Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carotenoids, plant pigments with potent antioxidant activity, are implicated in chronic disease protection. They are absorbed from the diet and transported by plasma lipoproteins. Monocytes, as circulating blood cells, are exposed to carotenoid-rich lipoproteins. Such exposure may lead to enrichment with carotenoids and may affect the functions of monocyte-derived macrophages. This study explored the effect of cellular enrichment in vitro with beta-carotene, lycopene, or lutein on monocyte/macrophage function, using U937 cells as a model. Cell proliferation, production of reactive oxygen species, and cell-substrate adhesion were examined. Maximal carotenoid levels in medium supplemented with preenriched human serum were 2-8 mumol/L; incubation for 1-6 d resulted in 0.2-1.1 nmol carotenoid/mg cell protein (0.25-1 nmol/10(6) cells), approximately 10-fold more than that reported in normal tissue in vivo but within the range that might be anticipated with dietary supplementation. beta-Carotene, lycopene, and lutein markedly inhibited the proliferation of U937 cells, to an extent similar to or greater than that due to phorbol myristic acetate, a known differentiation/activation agent. Lycopene, but not beta-carotene or lutein, caused a significant increase in reactive oxygen species, indicating the induction of cell differentiation. Adhesion and LDL oxidation were unaffected. Thus, cellular carotenoids inhibit proliferation, and for lycopene at least, this may involve cell differentiation. The effectiveness of lycopene, a nonprovitamin A carotenoid, is consistent with a vitamin A-independent pathway modulating cell function.
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PMID:Carotenoids normally present in serum inhibit proliferation and induce differentiation of a human monocyte/macrophage cell line (U937). 1567 Dec 7

Vitiligo is a chronic disease characterized by macules devoid of melanin and identifiable melanocytes. Adhesion of melanocytes to the basement membrane by integrin CCN3 is mediated through collagen IV receptor DDR1. We hypothesize that genetic variants of the DDR1 gene are associated with the occurrence of vitiligo. To test this hypothesis, we genotyped 10 DDR1 tag single-nucleotide polymorphisms (SNPs) in 212 trios composed of an affected child and both parents. Associated markers were then genotyped in 134 independent, unrelated individuals with vitiligo and 134 unrelated controls. Allele T of tag SNP rs4618569 was associated with an increased risk for vitiligo in the family trios (P=0.002, odds ratio (OR)=5.27; 95% confidence interval (CI)=1.59-17.40), whereas allele C of tag SNP rs2267641 was associated with an increased risk for vitiligo in both family-based and case-control populations (P=0.01, OR=3.47; 95% CI=1.22-9.17; P=0.04, OR=6.00; 95% CI=1.73-52.33, respectively). The best evidence for association in the trios was obtained for a haplotype composed of risk alleles of markers rs4618569 and rs2267641 (P=0.0006). There was an age-dependent enrichment of rs4618569 T allele and rs2267641 C allele in early-onset affected individuals. In conclusion, we propose DDR1 as a susceptibility gene for vitiligo, possibly implicating a defective cell adhesion in vitiligo pathogenesis.
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PMID:Genetic variants of the DDR1 gene are associated with vitiligo in two independent Brazilian population samples. 2018 41