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J Occup Health year 2001 volume 43 number 3 page 111 - 117
Classification Original
Title Gene Expression of Clara Cell Secretory Protein, Surfactant Protein-A and Thyroid Transcription Factor-1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers in vivo
Author Li DING1, Yasuo MORIMOTO1, Takako OYABU1, Heungnam KIM1, Akira OHGAMI1, Kazuhiro YATERA2, Masami HIROHASHI1, Hiroshi YAMATO1, Hajime HORI3, Toshiaki HIGASHI1 and Isamu TANAKA1
Organization 1Institute of Industrial and Ecological Sciences,
2Department of Respiratory Diseases,
3School of Health Sciences, University of Occupational and Environmental Health, Japan
Keywords CCSP, SP-A, TTF-1, Potassium octatitanate whiskers, RT-PCR, Lung
Correspondence Y. Morimoto, Department of Occupational Pneumology, Institute of Industrial and Ecological Sciences, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu 807-8555, Japan
Abstract Gene Expression of Clara Cell Secretory Protein, Surfactant Protein-A and Thyroid Transcription Factor-1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers in vivo: Li DING, et al. Institute of Industrial and Ecological Sciences, University of Occupational and Environmental Health, Japan-Inhalation studies have shown that exposure to potassium octatitanate whiskers (PT1), an asbestos substitute, produces pulmonary fibrotic changes, suggesting that PT1 might have fibrogenic potential. It has been theorized that Clara cell secretion protein (CCSP) and surfactant protein-A (SP-A) play a critical role in regulating the acute inflammatory response in the lung. The present study was conducted to investigate the time course (3 days, 1 wk, 1 month, 3 months, and 6 months) of the expression of mRNA of CCSP, SP-A and thyroid transcription factor-1 (TTF-1), a common transcription factor of CCSP and SP-A, in lungs exposed to PT1 in vivo. PT1 suspended in saline was administered to male Wistar rats at a dose of 2 mg or 10 mg by single intratracheal instillation, and RNA was then extracted from the lungs. Expression of CCSP, SP-A and TTF-1 mRNA from the lungs was examined by reverse transcription-polymerase chain reaction. Exposure to 2 mg of PT1 did not increase levels of CCSP, SP-A or TTF-1 mRNA. The level of SP-A mRNA in PT1-exposed rats was decreased at 1, 3 and 6 months after a single instillation of 10 mg. Levels of CCSP and TTF-1 mRNA were also decreased at 3 days, 3 and 6 months after a single instillation. These findings suggest that CCSP and SP-A are involved not only in the acute inflammatory response but also in the chronic response of the lung exposed to PT1.