Repetitive acute XXXX in the @entity19 induces procollagen alpha1(I) expression colocalized to pancreatic stellate cells.

@entity788 @entity82 @entity19 @entity660 @entity8629 @entity130
@entity788 stellate cells may be a major source of extracellular matrix deposition during injury. This study was undertaken to establish whether pancreatic stellate cells are a source of Type I collagen in vivo and whether they continue to be a source of matrix production in the @entity130 . To induce pancreatic fibrogenesis, acute @entity660 was induced in @entity19 three times weekly with supraphysiologic doses of @entity8629 . Animals were treated for 6 weeks and allowed to recover for an additional 6 weeks. Stellate cell activation and pancreatic collagen expression were measured by immunohistochemistry, whole tissue RNA analysis, and in situ hybridization. Histology and digital image analysis demonstrated the development of substantial pancreatic @entity82 after 6 weeks of treatment. During recovery, incomplete resolution of the @entity82 was found. Procollagen alpha1(I) mRNA increased more than 15-fold during treatment and continued to be 5-fold elevated during the post-injury phase. In situ hybridization studies demonstrated that collagen gene expression was colocalized to activated pancreatic stellate cells. Collagen expression and @entity82 persisted in focal areas during recovery. These findings show that pancreatic stellate cells are the major source of collagen during @entity130 in vivo. Additionally, focal areas of sustained pancreatic fibrogenesis persist after cessation of @entity8629 treatment, and these areas may contribute to sustained total organ collagen expression in the absence of @entity130 .
