, tissue inhibitor of metalloproteinase (TIMP)- 1 and TIMP-2, were investigated in lung tissue obtained from infants who died during different phases of BPD development. In all studied cases (n = 50) type-II pneumocytes were found to be immunoreactive for MMP-1, TEMP-1, and TIMP-2. During the acute and regenerative phase of BPD, type-II pneumocytes re-epithelialize the injured alveoli. This may suggest that MMP-1 and its inhibitors, expressed by type-II pneumocytes, play a role in the reepithelialization process after acute lung injury. Although MMP-1 staining intensity remained constant in type-II pneumocytes during BPD development, TIMP-1 increased during the chronic fibrotic phase. This relative elevation of TIMP-1 compared with MMP-1 is indicative for reduced collagenolytic activity by type-H pneumocytes in chronic BPD and may contribute to fibrosis. Fibrotic foci in chronic BPD contained fibroblasts immunoreactive for MMP- I and TIMP- and -2. This may indicate that decreased collagen turnover by fibroblasts contributes to fibrosis in BPD development.
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页码:761 / 766
页数:6
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