Interleukin-22 regulating fibrosis on mouse cardiac fibroblasts through STAT3 signaling pathway

Objective:To observe the effects of interleukin-22(IL-22)on the expression of type Ⅲ collagen,cytokines,growth factors and chemokines in mouse cardiac fibroblasts in vitro.Methods:Mouse cardiac fibroblasts were treated with0μg/L(control),1μg/L(low concentration)and 100μg/L(high concentration)IL-22,respectively.In addition,cells treated with 100μmol/L static(an STAT3 pathway inhibitor)and 100μg/L IL-22 was defined as the block group.After treatment for 48 hours,the mRNA level of collagen type Ⅲ A1(Col3-A1),matrix metalloproteinase-1(Timp-1),IL-22receptor(IL-22R),interleukin 10-related T cellderived inducible factor beta(Iltifb),fibroblast growth factor1(Fgf1)and C-C motif chemokine ligand 4(Ccl4)were determined by RT-PCR.The expression of Col3-A1 in cardiac fibroblasts was also semi-quantified by immunofluorescence.Results:Expression of Col3-A1 decreased in the low and high concentration groups,but significantly increased in the block group(all P <0.05).The expression of Timp-1increased in the low,high concentration and block groups compared with that in the control group,but it was significantly lower in the high concentration group than that in the low concentration group(P <0.05).The expression of IL-22 Rand Iltifb was significantly increased in the low,high concentration and block groups compared with that in the control group(P <0.05),but there was no statistical difference between the high concentration group and block group.The expression of Fgf1 and Ccl4 was significantly decreased in the low,high concentration and block groups compared with that in the control group(P <0.05),but there was no statistic difference between the high concentration group and block group as well.Conclusion:IL-22 effected on the expression of Col3-A1 and Timp-1,which was possibly through the JAK-STAT3 signaling pathway in mice cardiac fibroblasts.

Objective： To observe the effects of interleukin-22 （IL-22） on the expression of type Ⅲ collagen, cytokines, growth factors and chemokines in mouse cardiac fibroblasts in vitro. Methods： Mouse cardiac fibroblasts were treated with 0 μg/L （control）, 1μg/L （low concentration） and 100 μg/L （high concentration） IL-22, respectively. In addition, cells treated with 100 μmol/L static （an STAT3 pathway inhibitor） and 100 μg/L IL-22 was defined as the block group. After treatment for 48 hours, the mRNA level of collagen type Ⅲ A1 （Co13-A1）, matrix metalloproteinase-1 （Timp- 1）, IL-22 receptor （IL-22R）, interleukin 10-related T cell- derived inducible factor beta （Iltifb）, fibroblast growth factor 1 （Fgf1） and C-C motif chemokine ligand 4 （Cc14） were determined by RT-PCR. The expression of Co13-A1 in cardiac fibroblasts was also semi-quantified by immunofluorescence. Results： Expression of Co13-A1 decreased in the low and high concentration groups, but significantly increased in the block group （all P 〈0.05）. The expression of Timp-1 increased in the low, high concentration and block groups compared with that in the control group, but it was significantly lower in the high concentration group than that in the low concentration group （ P 〈0.05）. The expression of IL-22R and Iltifb was significantly increased in the low, high concentration and block groups compared with that in the control group （ P 〈0.05）, but there was no statistical difference between the high concentration group and block group. The expression of Fgfl and Cc14 was significantly decreased in the low, high concentration and block groups compared with that in the control group （ P 〈0.05）, but there was no statistic difference between the high concentration group and block group as well. Conclusion：IL-22 effected on the expression of Col3-A1 and Timp-1, which was possibly through the JAK-STAT3 signaling pathway in mice cardiac fibroblasts.