Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression is abnormally regulated in multiple myeloma (MM) owing to imbalanced expression of the acute myeloid leukemia-1A (AML-1A) and AML-1B transcription factors. We hypothesized that the increased expression ratios of AML-1A to AML-1B also induced abnormal expression of other hematopoietic and bone-specific genes that contribute to the poor prognosis of MM patients with high levels of MIP-1 alpha. We found that interleukin-3 (IL-3) was also induced by the imbalanced AML-1A and AML-1B expression in myeloma. IL-3 mRNA levels were increased in CD138+ purified myeloma cells with increased AML-1A-to-AML-1B expression from MM patients, and IL-3 protein levels were significantly increased in freshly isolated bone marrow plasma from MM patients (66.4 +/- 12 versus 22.1 +/- 8.2 pg/mL; P = .038). IL-3 in combination with MIP-1 alpha or receptor activator of nuclear factor-kappa B ligand (RANKL) significantly enhanced human osteoclast (OCL) formation and bone resorption compared with MIP-1 alpha or RANKL alone. IL-3 stimulated the growth of interleukin-6 (IL-6)-dependent and IL-6-independent myeloma cells in the absence of IL-6, even though IL-3 did not induce IL-6 expression by myeloma cells. These data suggest that increased IL-3 levels in the bone marrow microenvironment of MM patients with imbalanced AML-1A and AML-1B expression can increase bone destruction and tumor cell growth.
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PMID:IL-3 expression by myeloma cells increases both osteoclast formation and growth of myeloma cells. 1461 78

The purpose of this study was to examine changes in serum cytokines after repeated bouts of aerobically biased eccentric exercise. Six untrained males ran down a -13.5% treadmill grade for 60 min on two occasions (RUN1 and RUN2) at a speed equal to 75% of their VO2 peak on a level grade; runs were spaced 14 d apart. Serum was collected before, after, and every hour for 12 h, and every 24 h for 6 d. Cytokines were assessed using 17 multiplex bead technology (Bio-Rad). Creatine kinase (CK) and delayed-onset muscle soreness (DOMS) were assessed before and 24-120 h after. Results were analyzed using a repeated measures analysis of variance (p <or= 0.05). All comparisons were between RUN1 and RUN2. CK and DOMS were significantly elevated after RUN1 compared with RUN2, indicative of a repeated bout effect. Regarding cytokines, during the initial 12 h period after RUN2, there was a 50% decrease in pro-inflammatory interleukin-6 (IL-6), a 10% decrease in pro-inflammatory macrophage chemotactic protein-1, and a 95% elevation in anti-inflammatory interleukin-10 (IL-10). Regarding 24 h periods, after RUN2 there was an 8% reduction in pro-inflammatory interleukin-8 (IL-8). However, pro-inflammatory macrophage inflammatory factor-1beta (MIF-1beta) was 18% higher during the 12 h after RUN2. The overall cytokine profile suggests a slight reduction in systemic inflammation after RUN2.
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PMID:Changes in serum cytokines after repeated bouts of downhill running. 1748 64