| Objective: Pregnancy Induced Hypertension (PIH) is one of the leading cause of maternal and fetal morbidity and mortality. The study on it's etiology and pathogensis is remain one of important subject of obstetrics. Endothelial dysfunction and defective endovascular invasion of cytotrophoblast are two important links of PIH. Cell adhesion molecules (CAMs) play a key role in cell-cell action and in cell-extracellular matrix interactions. They are essential to the successful pregnancy. The immuno-microenvironment of decidua contains immunocyte and cytokines secreted by these cell, and which is essential to successful pregnancy. The change of adhesion molecules expression on decidual immunocytes may cause PIH. We investigated the expression of adhesion molecule: integrin β1(CD29) integrin α3(CD49c), integrin αV (CD51), ntegrin αE (CD103), selectin-L (CD62L) vascular cell adhesion molecule-1 VCAM-1,(CD106) on decidua lymphocyte and macrophage in PIH, in order to find out the mechanism of PIH, further the way of prevention and therapy to PIH. Methods: The study group consisted of 10 women with PIH, the control group consisted of 10 women withuncomplicated pregnancies. Women with previous history of underlying hypertension, diabetes, chronic renal disease, platelet disorder, infection were excluded from the study. Two group was matched for age and parity. The decidual tissue was separated by lymphocyte separation fluid after digested by Trypsin, then purer lymphocyte and macrophage are get with the way attached cells to the wall of culture medium. Assay of flow cytometry is used for phenotypes of adhesion molecule: integrin β1(CD29), integrin α3 (CD49c), integrin αV (CD51), integrin αE (CD103), selectin-L (CD62L), vascular cell adhesion molecule-1 VCAM-1 (CD106) on decidua lymphocyte and macrophage. Results: 1 The comparison of adhesion molecule expression on lymphocyte in PIH and controls: Compared to the control group, the expression of integrin β1 (CD29) on decidua lymphocyte in middle and sever PIH is obviously higher, (P<0.01, P<0.01). The expression of integrin β1 (CD29) on decidua lymphocyte in mild PIH is not higher than that in control group (P>0.05). Compared to the control group, the expression of integrin α3 (CD49c) on decidual lymphocyte in sever PIH is obviously higher, (P<0.01). the expression of integrin α3 (CD49c) on decidua lymphocyte in middle and mild PIH is not obviously higher than that in control group (P>0.05, P>0.05). The expression of integrin αV (CD51), selectin-L (CD62L), vascular cell adhesion molecule-1 VCAM-1 (CD106) on decidua lymphocyte inmiddle and mild and sever PIH are all slightly higher than that of the control group, but no statistical significant difference. (all P>0.05). Compared to the control group , the expression of integrin αE (CD103) on decidual lymphocyte in sever PIH is obviously higher, (P<0.01). the expression of integrin αE (CD103) on decidual lymphocyte in middle and mild PIH is not higher than that in control group (P>0.05, P>0.05). 2 The comparison of adhesion molecule expression on macrophage in PIH and controls: Compared to the control group , the expression of integrin β1 (CD29) on decidual macrophage in sever PIH is obviously higher, (P<0.01). the expression of integrin β1 (CD29) on decidual macrophage in middle and mild PIH is not obviously higher than that in control group (P>0.05). Compared to the control group, the expression of integrin α3 (CD49c) on decidua macrophage in middle and mild and sever PIH are all obviously higher, (P<0.01, P<0.01, P<0.01). Compared to the control group, the expression of integrin αV (CD51) on decidual macrophage in middle and mild and sever PIH are all obviously higher, (P<0.01, P<0.01, P<0.01). the expression of selectin-L (CD62L) on decidual macrophage in middle and mild and sever PIH are all slightly higher than the control group, but no statistical significant difference (P>0.05). Compared to the control group, the expression of vascular cell adhesion molecule-1 VC...
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