Morimoto Y, Tsuda T, Nakamura H, Hori H, Yamato H, Nagata N, Higashi T, Kido M, Tanaka I
Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Kitakyushu, Japan.
Environ Health Perspect. 1997 Sep;105 Suppl 5(Suppl 5):1247-51. doi: 10.1289/ehp.97105s51247.
To determine the effect of mineral fibers and cigarette smoke on remodeling of lung tissues, we examined matrix metalloproteinase-1 (MMP-1), MMP-2, tissue inhibitors of metalloproteinase-1 (TIMP-1), TIMP-2, and types I and IV collagen mRNA levels from rat lungs exposed to mineral fibers and/or cigarette smoke in vivo. Male Wistar rats (10 weeks of age) were given a single intratracheal instillation of 2 mg of chrysotile or alumina silicate ceramic fibers (RCF). Animals were then exposed to cigarette smoke (side stream) 5 days per week for 4 weeks. Transcriptional levels of mRNA extracted from the lungs were assessed by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). Exposure to cigarette smoke induced increases in MMP-1 and TIMP-1 mRNA levels and decreased TIMP-2 and type I collagen mRNA levels in lung. Chrysotile or RCF stimulated the expression of MMP-1 mRNA in the lung. The mineral fibers and cigarette smoke had more than additive effects on the expression of MMP-2 and TIMP-1 in the lung. These data suggest that the imbalance of the expression of MMPs, TIMPs, and extracellular matrix may be associated with the remodeling of lung tissues induced by mineral fibers and/or cigarette smoke.
为了确定矿物纤维和香烟烟雾对肺组织重塑的影响，我们检测了体内暴露于矿物纤维和/或香烟烟雾的大鼠肺组织中基质金属蛋白酶-1（MMP-1）、MMP-2、金属蛋白酶组织抑制剂-1（TIMP-1）、TIMP-2以及I型和IV型胶原mRNA的水平。将雄性Wistar大鼠（10周龄）经气管内单次注入2mg温石棉或硅酸铝陶瓷纤维（RCF）。然后动物每周5天暴露于香烟烟雾（侧流）中，持续4周。通过半定量逆转录-聚合酶链反应（RT-PCR）评估从肺中提取的mRNA的转录水平。暴露于香烟烟雾会导致肺中MMP-1和TIMP-1 mRNA水平升高，而TIMP-2和I型胶原mRNA水平降低。温石棉或RCF刺激肺中MMP-1 mRNA的表达。矿物纤维和香烟烟雾对肺中MMP-2和TIMP-1的表达具有超过相加的作用。这些数据表明，MMPs、TIMPs和细胞外基质表达的失衡可能与矿物纤维和/或香烟烟雾诱导的肺组织重塑有关。
