Synthesis and Degradation of Collagen in Pancreatic Fibrogenesis

Valderrama, Rodrigo; Navarro, S; Jm, López Novoa; Caballería, Joan; Giménez, America; Parés, Albert; Mj, Adrián; Fernández‐Cruz, Laureano; Terés, J

doi:10.1097/00006676-199901000-00005

Cited by 7 publications

(1 citation statement)

References 10 publications

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“…Active pancreatic matrix remodeling has been observed after acute injury in rat models when the expression of the matrix-degrading enzyme MMP-2 was transiently elevated (Elsä sser et al, 1989;Mü ller-Pillasch et al, 1997). The activity of MMP-2 was also increased in human chronic pancreatitis (Gress et al, 1994b), although the overall pancreatic collagenase activity was low in human chronic pancreatitis compared with that in normal people (Valderrama et al, 1998). Pancreatic stellate cells may be lost or deactivated through apoptosis or terminal differentiation.…”

Section: Stellate Cells and Pancreatic Fibrogenesismentioning

confidence: 99%

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Neuschwander‐Tetri¹,

Bridle

Wells³

et al. 2000

Laboratory Investigation

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SUMMARY:Pancreatic 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 post-injury fibrotic pancreas. To induce pancreatic fibrogenesis, acute pancreatic injury was induced in mice three times weekly with supraphysiologic doses of cerulein. 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 fibrosis after 6 weeks of treatment. During recovery, incomplete resolution of the fibrosis was found. Procollagen ␣ 1 (I) mRNA increased more than15-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 fibrosis persisted in focal areas during recovery. These findings show that pancreatic stellate cells are the major source of collagen during repetitive injury in vivo. Additionally, focal areas of sustained pancreatic fibrogenesis persist after cessation of cerulein treatment, and these areas may contribute to sustained total organ collagen expression in the absence of ongoing injury. (Lab Invest 2000, 80:143-150).

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Section: Stellate Cells and Pancreatic Fibrogenesismentioning

confidence: 99%

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Neuschwander‐Tetri¹,

Bridle

Wells³

et al. 2000

Laboratory Investigation

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Decreased Type IV Collagenase Activity in Experimental Pancreatic Fibrosis

Ng¹,

Barent²,

Smith³

et al. 2001

Journal of Surgical Research

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Motoo

Xie

et al. 2000

Digestive Diseases and Sciences

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Transforming growth factor-beta1 (TGF-beta1) is suggested to be a mediator of fibrosis in chronic pancreatitis, but the serial change of TGF-beta1 expression in the onset and progression of chronic pancreatitis is still unclear. We investigated the TGF-beta1 expression in the spontaneous chronic pancreatitis model. Four-week-old male WBN/Kob rats were fed with special pellet diet (MB-3) for 20 weeks. TGF-beta1 mRNA in the pancreas was detected by reverse transcription-polymerase chain reaction assay from four weeks, and its expression peaked at 12 weeks when the pancreatic fibrosis first appeared. The localizations of TGF-beta1 mRNA and protein were confirmed in the cytoplasm of pancreatic acinar and ductal cells by in situ hybridization and immunohistochemistry, respectively. Although fibronectin expression peaked at 12 weeks and correlated with that of TGF-beta1, its elevated expression tended to be prolonged. Pancreatic fibrosis peaked at 16 weeks after the peak of TGF-beta1 expression. These results suggest that TGF-beta1 expression may be a trigger of the fibrotic process of chronic pancreatitis in the WBN/Kob rat.

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Synthesis and Degradation of Collagen in Pancreatic Fibrogenesis

Cited by 7 publications

References 10 publications

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Decreased Type IV Collagenase Activity in Experimental Pancreatic Fibrosis

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