| Objeetive:Scleroderma is a kind of connective tissue disease which pathological feature is expressed by the skin and the collagen fiber progressive hardening of each system.Skin fibroblasts excessive synthesis Ⅰ,Ⅲ collagen type that play a vital role in pathogenesis of scleroderma.At present,the domestic and foreign research have found that the collagen triple helix repeat containing 1 and the transforming growth factor-β1/Smad play an important role in the process of the whole body many organs abnormal fibering and this process is caused by the skin fibroblasts excessive synthesis Ⅰ,Ⅲ collagen type.However,researches refer to Cthrcl and TGF-β1/Smad signaling pathway in the pathogenic mechanism of scleroderma is so little.To explore the effect of Cthrcl and TGF-β1/Smad signaling pathway in the pathogenic mecha-nism of scleroderma,the expression level of Cthrcl,TGF-β1,Smad2,Smad3 and Smad7 was tested by immunohistochemistry technique in the skin tissues from the scleroderma patients and normal people,also the difference of their expression and relationship of each other was analyzed.Method:Using case-control study,we collected skin tissues with scleroderma patients and normal.The expression of Cthrcl,TGF-β1,Smad2,Smad3 and Smad7 in 30 cases of scleroderma skin tissue and 15 cases of normal skin fibroblasts was detected by immunohistochemistry technique to find the difference and connect with each other of them.Collected images positive staining results of Collected images were semi-quantitative analyzed with the the Media Cybernetics professional image analysis software(image pro plu6.0,IPP),and evaluation of the integral optical density(IOD)as positive staining.Data were analyzed by SPSS 17.0 software.The t-test was used for the comparison between the measurement data,and Pearson correlation analysis was used for the associativity of each sample.Results:1.HE staining:we found that Collagen fiber homogenization,collagen fiber bundle of parallel arrangement with the skin increased,collagen fiber volume increased significantly,elastic fibers were damaged.only a few blood vessels inside of the collagen dermal sclerosis,hemal wall became stenosis,fibroblasts were squeezed and deformation,no had obvious skin atrophy.2.The expression of Cthrcl,TGF-β1 Smad2,Smad3,Smad7 by immunohistochemistry:(1)Cthrc1:Scleroderma lesion group(IOD):6620.40±1758.34,normal control group(IOD):852.33±224.24.The expression of Cthrcl in Scleroderma lesion group were higher than those in normal control group(P<0.05).(2)TGF-β3:Scleroderma lesion group(IOD):1098.97±441.08,normal control group(IOD):221.33±84.27.The expression of TGF/β1 in Scleroderma lesion group were higher than those in normal control group(P<0.05).(3)Smad2:Scleroderma lesion group(IOD):24008.58±7431.01,normal control group(IOD):1816.72±447.09.The expression of Smad2 in Scleroderma lesion group were higher than those in normal control group(P<0.05).(4)Smad3:Scleroderma lesion group(IOD):54983.22±17741.32,normal control group(IOD):2035.23±720.94.The expression of Smad3 in Scleroderma lesion group were higher than those in normal control group(P<0.05).(5)Smad7:Scleroderma lesion group(IOD):1098.34±332.00,normal control group(IOD):132.27±87.48.The expression of Smad7 in Scleroderma lesion group were higher than those in normal control group(P<0.05).3.Correlation analysis for Cthrc1,TGF-β1,Smad2,Smad3,Smad7:(1)In scleroderma lesion group:There was a positive linear correlation between the abnormal expression of Cthrc1 and TGF-β1(r=0.775,P<0.05);There was a positive linear correlation between the abnormal expression of TGF-β1 and Smad2(r=0.756,P<0.05);There was a positive linear correlation between the abnormal expression of TGF-β1 and Smad3(r=0.722,P<0.05);There was a positive linear correlation between the abnormal expression of TGF-(31 and Smad7(r=0.822,P<0.05);(2)In Normal skin group:There was no obvious correlation between the abnormal expression of Cthrcl and TGF-β1(r= 1.108,P>0.05);There was no obvious correlation between the abnormal expression of TGF-β1 and Smad2(r=1.284,P>0.05);There was no obvious correlation between the abnormal expression of TGF-β1 and Smad3(r=1.402,P>0.05);There was no obvious correlation between the abnormal expression of TGF-β1 and Smad7(r=1.256,P>0.05).Conelusions:1.HE staining:Collagen fiber in scleroderma patients skin tissue was swelled and increased,showed that associated with the pathogenesis of scleroderma.2.The abnormal expression of Cthrcl in Scleroderma lesion group were higher than those in normal control group,suggested Cthrc1 may play a role in the pathogenesis of scleroderma.3.The abnormal expression of TGF-β1 Smad2 and Smad3 in Scleroderma lesion group were higher than those in normal control group,Smad2 and Smad3 the most expressed in cell nucleus,and the expression of TGF-β1 and Smad2,Smad3,Smad7 expression was negatively significant correlation,so we extrapolate TGF-β1/Smad signaling pathway may be actived in scleroderma.4.There was a positive linear correlation between the abnormal expression of Cthrc1 and TGF-β1,suggested the abnormal expression of Cthrc1 and TGF-β1/Smad signaling pathways abnormal activation affected with each other.5.The abnormal expression of Cthrcl and TGF-β1/Smad signaling pathways abnormal activation in skin fibroblasts affected with each other,they may participate in skin collagen fiber progressive hardening process,and may be associated with the pathogenesis of scleroderma. |
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