Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophoresis and isoelectrofocusing were used to study polymorphism by 7 genetic loci: haptoglobin (Hp), proteinase inhibitor (PI), transferrin (TF), Vitamin D-transporting protein (GC), complement 3 (C3), phosphoglucomutase 1 (PGM1) and glyoxalase (GLO1) in 60 patients with silicosis and in 70 apparently healthy workers of the Dynamo plant. Comparison of the study groups by significant differences in the summary of the genetic information obtained suggests that 5 (Hp, C3, TF, PI, PGM1) of the 7 studied systems showed the hereditary features of silicosis. The gene carriers Hp*2, C3*F, PGM1*2-, PI*M1, TF*C1, TF*C16 TF*D, GC*R due to peculiar biochemical processes appear to have less adaptive potentialities and a greater likelihood of the disease on exposure to industrial factors.
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PMID:[Genetic aspects of silicosis: polymorphic gene distribution frequency]. 966 90

Glyoxalase I (Glo1) is the main scavenging enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs). AGEs are known to control multiple biological processes, including epithelial to mesenchymal transition (EMT), a multistep phenomenon associated with cell transformation, playing a major role in a variety of diseases, including cancer. Crystalline silica is a well-known occupational health hazard, responsible for a great number of human pulmonary diseases, such as silicosis. There is still much debate concerning the carcinogenic role of crystalline silica, mainly due to the lack of a causal demonstration between silica exposure and carcinogenesis. It has been suggested that EMT might play a role in crystalline silica-induced lung neoplastic transformation. The aim of this study was to investigate whether, and by means of which mechanism, the antiglycation defence Glo1 is involved in Min-U-Sil 5 (MS5) crystalline silica-induced EMT in BEAS-2B human bronchial epithelial cells chronically exposed, and whether this is associated with the beginning of a neoplastic-like transformation process. By using gene silencing/overexpression and scavenging/inhibitory agents, we demonstrated that MS5 induced hydrogen peroxide-mediated c-Jun-dependent Glo1 up-regulation which resulted in a decrease in the Argpyrimidine-modified Hsp70 protein level which triggered EMT in a novel mechanism involving miR-21 and SMAD signalling. The observed EMT was associated with a neoplastic-like phenotype. The results obtained provide a causal in vitro demonstration of the MS5 pro-carcinogenic transforming role and more importantly they provide new insights into the mechanisms involved in this process, thus opening new paths in research concerning the in vivo study of the carcinogenic potential of crystalline silica.
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PMID:Glyoxalase I drives epithelial-to-mesenchymal transition via argpyrimidine-modified Hsp70, miR-21 and SMAD signalling in human bronchial cells BEAS-2B chronically exposed to crystalline silica Min-U-Sil 5: Transformation into a neoplastic-like phenotype. 2678 15