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자료유형
학술저널
저자정보
Shin, Chan-Young (Department of Pharmacology, College of Pharmacy, Seoul National University, Department of Molecular, Cellular and Developmental Biology, Yale University) Lee, Woo-Jong (Department of Pharmacology, College of Pharmacy, Seoul National University) Park, Kyu-Hwan (Department of Pharmacology, College of Pharmacy, Seoul National University) Ryu, Jae-Ryun (Department of Pharmacology, College of Pharmacy, Seoul National University) Ko, Kwang-Ho (Department of Molecular, Cellular and Developmental Biology, Yale University)
저널정보
한국응용약물학회 The journal of applied pharmacology : the official journal of the Korean Society of Applied Pharmacology The journal of applied pharmacology : the official journal of the Korean Society of Applied Pharmacology 제12권 제1호
발행연도
2004.1
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1 - 8 (8page)

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In chronic airway inflammatory diseases such as asthma and chronic bronchitis, it has been suggested that matrix metalloproteinases secreted from infiltrating neutrophil contribute the pathogenesis of the disease and have been a focus of intense investigation. We report here that hamster tracheal surface epithelial goblet cells (HTSE cells) produce matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2). Matrix metalloproteinase activities were investigated using [$^3H$]collagen-digestion assay and gelatin zymography. The subtype of matrix metalloproteinases expressed from HTSE cells was MMP-2 (gelatinase A), which was determined by Western blot with various subtype selective anti-matrix metalloproteinase antibodies. The MMP-2 and TIMP-2 cDNAs from HTSE cells were partially cloned by RT-PCR and they reveal more than 90% of sequence homology with those from human, rat and mouse. The collagenolytic activity was increased with the secretory differentiation of the HTSE cell and it was found that zymogen activation was responsible for the increased MMP-2 activity in HTSE cells. The results from the present study suggest that the metaplastic secretory differentiation of airway goblet cells may affect chronic airway inflammatory process by augmenting the zymogen activation of MMP-2.

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