Characterization of Pancreatic Collagen-Expressing Fibroblasts in Mouse Acute Pancreatitis

Amy Qin , Kevin Shi , Rachel R. Tindall , Jiajing Li , Binglu Cheng , Jing Li , Baibing Yang , Qiang Yu , Yinjie Zhang , Bangxing Hong , Balveen Kaur , Mamoun Younes , Qiang Shen , Jennifer M. Bailey-Lundberg , Yanna Cao , Tien C. Ko
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Abstract

Background and Aims

Pancreatic stellate cells (PSCs) are critical mediators in chronic pancreatitis with an undefined role in acute pancreatitis (AP). PSCs consist of a heterogenous group of cells and are considered interchangeable with pancreatic fibroblasts. This study explored the heterogeneous nature of PSCs by characterizing pancreatic collagen-expressing fibroblasts (PCFs) via lineage tracing in mouse normal and AP pancreas and determining the effect of PCF depletion in AP.

Methods

Tandem dimer Tomato (tdTom+) PCFs in collagen type 1 (Col1)a2CreERtdTomato (Tom) mice receiving tamoxifen were characterized via fluorescence, Oil Red staining, and flow cytometry. AP was induced by cerulein, AP injury was assessed, and tdTom+ PCFs were monitored. The effect of PCF depletion on AP injury was evaluated in Col1a2CreERdiphtheria toxin A mice.

Results

Approximately 13% of pancreatic cells in Col1a2CreERTom mice were labeled by tdTom (tdTom+ PCFs), which surrounded acini, ducts, and blood vessels, and stained with Oil Red, collagen type I, vimentin, and desmin. tdTom+ PCFs increased 2-fold during AP, correlating with AP score, amylase, and alpha-smooth muscle actin+ and Ki67+ staining. PCF depletion in Col1a2CreERdiphtheria toxin A mice receiving tamoxifen resulted in enhanced inflammation compared to control.

Conclusion

PCFs may constitute a subset of PSCs and can be activated during AP. PCF depletion aggravates AP, suggesting a protective role for PCFs.

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Gastro hep advances
Gastro hep advances Gastroenterology
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