|
|
- ADIPOQ (adiponectin, C1Q and collagen domain containing)
[ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1, GBP28, adiponectin]
Total and high-molecular weight (HMW) adiponectin are correlated with markers of insulin secretion and insulinemia, endothelial function, and inflammation (Fargnoli et al., 2010).
HMW adiponectin has been found to contribute to the renal inflammation of systemic lupus erythematosus (SLE) (Song et al., 2009).
High-grade inflammation was found to be negatively correlated with circulating adiponectin concentrations (Gonzalez-Gay et al., 2008). Low adiponectin levels were found to be clustered with metabolic syndrome features associated with atherogenesis in rheumatoid arthritis (RA). Circulating adiponectin is linked to cardiovascular disease in RA.
In patients undergoing percutaneous coronary intervention (PCI), the persistence of a low adiponectin (APO) plasma level at discharge and 6 months afterwards have been suggested to be used as a clinical marker for in-stent restenosis (ISR) prediction (Moldoveanu et al., 2008).
Adiponectin level and markers of low-grade inflammation are associated with insulin sensitivity (Saltevo et al., 2008). Adiponectin and interleukin-1 receptor antagonist (IL-1 Ra) levels have been suggested to be better markers for the risk of obesity and type 2 diabetes than high-sensitivity C-reactive protein (hs-CRP).
The secreted liver protein fetuin-A causes low-grade inflammation and inhibits adiponectin production in animals and in humans (Hennige et al., 2008). Fatty liver plays an important role in the pathophysiology of insulin resistance and atherosclerosis.
In patients with chronic hepatitis C virus (HCV), adiponectin was linked to steatosis only in males and was increased with inflammation (Jonsson et al., 2005). The expression of adiponectin in chronic liver diseases may be related to gender and etiology.
Related diseases:
insulinemia, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), obesity, type 2 diabetes, fatty liver, atherosclerosis, hepatitis C virus (HCV)
References:
Fargnoli, J. L., Sun, Q., et al. Resistin is associated with biomarkers of inflammation while total and high-molecular weight adiponectin are associated with biomarkers of inflammation, insulin resistance, and endothelial function. Eur J Endocrinol 162, 281-288.
Gonzalez-Gay, M. A., Llorca, J., et al. (2008) High-grade inflammation, circulating adiponectin concentrations and cardiovascular risk factors in severe rheumatoid arthritis. Clin Exp Rheumatol 26, 596-603.
Hennige, A. M., Staiger, H., et al. (2008) Fetuin-A induces cytokine expression and suppresses adiponectin production. PLoS One 3, e1765.
Jonsson, J. R., Moschen, A. R., et al. (2005) Adiponectin and its receptors in patients with chronic hepatitis C. J Hepatol 43, 929-936.
Moldoveanu, E., Mut-Vitcu, B., et al. (2008) Low basal levels of circulating adiponectin in patients undergoing coronary stenting predict in-stent restenosis, independently of basal levels of inflammatory markers: lipoprotein associated phospholipase A2, and myeloperoxidase. Clin Biochem 41, 1429-1433.
Saltevo, J., Laakso, M., et al. (2008) Levels of adiponectin, C-reactive protein and interleukin-1 receptor antagonist are associated with insulin sensitivity: a population-based study. Diabetes Metab Res Rev 24, 378-383.
Song, H., Chan, J., et al. (2009) Induction of chemokine expression by adiponectin in vitro is isoform dependent. Transl Res 154, 18-26.
- ADAMTS13 (ADAM metallopeptidase with thrombospondin type 1 motif, 13)
[C9orf8, DKFZp434C2322, FLJ42993, MGC118899, MGC118900, TTP, VWFCP, vWF-CP]
ADAMTS13 activity was found to decline with the extent of inflammatory responses (Bockmeyer et al., 2008). Systemic inflammation results in the deficiency of ADAMTS13, and such effect activates hemostasis. Thrombotic microangiopathy (TMA) is one of the sequelae of sepsis. The ratio of Von Willebrand factor (VWF) antigen level and ADAMTS13 activity was found higher in patients with inflammation and sepsis (Claus et al., 2009). ADAMTS13, VWF and related parameters, even combined, can be used for the diagnosis and the therapeutic monitoring of patients with sepsis associated TMA.
Related diseases: Thrombotic microangiopathy (TMA), sepsis
References:
Bockmeyer, C. L., Claus, R. A., et al. (2008) Inflammation-associated ADAMTS13 deficiency promotes formation of ultra-large von Willebrand factor. Haematologica 93, 137-140.
