Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.6.1 (sulfatase)
 3,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known that prostaglandin (PG)E2 and PGI2 can contribute to the ripening of the uterine cervix. To study the PG biosynthesis in cervical tissue, 14C-arachidonic acid was used to incubate the preparation of human cervical tissue obtained from pregnant women at delivery and non pregnant women at hysterectomy. Labeled PGE2 and 6-keto-PGF1 alpha (6PG), a stable metabolite of PGI2 were isolated on TLC, and the enzymatic activity was calculated from the formation of PGE2 and 6PG from arachidonic acid. The capacity to metabolize arachidonic acid to PGE2 and 6PG in cervical tissue obtained from pregnant women was 6 times higher than that from non pregnant women. Low enzymatic activity in the formation of PGE2 and 6PG were observed in cervical tissues from the patients with placental sulfatase deficiency and preterm delivery which were known to have a low estrogen environment. On the other hand, DHA-S administration to patients increased the formation of both PGE2 and 6PG. These results demonstrate that human cervical tissue possesses the ability to synthesize PGE2 and PGI2, and enzymatic activity increased during pregnancy, and was further enhanced by the administration of DHA-S. The results suggest that the steroids in the fetoplacental unit may be involved in the mechanism controlling the formation of PGs in the cervical tissue which lead the cervix to ripen at term.
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PMID:[Biosynthesis of prostaglandin in human cervical tissue]. 331 40

Introduction: Focal segmental glomerulosclerosis (FSGS), the most common primary glomerular disease, is a diverse clinical entity that occurs after podocyte injury. Although numerous studies have suggested molecular pathways responsible for the development of FSGS, many still remain unknown about its pathogenic mechanisms. Two important pathways were predicted as candidates for the pathogenesis of FSGS in our previous in silico analysis, whom we aim to confirm experimentally in the present study. Methods: The expression levels of 4 enzyme genes that are representative of "chondroitin sulfate degradation" and "eicosanoid metabolism" pathways were investigated in the urinary sediments of biopsy-proven FSGS patients and healthy subjects using real-time polymerase chain reaction (RT-PCR). These target genes were arylsulfatase, hexosaminidase, cyclooxygenase-2 (COX-2), and prostaglandin I2 synthase. The patients were sub-divided into 2 groups based on the range of proteinuria and glomerular filtration rate and were compared for variation in the expression of target genes. Correlation of target genes with clinical and pathological characteristics of the disease was calculated and receiver operating characteristic (ROC) analysis was performed. Results: A combined panel of arylsulfatase, hexosaminidase, and COX-2 improved the diagnosis of FSGS by 76%. Hexosaminidase was correlated with the level of proteinuria, while COX-2 was correlated with interstitial inflammation and serum creatinine level in the disease group. Conclusion: Our data supported the implication of these target genes and pathways in the pathogenesis of FSGS. In addition, these genes can be considered as non-invasive biomarkers for FSGS.
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PMID:Chondroitin sulfate degradation and eicosanoid metabolism pathways are impaired in focal segmental glomerulosclerosis: Experimental confirmation of an in silico prediction. 3133 40