Next-generation sequencing profiling of miRNAs in individuals with 22q11.2 deletion syndrome revealed altered expression of miR-185-5p.


Journal

Human genomics
ISSN: 1479-7364
Titre abrégé: Hum Genomics
Pays: England
ID NLM: 101202210

Informations de publication

Date de publication:
13 Jun 2024
Historique:
received: 16 10 2023
accepted: 25 05 2024
medline: 14 6 2024
pubmed: 14 6 2024
entrez: 13 6 2024
Statut: epublish

Résumé

The 22q11.2 deletion syndrome (22q11.2DS) is a microdeletion syndrome with highly variable phenotypic manifestations, even though most patients present the typical 3 Mb microdeletion, usually affecting the same ~ 106 genes. One of the genes affected by this deletion is DGCR8, which plays a crucial role in miRNA biogenesis. Therefore, the haploinsufficiency of DGCR8 due to this microdeletion can alter the modulation of the expression of several miRNAs involved in a range of biological processes. In this study, we used next-generation sequencing to evaluate the miRNAs profiles in the peripheral blood of 12 individuals with typical 22q11DS compared to 12 healthy matched controls. We used the DESeq2 package for differential gene expression analysis and the DIANA-miTED dataset to verify the expression of differentially expressed miRNAs in other tissues. We used miRWalk to predict the target genes of differentially expressed miRNAs. Here, we described two differentially expressed miRNAs in patients compared to controls: hsa-miR-1304-3p, located outside the 22q11.2 region, upregulated in patients, and hsa-miR-185-5p, located in the 22q11.2 region, which showed downregulation. Expression of miR-185-5p is observed in tissues frequently affected in patients with 22q11DS, and previous studies have reported its downregulation in individuals with 22q11DS. hsa-miR-1304-3p has low expression in blood and, thus, needs more validation, though using a sensitive technology allowed us to identify differences in expression between patients and controls. Thus, lower expression of miR-185-5p can be related to the 22q11.2 deletion and DGCR8 haploinsufficiency, leading to phenotypic consequences in 22q11.2DS patients, while higher expression of hsa-miR-1304-3p might be related to individual genomic variances due to the heterogeneous background of the Brazilian population.

Sections du résumé

BACKGROUND BACKGROUND
The 22q11.2 deletion syndrome (22q11.2DS) is a microdeletion syndrome with highly variable phenotypic manifestations, even though most patients present the typical 3 Mb microdeletion, usually affecting the same ~ 106 genes. One of the genes affected by this deletion is DGCR8, which plays a crucial role in miRNA biogenesis. Therefore, the haploinsufficiency of DGCR8 due to this microdeletion can alter the modulation of the expression of several miRNAs involved in a range of biological processes.
RESULTS RESULTS
In this study, we used next-generation sequencing to evaluate the miRNAs profiles in the peripheral blood of 12 individuals with typical 22q11DS compared to 12 healthy matched controls. We used the DESeq2 package for differential gene expression analysis and the DIANA-miTED dataset to verify the expression of differentially expressed miRNAs in other tissues. We used miRWalk to predict the target genes of differentially expressed miRNAs. Here, we described two differentially expressed miRNAs in patients compared to controls: hsa-miR-1304-3p, located outside the 22q11.2 region, upregulated in patients, and hsa-miR-185-5p, located in the 22q11.2 region, which showed downregulation. Expression of miR-185-5p is observed in tissues frequently affected in patients with 22q11DS, and previous studies have reported its downregulation in individuals with 22q11DS. hsa-miR-1304-3p has low expression in blood and, thus, needs more validation, though using a sensitive technology allowed us to identify differences in expression between patients and controls.
CONCLUSIONS CONCLUSIONS
Thus, lower expression of miR-185-5p can be related to the 22q11.2 deletion and DGCR8 haploinsufficiency, leading to phenotypic consequences in 22q11.2DS patients, while higher expression of hsa-miR-1304-3p might be related to individual genomic variances due to the heterogeneous background of the Brazilian population.

Identifiants

pubmed: 38872198
doi: 10.1186/s40246-024-00625-5
pii: 10.1186/s40246-024-00625-5
doi:

Substances chimiques

MicroRNAs 0
MIRN185 microRNA, human 0
DGCR8 protein, human 0
RNA-Binding Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

64

Subventions

Organisme : Fundação de Amparo à Pesquisa do Estado de São Paulo
ID : #2019/21644-0

Informations de copyright

© 2024. The Author(s).