Claus, R. A., Bockmeyer, C. L., et al. (2009) Variations in the ratio between von Willebrand factor and its cleaving protease during systemic inflammation and association with severity and prognosis of organ failure. Thromb Haemost 101, 239-247.
- ADAR (adenosine deaminase, RNA-specific)
[RP11-61L14.5, ADAR1, DRADA, DSH, DSRAD, G1P1, IFI-4, IFI4, K88dsRBP, p136]
ADAR1 variants (e.g., p150, p80, and p110) are differentially regulated during acute inflammation (Yang et al., 2003). Upon inflammatory stimulation, the localization of these variants and adenosine-to-inosine (A-to-I) editing in the cytoplasm, nucleus, and nucleolus are intracellularly reorganized.
Reference:
Yang, J. H., Nie, Y., et al. (2003) Intracellular localization of differentially regulated RNA-specific adenosine deaminase isoforms in inflammation. J Biol Chem 278, 45833-45842.
- ADCYAP1 (adenylate cyclase activating polypeptide 1 (pituitary))
[MGC126852, PACAP]
In chronic pancreatitis (CP), responsiveness of peripheral blood mononuclear cells (PBMC) to the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is changed, from inhibiting TNF-alpha to decreasing IL-1beta and increasing IL-10 secretion (Michalski et al., 2008). Such change of PACAP-mediated anti-inflammatory pattern was related to altered activation of NF-kappaB, as NF-kappaB was decreased in donor PBMC. The ability of PBMC to generate and to respond to PACAP may influence neuroimmune interactions that affect pain and inflammation in CP.
Related disease: chronic pancreatitis (CP)
Reference:
Michalski, C. W., Selvaggi, F., et al. (2008) Altered anti-inflammatory response of mononuclear cells to neuropeptide PACAP is associated with deregulation of NF-{kappa}B in chronic pancreatitis. Am J Physiol Gastrointest Liver Physiol 294, G50-57.
- ADA (adenosine deaminase)
Adenosine elimination on human airway epithelia is mediated by proteins including adenosine deaminase 1 (ADA1), concentrative nucleoside transporter (CNT)2, and CNT3 (Hirsh et al., 2007). These proteins are important regulators of adenosine-mediated inflammation. The study of pediatric patients with chronic hypoxia having cardiac surgery showed significant elevation in plasma adenosine deaminase (ADA) activity compared with controls (Eltzschig et al., 2006). In acute hypoxia associated with vascular leakage and excessive inflammation, the inhibition of ADA can be used as a potential therapeutic strategy. Familial Mediterranean Fever (FMF) is a systemic autoinflammatory disorder. ADA can be used as a marker to differentiate FMF attacks from attack-free periods. FMF patients with acute attacks had higher serum levels of ADA than attack-free periods and healthy controls (Kisacik et al., 2009).
Related diseases: chronic and acute hypoxia, Familial Mediterranean Fever
References:
Eltzschig, H. K., Faigle, M., et al. (2006) Endothelial catabolism of extracellular adenosine during hypoxia: the role of surface adenosine deaminase and CD26. Blood 108, 1602-1610.
Hirsh, A. J., Stonebraker, J. R., et al. (2007) Adenosine deaminase 1 and concentrative nucleoside transporters 2 and 3 regulate adenosine on the apical surface of human airway epithelia: implications for inflammatory lung diseases. Biochemistry 46, 10373-10383.
Kisacik, B., Akdogan, A., et al. (2009) Serum adenosine deaminase activities during acute attacks and attack-free periods of familial Mediterranean fever. Eur J Intern Med 20, 44-47.
- ADAM33 (ADAM metallopeptidase domain 33)
[RP5-964F7.2, C20orf153, DJ964F7.1, DKFZp434K0521, FLJ35308, FLJ36751, MGC149823, MGC71889]
Th2 cytokines IL-4 and IL-13 can up-regulate the mRNA expression of ADAM33 in human fibroblasts (Jie et al., 2009). ADAM33 may be involved in the development of airway remodeling in allergen-induced chronic airway inflammation.
Reference:
Jie, Z., Jin, M., et al. (2009) The effects of Th2 cytokines on the expression of ADAM33 in allergen-induced chronic airway inflammation. Respir Physiol Neurobiol 168, 289-294.
- ADAMTS10 (ADAM metallopeptidase with thrombospondin type 1 motif, 10)
[ADAM-TS10, WMS]
This gene is a member of the ADAMTS (a disintegrin and metalloproteinase domain with thrombospondin type-1 motifs) family of zinc-dependent proteases. ADAMTS plays important roles in inflammation, connective tissue organization, coagulation, arthritis, angiogenesis and cell migration (RefSeq, 2010).
|
|
