Control of type I collagen formation in the lung.
Type I collagen is a major structural protein in the lung, the accumulation of which is stimulated during certain inflammatory reactions in the lung. Accumulating evidence suggests that type I collagen formation parallels changes in steady-state mRNA levels. Specific inflammatory substances modulate transcription of collagen genes and stabilization of collagen mRNA in vitro. However, the precise role for any particular mediator during fibrotic processes is difficult to identify because of the complex nature of the inflammatory reaction and potential interaction among mediators. The signal transduction mechanisms that regulate collagen accumulation remain to be defined. This review focuses on the regulation of collagen accumulation in the lung by specific inflammatory substances.
Goldstein
R H
RH
Pulmonary Center, Boston University School of Medicine 02118.
D000818:Animals; D003094:Collagen / Q000096:biosynthesis* / Q000235:genetics; D005347:Fibroblasts / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D008168:Lung / Q000166:cytology / Q000378:metabolism*; D008954:Models, Biological; D011658:Pulmonary Fibrosis / Q000209:etiology; D015398:Signal Transduction
D003094:Collagen