Open AccessGene 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(s) -
Ding Li,
Morimoto Yasuo,
Oyabu Takako,
Kim Heungnam,
Ohgami Akira,
Yatera Kazuhiro,
Hirohashi Masami,
Yamato Hiroshi,
Hori Hajime,
Higashi Toshiaki,
Tanaka Isamu
Publication year - 2001
Publication title -
journal of occupational health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 59
ISSN - 1348-9585
DOI - 10.1539/joh.43.111
Subject(s) - thyroid transcription factor 1 , messenger rna , in vivo , thyroid , gene expression , lung , medicine , pulmonary surfactant , endocrinology , transcription factor , reverse transcription polymerase chain reaction , biology , chemistry , andrology , gene , biochemistry , microbiology and biotechnology
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 SPA 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.