Références

McDonald-McGinn DM, Sullivan KE, Marino B, Philip N, Swillen A, Vorstman JAS, et al. 22q11.2 deletion syndrome. Nat Rev Dis Primers. 2015;1(1):15071.
pubmed: 27189754 pmcid: 4900471 doi: 10.1038/nrdp.2015.71
Grati FR, Molina Gomes D, Ferreira JCPB, Dupont C, Alesi V, Gouas L, et al. Prevalence of recurrent pathogenic microdeletions and microduplications in over 9500 pregnancies. Prenat Diagn. 2015;35(8):801–9.
pubmed: 25962607 doi: 10.1002/pd.4613
Shaikh TH, Kurahashi H, Saitta SC, O’Hare AM, Hu P, Roe BA, et al. Chromosome 22-specific low copy repeats and the 22q11.2 deletion syndrome: genomic organization and deletion endpoint analysis. Hum Mol Genet. 2000;9(4):489–501.
pubmed: 10699172 doi: 10.1093/hmg/9.4.489
Edelmann L, Pandita RK, Morrow BE. Low-Copy repeats mediate the common 3-Mb deletion in patients with Velo-cardio-facial syndrome. Am J Hum Genet. 1999;64(4):1076–86.
pubmed: 10090893 pmcid: 1377832 doi: 10.1086/302343
Karbarz M. Consequences of 22q11.2 Microdeletion on the genome, Individual and Population levels. Genes (Basel). 2020;11(9):977.
pubmed: 32842603 doi: 10.3390/genes11090977
Robin NH, Shprintzen RJ. Defining the clinical spectrum of deletion 22q11.2. J Pediatr. 2005;147(1):90–6.
pubmed: 16027702 doi: 10.1016/j.jpeds.2005.03.007
Du Q, de la Morena MT, van Oers NSC. The Genetics and epigenetics of 22q11.2 deletion syndrome. Front Genet. 2020;10.
Racedo SE, Liu Y, Shi L, Zheng D, Morrow BE. Dgcr8 functions in the secondary heart field for outflow tract and right ventricle development in mammals. Dev Biol. 2023.
Leitão AL, Enguita FJ. A structural view of miRNA Biogenesis and function. Noncoding RNA. 2022;8(1):10.
pubmed: 35202084 pmcid: 8874510
Kozomara A, Birgaoanu M, Griffiths-Jones S. miRBase: from microRNA sequences to function. Nucleic Acids Res. 2019;47(D1):D155–62.
pubmed: 30423142 doi: 10.1093/nar/gky1141
Bartel DP, MicroRNAs. Cell. 2004;116(2):281–97.
pubmed: 14744438 doi: 10.1016/S0092-8674(04)00045-5
Brzustowicz LM, Bassett AS. miRNA-mediated risk for schizophrenia in 22q11.2 deletion syndrome. Front Genet. 2012;3(DEC).
Sellier C, Hwang VJ, Dandekar R, Durbin-Johnson B, Charlet-Berguerand N, Ander BP, et al. Decreased DGCR8 expression and miRNA dysregulation in individuals with 22q11.2 deletion syndrome. PLoS ONE. 2014;9(8):e103884.
pubmed: 25084529 pmcid: 4118991 doi: 10.1371/journal.pone.0103884
de la Morena MT, Eitson JL, Dozmorov IM, Belkaya S, Hoover AR, Anguiano E, et al. Signature MicroRNA expression patterns identified in humans with 22q11.2 deletion/DiGeorge syndrome. Clin Immunol. 2013;147(1):11–22.
pubmed: 23454892 pmcid: 3748608 doi: 10.1016/j.clim.2013.01.011
Koshiol J, Wang E, Zhao Y, Marincola F, Landi MT. Strengths and limitations of Laboratory procedures for MicroRNA Detection. Cancer Epidemiol Biomarkers Prev. 2010;19(4):907–11.
pubmed: 20332265 pmcid: 2852469 doi: 10.1158/1055-9965.EPI-10-0071
Ibberson D, Benes V, Muckenthaler MU, Castoldi M. RNA degradation compromises the reliability of microRNA expression profiling. BMC Biotechnol. 2009;9(1):102.
pubmed: 20025722 pmcid: 2805631 doi: 10.1186/1472-6750-9-102
Patil AH, Halushka MK. miRge3.0: a comprehensive microRNA and tRF sequencing analysis pipeline. NAR Genom Bioinform. 2021;3(3).
Love MI, Huber W, Anders S. Moderated estimation of Fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 2014;15(12):550.
pubmed: 25516281 pmcid: 4302049 doi: 10.1186/s13059-014-0550-8
Potla P, Ali SA, Kapoor M. A bioinformatics approach to microRNA-sequencing analysis. Osteoarthr Cartil Open. 2021;3(1):100131.
