Anti-HSPD1 (internal region) Monoclonal Antibody, clone FQ2007Z

We identified increased expression and redistribution of the intracellular protein 60-kDa human heat shock protein (hHSP60) (HSPD1) to the cell surface in human endothelial cells subjected to classical atherosclerosis risk factors and subsequent immunologic cross-reactivity against this highly conserved molecule, as key events occurring early in the process of atherosclerosis. The present study aimed at investigating the role of infectious pathogens as stress factors for vascular endothelial cells and, as such, contributors to early atherosclerotic lesion formation. Using primary donor-matched arterial and venous human endothelial cells, we show that infection with Chlamydia pneumoniae leads to marked upregulation and surface expression of hHSP60 and adhesion molecules. Moreover, we provide evidence for an increased susceptibility of arterial endothelial cells for redistribution of hHSP60 to the cellular membrane in response to C. pneumoniae infection as compared to autologous venous endothelial cells. We also show that oxidative stress has a central role to play in endothelial cell activation in response to chlamydial infection. These data provide evidence for a role of C. pneumoniae as a potent primary endothelial stressor for arterial endothelial cells leading to enrichment of hHSP60 on the cellular membrane and, as such, a potential initiator of atherosclerosis.

MiR-206 acts as a potential tumor suppressor during carcinogenesis and a regulatory factor in osteoblasts differentiation, but its modulatory mechanism remains unclear. In this study, we used a quantitative proteomics method, difference gel electrophoresis (DIGE), to profile the protein variation in A549 lung cancer cells with and without miR-206 transfection. We identified a total of 17 differently expressed proteins including 5 up-regulated and 12 down-regulated proteins affected by miR-206 in A549 cells. We further constructed a protein network linked 17 differently expressed proteins with 106 computationally predicted miR-206 targets, and identified 8 "hub" genes (CALR, CTSD, ENO1, HSPA5, CDC42, HSPD1, POLA1, and SMARCA4) within the network, which may represent important miR-206 functional gene targets. In conclusion, in this study, we identified several candidate functional target genes for miR-206, which is helpful to further explore its mechanisms during carcinogenesis and osteogenesis, and we also proposed a novel proteomic strategy to identify functionally important gene targets for microRNA.