The Role And The Molecular Mechanism Of 1, 25 Dihydroxyvitamin D And It's Receptor In Kawasaki Disease

PartⅠThe role and the molecular mechanism of 1,alpha,25 dihydroxyvitamin D and it's receptor in JurkatObjective: To study the expression and the role of 1,alpha,25 dihydroxyvitamin D (1,25(OH)2D3) and it's receptor(VDR) in Jurkat, moreover to research the mocular regulation, which can supply basic data for next experiment. Methods: Different concentration 1,25(OH)2D3 were used to culure Jurkat .Western Blot were used to study the protein of vitamin D3 receptor and signal transducers and activations and Transcription3 (STAT3), Exacellular signal regulation kinase (ERK), Nuclear factor-κB (NF-κB), Protein 53(P53).Results: The maximum harmless concentration of 1,25(OH)2D3 was 10-1mg/ml. The protein of VDR was expressed in Jurkat,but was not regulated by 1,25(OH)2D3. ERK can be inhibited by 1,25(OH)2D3, and be related to the concentration. NF-κB was activated in Jurkat, was not related to 1,25(OH)2D3. P53can be regulated by 1,25(OH)2D3.Conclusion: The role of 1,25(OH)2D3 to Jurkat was inhibition of cell growth.PartⅡThe role and the molecular mechanism of 1,25(OH)2D3 and it's receptorin T cell in Kawasaki DiseaseObjective: To study the expression and the role of 1,25(OH)2D3and it's receptor(VDR) in T cell in Kawasaki Disease, moreover to research the mocular regulation.Methods: Collecting PBMC of 30 patients of Kawasaki Disease, 60 patients of infecting febrile, 60 patients of normal childrens. Culuring human peripheral T cell .Western Blot were used to study the protein of VDR and STAT3, ERK, NF-ΚB,P53. And research the regulation of 1,25(OH)2D3 to them.Results: The maximum harmless concentration of 1,25(OH)2D3was 10-3mg/ml in T cell. The protein of VDR was highest in Kawasaki Disease, but was not regulated by 1,25(OH)2D3.STAT3 was activated in Kawasaki Disease, but could not be regulated by 1,25(OH)2D3. P53 did not response in Kawasaki disease. ERK and NF-κB were activatied in Kawasaki disease.1,25(OH)2D3 can regulate P53 and ERK. Conclusion: Activating STAT3 inhibited cell apoptosis. Theinactive of P53, the anti-apoptosis of NF-Κb, and activation ofERK can accelerate cell growth. In this time, the up-regulationof VDR was not able to inhibite this phenomenon. However, adding 1,25(OH)2D3 to culture T cell can revolt all.PartⅢThe role of STAT3 in Kawasaki DiseaseObjective: In second part , we found STAT3 STAT3 was activated in Kawasaki Disease, which is special, So in this part, it is important to study the role of STAT3-SOCS1 in Kawasaki Disease,so that to research the molecular mechanical in Kawasaki Disease.Methods: Construction of the green fluorescence eukaryoti expression vector of the SOCS1 gene, and express in the peripheryblood mononuclear cell in Kawasaki Disease. Western Blot were used to study the protein of STAT3. Results: The green fluorescence of the green fluorescence eukaryotiexpression vector of the SOCS1 gene was constructed correctly and was expressed in the periphery blood mononuclear cell in KawasakiDisease. And SOCS1 can decrease the expression of STAT3.Conclusions: The up-regulation of SOCS1 can balance the STAT3-SOCS1 in Kawasaki Disease.