Inflammation protein expression

McDuffie, E., et al. (2006) Detection of cytokine protein expression in mouse lung homogenates using suspension bead array. J Inflamm (Land). 3, 15. 

In line with expression of A3 adenosine receptors in cells and tissues like mast cells, spleen and thymus putative binding sites for a number of transcription factors relevant for protein expression in inflammation and infection were identified in the promoter region of the A3 receptor gene (Atkinson et al. 1997 Zhao et al. 1999). These include activator protein 1 (AP-1) which regulates gene expression in response to viral and bacterial infections or to stimulation by cytokines. Additional binding sites for transcription factors with specificity for immune cells are for the T cell-specific T cell factor F-2-a (TcF-2-a) and for the B cell-specific E2aECB. 

Biosynthesis of Ial and Pal starts from a-l-microglobulin/Bik precursor protein (AMBP) ( 43 63 kDa), consisting of three connected proteins (Bik, a-1-microglobulin, and a signal peptide) [8, 11, 12]. AMBP is an intracellular protein expressed constitutively and is generally suppressed during acute inflammation. Only trace amount of AMBP is found in blood or urine [13-15],... 

Site of therapeutic action (if different from plasma circulation) local protein expression and transport rates between the site and blood circulation (e.g., a target in brain will see very small fraction of injected dose due to poor mAb brain penetration, and synovial fluid may have higher concentration of a target inflammation factor than plasma in rheumatoid arthritis)... 

Heat shock proteins (HSPs) are a family of proteins expressed in almost all organisms from prokaryotes to humans. HSPs were originally described about four decades ago as proteins that were induced in the Drosophila melanogaster in response to a heat stress and hence derive the name HSR However, research over the years has uncovered these proteins to have a multitude of functions. Primarily, all HSPs act as molecular chaperons and assist in proper folding of naive proteins. Furthermore, HSPs have important roles in cellular processes including cell survival, inflammation, immunity, ion channel repair, and others. HSPs are also induced by a variety of stressors. Reactive oxygen species, cytotoxic injury, necrosis, ultraviolet radiation, metals, and many others are some examples. 

As in other organs, ABCBl is the best investigated transporter in the liver. It was demonstrated that turpentine-induced APR leads to a 50-70% reduction of ABCBl expression and function in rat liver tissue 48 h after treatment [103]. Similar results were observed in studies of endotoxin-triggered inflammation in which both constitutive and induced expression were affected in rodents [104]. Further experiments have shown that reduction of ABCBl expression is also linked to a reduction in ABCBl function. In two distinct experimental setups, Shiga-toxin II and endotoxin administration to rats prompted a substantial reduction in ABCBl function (assessed by hepatobiliary doxorubicin and "TC-sestamibi clearance), accompanied by a significant reduction in ABCBl protein expression [69, 105]. Likewise, endotoxin-treated mice displayed decreased liver-mediated doxorubcin clearance as a result of... 

Nackley AG, Makriyannis A, Hohmann AG (2003) Selective activation of cannabinoid CB(2) receptors suppresses spinal fos protein expression and pain behavior in a rat model of inflammation. Neuroscience 119 747-757... 

Expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) is known to be elevated at sites of inflammation. Studies have been conducted into the effects of EGCG and TF-3 on the expression of these adhesion molecules induced by interleukin-ip (IL-lp) in cultured human umbilical vein endothelial cells (HUVECs). Both compounds significantly inhibited IL-ip-induced protein expression of VCAM and ICAM in dose-dependent manners and were associated with reduced adhesion of leukocytes to HUVECs. The m-RNA level of VCAM-1 was also inhibited by these tea polyphenolics, as was the NF-KB-dependent transcriptional activity induced by IL-lp. It is concluded that these molecules exhibit anti-inflammatory and anti-invasion properties, probably via a route involving blockage of IkB kinase. 

During infection and inflammation, the expression of CYP450 and its dependent biotransformation are also modified at the pre-translational steps in protein synthesis [9]. 

AD. Also, they found increases in transcript levels of 19 genes involved in proapoptotic activities and inflammation, also consistent with AD pathology. Interpretation and integration of such data with that obtained from proteomic experiments is presently difficult as specific changes in transcripts and protein levels are not seen in many consistent sets of proteins/genes. Also, expression levels (mRNA/protein) seen in normal versus diseased experiments can be due to secondary effects and not central to the pathogenesis. However, consolidation of mRNA/protein expression data for a particular disease in a database, may uncover common disturbances in pathways relevant to the actual pathology and not due to secondary effects. 

Tripp RA, Moore D, Winter J et al. Respiratory syncytial virus infection and G and/or SH protein expression contribute to substance P, which mediates inflammation and enhanced pulmonary disease in BALB/c mice. J Virol 2000 74(4) l6l4 22. 

Whereas most of these chemokines and their receptors are functional on cells of the immune system, it has become clear that the expression of these proteins is not restricted to immune cells. Under the influence of proinflammatory cytokines, such as IL-ip, TNF-a and IFNy, that are released during inflammation, many cell types are able to produce chemokines or upregulate receptor expression. Some representative cell types include endothelial cells, smooth muscle cells, tumor cells, and cells of the central nervous system (CNS)—specifically astrocytes, microglia, and neurons. Endothelial cells under the appropriate stimuli are able to upregulate chemokine expression to attract cells from the periphery to sites of inflammation. Once attracted to a site of inflammation the immune cells express a number of counter molecules for attachment to adhesion proteins expressed on the surface of endothelium. This... 

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