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It has been shown that atherogenesis is a chronic infectious process involving various kinds of immune cells caused by endothelial cell injuries. The adhesion process which promotes inflammatory reactions is mediated by adhesion molecules among injured intima and activated leukocytes, platelets and endothelial cells. Integrin β2 is specifically expressed on surface of leukocytes, including αDβ2, αLβ2, αMβ2 and αXβ2. Abnormalities of human integrin β2 gene (ITGB2) expressions could cause changes in adhesion depended processes, such as chemotaxis, phagocytosis and aggregation. This study aimed to detect and compare the expression intensity of integrin β2 and its related genes among acute myocardial infarction (AMI) patients, stable angina pectoris (SA) patients as well as healthy people, and analyze the gene expression characteristics of integrin β2 on the surface of leukocytes in different phases.
20 patients with AMI were enrolled into AMI group. Another 20 SA patients (18 males and 2 females, average age: 64±10 yrs) were recruited into SA group. There were no significant differences of age, gender, smoke, body mass index, systolic blood pressure, diastolic blood pressure, low density lipoprotein, high density lipoprotein and triglyceride among three groups (P>0.05).
A total of 76 genes associated with integrin β2 were detected. The mRNA expressions in three groups are shown as follows. Compared with controls, mRNA expressions of α/β subunit (ITGAD, ITGAL, ITGAM, ITGAX and ITGB2), ligands of integrin β2 (RAGE, JAM-1, Fibrinogen, ICAM-1, ICAM-3, ICAM-5 and uPAR), chemokine (fMLP and RAF), inside-out signaling pathway (RIAM, ADAP, SLP-76, PLCγ, RAPL, SPA1, α-actinin, calpain, Dok1, radixin, talin and 14-3-3ζ) andoutside-in signaling pathway (Fgr, Hck, Lyn, PKC, c-ab1, Syk, Vav1/3, cdc42, mDia, Rac, RhoA and ROCK1/2) in AMI patients were significantly upregulated. However there was no significant difference of gen expressions of integrin β2 and its signaling pathway in SA patients compared to control group.
Taken together, the inside-out signaling pathway of integrin β2 is inhibited while the outside-in signaling pathway activated in AMI patients, suggesting that activation of integrin β2 in AMI patients might be caused by extracellular factors.