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MicroRNAs as a therapeutic target in IgA nephropathy in Indian population

Immunoglobulin A nephropathy (IgAN) is the most frequent glomerular disease with rapid development to end stage renal disease, requiring renal replacement therapy. Genome-wide studies suggest geographical variations in genetic susceptibility to IgAN and disease progression. Specific ‘candidate genes...

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Autores principales: Tripathy, Anindita, Yedla, Poornachandra, Vishnubhotla, Ravikanth V, Sekaran, Anuradha, Keithi Reddy, Sai Ram
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10119669/
https://www.ncbi.nlm.nih.gov/pubmed/37089577
http://dx.doi.org/10.3892/br.2023.1617
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author Tripathy, Anindita
Yedla, Poornachandra
Vishnubhotla, Ravikanth V
Sekaran, Anuradha
Keithi Reddy, Sai Ram
author_facet Tripathy, Anindita
Yedla, Poornachandra
Vishnubhotla, Ravikanth V
Sekaran, Anuradha
Keithi Reddy, Sai Ram
author_sort Tripathy, Anindita
collection PubMed
description Immunoglobulin A nephropathy (IgAN) is the most frequent glomerular disease with rapid development to end stage renal disease, requiring renal replacement therapy. Genome-wide studies suggest geographical variations in genetic susceptibility to IgAN and disease progression. Specific ‘candidate genes’ were indicated to correlate with different functions that are involved in the pathogenesis of renal conditions. MicroRNAs (miRNAs/miRs) have a major role in mRNA degradation or translation repression, thereby regulating the expression of their target proteins. Previously, a small number of miRNAs were reported to have direct associations with IgAN. In the present study, new miRNAs linked to IgAN were identified in the Indian population. The miRNA was isolated from kidney biopsies of patients with IgAN (n=6) and healthy control tissue from patients with renal cell carcinoma (n=6). The sequencing results indicated that the miRNA percentage acquired from controls and patients with IgAN was 5.61 and 4.35%, respectively. From the results, 10 upregulated and 15 downregulated miRNAs were identified. Of the 25 differentially expressed miRNAs (DEMs), miR-181a-5p, miR-28-3p, let-7g-5p, miR-92a-3p and miR-30c-5p were not reported previously. Furthermore, Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses suggested that the target genes of the DEMs were mainly enriched in pathways such as cancer, ErbB signalling, proteoglycans in cancer, Hippo signalling and MAPK pathways. The newly identified miRNAs may impact the behaviour of tissues or IgA deposition by regulating signalling pathways, which forms a basis for future studies aimed at improving the diagnosis and care of patients with IgAN in the Indian community.
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spelling pubmed-101196692023-04-22 MicroRNAs as a therapeutic target in IgA nephropathy in Indian population Tripathy, Anindita Yedla, Poornachandra Vishnubhotla, Ravikanth V Sekaran, Anuradha Keithi Reddy, Sai Ram Biomed Rep Articles Immunoglobulin A nephropathy (IgAN) is the most frequent glomerular disease with rapid development to end stage renal disease, requiring renal replacement therapy. Genome-wide studies suggest geographical variations in genetic susceptibility to IgAN and disease progression. Specific ‘candidate genes’ were indicated to correlate with different functions that are involved in the pathogenesis of renal conditions. MicroRNAs (miRNAs/miRs) have a major role in mRNA degradation or translation repression, thereby regulating the expression of their target proteins. Previously, a small number of miRNAs were reported to have direct associations with IgAN. In the present study, new miRNAs linked to IgAN were identified in the Indian population. The miRNA was isolated from kidney biopsies of patients with IgAN (n=6) and healthy control tissue from patients with renal cell carcinoma (n=6). The sequencing results indicated that the miRNA percentage acquired from controls and patients with IgAN was 5.61 and 4.35%, respectively. From the results, 10 upregulated and 15 downregulated miRNAs were identified. Of the 25 differentially expressed miRNAs (DEMs), miR-181a-5p, miR-28-3p, let-7g-5p, miR-92a-3p and miR-30c-5p were not reported previously. Furthermore, Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyses suggested that the target genes of the DEMs were mainly enriched in pathways such as cancer, ErbB signalling, proteoglycans in cancer, Hippo signalling and MAPK pathways. The newly identified miRNAs may impact the behaviour of tissues or IgA deposition by regulating signalling pathways, which forms a basis for future studies aimed at improving the diagnosis and care of patients with IgAN in the Indian community. D.A. Spandidos 2023-04-04 /pmc/articles/PMC10119669/ /pubmed/37089577 http://dx.doi.org/10.3892/br.2023.1617 Text en Copyright: © Tripathy et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Tripathy, Anindita
Yedla, Poornachandra
Vishnubhotla, Ravikanth V
Sekaran, Anuradha
Keithi Reddy, Sai Ram
MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title_full MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title_fullStr MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title_full_unstemmed MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title_short MicroRNAs as a therapeutic target in IgA nephropathy in Indian population
title_sort micrornas as a therapeutic target in iga nephropathy in indian population
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10119669/
https://www.ncbi.nlm.nih.gov/pubmed/37089577
http://dx.doi.org/10.3892/br.2023.1617
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