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BioImpacts. 2022;12(2): 89-105.
doi: 10.34172/bi.2022.23467
PMID: 35411297
PMCID: PMC8905584
Scopus ID: 85127154960
  Abstract View: 1015
  PDF Download: 969
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Original Research

To detect potential pathways and target genes in infantile Pompe patients using computational analysis

Aynur Karadağ Gürel 1* ORCID logo, Selçuk Gürel 2 ORCID logo

1 Department of Medical Biology, School of Medicine, Usak University, Usak, Turkey
2 Department of Pediatrics, School of Medicine, Bahcesehir University, İstanbul, Turkey
*Corresponding Author: Email: aynur.karadag@usak.edu.tr

Abstract

Introduction: Pompe disease (PD) is a disease caused by pathogenic variations in the GAA gene known as glycogen storage disease type II, characterized by heart hypertrophy, respiratory failure, and muscle hypotonia, leading to premature death if not treated early. The only treatment option, enzyme replacement therapy (ERT), significantly improves the prognosis for some patients while failing to help others. In this study, the determination of key genes involved in the response to ERT and potential molecular mechanisms were investigated.
Methods: Gene Expression Omnibus (GEO) data, accession number GSE38680, containing samples of biceps and quadriceps muscles was used. Expression array data were analyzed using BRB-Array Tools. Biceps group patients did not receive ERT, while quadriceps received treatment with rhGAA at 0, 12, and 52 weeks. Differentially expressed genes (DEGs) were deeply analyzed by DAVID, GO, KEGG and STRING online analyses, respectively.
Results: A total of 1727 genes in the biceps group and 1198 genes in the quadriceps group are expressed differently. It was observed that DEGs were enriched in the group that responded poorly to ERT in the 52nd week. Genes frequently changed in the weak response group; the expression of 530 genes increased and 1245 genes decreased compared to 0 and 12 weeks. The GO analysis demonstrated that the DEGs were mainly involved in vascular smooth muscle contraction, lysosomes, autophagy, regulation of actin cytoskeleton, inflammatory response, and the WNT signaling pathway. We also discovered that the WNT signaling pathway is highly correlated with DEGs. Several DEGs, such as WNT11, WNT5A, CTNNB1, M6PR, MYL12A, VCL, TLN, FYN, YES1, and BCL2, may be important in elucidating the mechanisms underlying poor response to ERT.
Conclusion: Early diagnosis and treatment of PD are very important for the clinic of the disease. As a result, it suggests that the enriched genes and new pathways emerging as a result of the analysis may help identify the group that responds poorly to treatment and the outcome of the treatment. Obtained genes and pathways in neonatal screening will guide diagnosis and treatment.


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Submitted: 20 Oct 2020
Revision: 08 Feb 2021
Accepted: 13 Feb 2021
ePublished: 22 Jan 2022
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