pubmed: 36475076 doi: 10.1016/j.ocarto.2020.100131
Kavakiotis I, Alexiou A, Tastsoglou S, Vlachos IS, Hatzigeorgiou AG. DIANA-miTED: a microRNA tissue expression database. Nucleic Acids Res. 2022;50(D1):D1055–61.
pubmed: 34469540 doi: 10.1093/nar/gkab733
Sticht C, De La Torre C, Parveen A, Gretz N. miRWalk: an online resource for prediction of microRNA binding sites. PLoS ONE. 2018;13(10):e0206239.
pubmed: 30335862 pmcid: 6193719 doi: 10.1371/journal.pone.0206239
Kuleshov MV, Jones MR, Rouillard AD, Fernandez NF, Duan Q, Wang Z, et al. Enrichr: a comprehensive gene set enrichment analysis web server 2016 update. Nucleic Acids Res. 2016;44(W1):W90–7.
pubmed: 27141961 pmcid: 4987924 doi: 10.1093/nar/gkw377
Chen EY, Tan CM, Kou Y, Duan Q, Wang Z, Meirelles GV, et al. Enrichr: interactive and collaborative HTML5 gene list enrichment analysis tool. BMC Bioinformatics. 2013;14(1):128.
pubmed: 23586463 pmcid: 3637064 doi: 10.1186/1471-2105-14-128
Xie Z, Bailey A, Kuleshov MV, Clarke DJB, Evangelista JE, Jenkins SL et al. Gene Set Knowledge Discovery with Enrichr. Curr Protoc. 2021;1(3).
Dantas AG, Santoro ML, Nunes N, de Mello CB, Pimenta LSE, Meloni VA, et al. Downregulation of genes outside the deleted region in individuals with 22q11.2 deletion syndrome. Hum Genet. 2019;138(1):93–103.
pubmed: 30627818 doi: 10.1007/s00439-018-01967-6
Stark KL, Xu B, Bagchi A, Lai WS, Liu H, Hsu R, et al. Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model. Nat Genet. 2008;40(6):751–60.
pubmed: 18469815 doi: 10.1038/ng.138
Earls LR, Fricke RG, Yu J, Berry RB, Baldwin LT, Zakharenko SS. Age-dependent MicroRNA control of synaptic plasticity in 22q11 deletion syndrome and Schizophrenia. J Neurosci. 2012;32(41):14132–44.
pubmed: 23055483 pmcid: 3486522 doi: 10.1523/JNEUROSCI.1312-12.2012
Chun S, Du F, Westmoreland JJ, Han SB, Wang YD, Eddins D, et al. Thalamic mir-338-3p mediates auditory thalamocortical disruption and its late onset in models of 22q11.2 microdeletion. Nat Med. 2017;23(1):39–48.
pubmed: 27892953 doi: 10.1038/nm.4240
Zhao D, Lin M, Chen J, Pedrosa E, Hrabovsky A, Fourcade HM, et al. MicroRNA profiling of neurons generated using Induced pluripotent stem cells derived from patients with Schizophrenia and Schizoaffective Disorder, and 22q11.2 Del. PLoS ONE. 2015;10(7):e0132387.
pubmed: 26173148 pmcid: 4501820 doi: 10.1371/journal.pone.0132387
Toyoshima M, Akamatsu W, Okada Y, Ohnishi T, Balan S, Hisano Y, et al. Analysis of induced pluripotent stem cells carrying 22q11.2 deletion. Transl Psychiatry. 2016;6(11):e934–934.
pubmed: 27801899 pmcid: 5314118 doi: 10.1038/tp.2016.206
Ying S, Heung T, Zhang Z, Yuen RKC, Bassett AS. Schizophrenia Risk mediated by microRNA target genes overlapped by genome-wide Rare Copy Number Variation in 22q11.2 deletion syndrome. Front Genet. 2022;13.
Kim JO, Song DW, Kwon EJ, Hong SE, Song HK, Min CK, et al. miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways. PLoS ONE. 2015;10(3):e0122509.
pubmed: 25767890 pmcid: 4358957 doi: 10.1371/journal.pone.0122509
Poirsier C, Besseau-Ayasse J, Schluth-Bolard C, Toutain J, Missirian C, Le Caignec C, et al. A French multicenter study of over 700 patients with 22q11 deletions diagnosed using FISH or aCGH. Eur J Hum Genet. 2016;24(6):844–51.
pubmed: 26508576 doi: 10.1038/ejhg.2015.219
Cancrini C, Puliafito P, Digilio MC, Soresina A, Martino S, Rondelli R, et al. Clinical features and Follow-Up in patients with 22q11.2 deletion syndrome. J Pediatr. 2014;164(6):1475–e14802.
