Bioimpacts. 2019;9(2): 89-95.
doi: 10.15171/bi.2019.12
PMID: 31334040
PMCID: PMC6637215
Scopus ID: 85067449429
WOSID: 000472051800003
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Original Research

Chondroitin sulfate degradation and eicosanoid metabolism pathways are impaired in focal segmental glomerulosclerosis: Experimental confirmation of an in silico prediction

Shiva Kalantari 1, Mohammad Naji 2, Mohsen Nafar 2 * ORCID logo, Hootan Yazdani-Kachooei 3, Nasrin Borumandnia 2, Mahmoud Parvin 4

1 Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Urology-Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Department of Biology, Faculty of Basic Sciences, Islamic Azad University, Science and Research Branch, Tehran, Iran
4 Department of Pathology, Shahid Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran


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.

Keywords: Biomarker, Chondroitin sulfate, Eicosanoid metabolism, Focal segmental glomerulosclerosis, Molecular pathway
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Submitted: 22 Oct 2018
Revision: 16 Dec 2018
Accepted: 22 Dec 2018
ePublished: 08 Mar 2019
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