Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.6.1 (
sulfatase
)
3,205
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID:Chondroitin sulfate degradation and eicosanoid metabolism pathways are impaired in focal segmental glomerulosclerosis: Experimental confirmation of an
in silico
prediction. 3133 40
