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Uncoupling protein 2 deficiency reduces proliferative capacity of murine pancreatic stellate cells

Hepatobiliary & Pancreatic Diseases International 2016年第6期15卷 647-654页

作者： Sarah Muller Sandra Maria Klingbeil Andreea Sandica Robert Jaster Department of Medicine II Division of Gastroen-terologyRostock University Medical CenterE.-Heydemann-Str.618057 RostockGermany

BACKGROUND： Uncoupling protein 2 （UCP2） has been suggested to inhibit mitochondrial production of reactive oxygen species （ROS） by decreasing the mitochondrial membrane potential. Experimental acute pancreatitis is associated with increased UCP2 expression, whereas UCP2 deficiency retards regeneration of aged mice from acute pancreatitis. Here, we have addressed biological and molecular functions of UCP2 in pancreatic stellate cells （PSCs）, which are involved in pancreatic wound repair and fibrogenesis. METHODS： PSCs were isolated from 12 months old （aged） UCP2^-/- mice and animals of the wild-type （WT） strain C57BL/6. Proliferation and cell death were assessed by em- ploying trypan blue staining and a 5-bromo-2＇-deoxyuridine incorporation assay. Intracellular fat droplets were visualized by oil red O staining. Levels of mRNA were determined by RT-PCR, while protein expression was analyzed by immunoblotting and immunofluorescence analysis. Intracellular ROS levels were measured with 2＇,7＇-dichlorofluorescin diacetate. Expression of senescence-associated β-galactosidase （SA β-Gal） was used as a surrogate marker of cellular senescence. RESULTS： PSCs derived from UCP2^-/- mice proliferated at a lower rate than cells from WT mice. In agreement with this observation, the UCP2 inhibitor genipin displayed dose- dependent inhibitory effects on WT PSC growth. Interestingly, ROS levels in PSCs did not differ between the two strains, and PSCs derived from UCP2^-/- mice did not senesce faster than those from corresponding WT cells. PSCs from UCP2^-/- mice and WT animals were also indistinguishable with respect to the activation-dependent loss of intracellular fat droplets, expression of the activation marker α-smooth muscle actin, type I collagen and the autocrine/paracrine mediators interleukin-6 and transforming growth factor-I~ 1. CONCLUSIONS： A reduced proliferative capacity of PSC from aged UCP2^-/- mice may contribute to the retarded regeneration after acute pancreatitis.

关键词： pancreatitis proliferation stellate cell biology uncoupling protein 2

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Trametinib and dactolisib but not regorafenib exert antiproliferative effects on rat pancreatic stellate cells

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Hepatobiliary & Pancreatic Diseases International 2015年第6期14卷 642-650页

作者： Laura Witteck Robert Jaster Department of Medicine Ⅱ Division of GastroenterologyRostock University Medical Center

BACKGROUND： Modulation of the stroma response is considered a promising approach for the treatment of chronic pancreatitis and pancreatic cancer. The aim of this study was to evaluate the effects of three clinically available small molecule kinase inhibitors, regorafenib, trametinib and dactolisib, on effector functions of activated pancreatic stellate cells （PSCs）, which play a key role in pancreatic fibrosis.

关键词： stellate cell biology pancreatic cancer chronic pancreatitis trametinib dactolisib

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