pubmed: 24657119 doi: 10.1016/j.jpeds.2014.01.056
Campbell IM, Sheppard SE, Crowley TB, McGinn DE, Bailey A, McGinn MJ, et al. What is new with 22q? An update from the 22q and you center at the children’s hospital of Philadelphia. Am J Med Genet A. 2018;176(10):2058–69.
pubmed: 30380191 pmcid: 6501214 doi: 10.1002/ajmg.a.40637
Sabaie H, Gharesouran J, Asadi MR, Farhang S, Ahangar NK, Brand S, et al. Downregulation of miR-185 is a common pathogenic event in 22q11.2 deletion syndrome-related and idiopathic schizophrenia. Metab Brain Dis. 2022;37(4):1175–84.
pubmed: 35075501 doi: 10.1007/s11011-022-00918-5
Forstner AJ, Basmanav FB, Mattheisen M, Böhmer AC, Hollegaard MV, Janson E, et al. Investigation of the involvement of MIR185 and its target genes in the development of schizophrenia. J Psychiatry Neurosci. 2014;39(6):386–96.
pubmed: 24936775 pmcid: 4214873 doi: 10.1503/jpn.130189
Benetti S, Mechelli A, Picchioni M, Broome M, Williams S, McGuire P. Functional integration between the posterior hippocampus and prefrontal cortex is impaired in both first episode schizophrenia and the at risk mental state. Brain. 2009;132(9):2426–36.
pubmed: 19420091 doi: 10.1093/brain/awp098
Karayiorgou M, Simon TJ, Gogos JA. 22q11.2 microdeletions: linking DNA structural variation to brain dysfunction and schizophrenia. Nat Rev Neurosci. 2010;11(6):402–16.
pubmed: 20485365 pmcid: 2977984 doi: 10.1038/nrn2841
Nicoletti A, S de, Visacri MB, Ronda da, SC da CR, do PE V, Quintanilha NS, de Souza JCF, et al. RN, et al. Differentially expressed plasmatic microRNAs in Brazilian patients with coronavirus disease 2019 (COVID-19): preliminary results. Mol Biol Rep. 2022;49(7):6931–43.
pubmed: 35301654 pmcid: 8929466 doi: 10.1007/s11033-022-07338-9
Ma X, Liu H, Zhu J, Zhang C, Peng Y, Mao Z, et al. Mir-185-5p regulates inflammation and Phagocytosis through CDC42/JNK Pathway in macrophages. Genes (Basel). 2022;13(3):468.
pubmed: 35328023 doi: 10.3390/genes13030468
Vaz C, Ahmad HM, Sharma P, Gupta R, Kumar L, Kulshreshtha R, et al. Analysis of microRNA transcriptome by deep sequencing of small RNA libraries of peripheral blood. BMC Genomics. 2010;11(1):288.
pubmed: 20459673 pmcid: 2885365 doi: 10.1186/1471-2164-11-288
Bo L, Wei B, Wang Z, Kong D, Gao Z, Miao Z. Screening of critical genes and MicroRNAs in blood samples of patients with ruptured intracranial aneurysms by Bioinformatic Analysis of Gene Expression Data. Med Sci Monit. 2017;23:4518–25.
pubmed: 28930970 pmcid: 5618721 doi: 10.12659/MSM.902953
McLean E, Bhattarai R, Hughes BW, Mahalingam K, Bagasra O. Computational identification of mutually homologous Zika virus miRNAs that target microcephaly genes. Libyan J Med. 2017;12(1):1304505.
pubmed: 28385119 pmcid: 5418939 doi: 10.1080/19932820.2017.1304505
Lopez-Valenzuela M, Ramirez O, Rosas A, Garcia-Vargas S, de la Rasilla M, Lalueza-Fox C, et al. An ancestral miR-1304 Allele Present in neanderthals regulates genes involved in enamel formation and could explain Dental differences with modern humans. Mol Biol Evol. 2012;29(7):1797–806.
pubmed: 22319171 doi: 10.1093/molbev/mss023
Eszlari N, Petschner P, Gonda X, Baksa D, Elliott R, Anderson IM et al. Childhood Adversity Moderates the Effects of HTR2A Epigenetic Regulatory Polymorphisms on rumination. Front Psychiatry. 2019;10.
Schneider M, Debbané M, Bassett AS, Chow EWC, Fung WLA, van den Bree MBM, et al. Psychiatric disorders from Childhood to Adulthood in 22q11.2 deletion syndrome: results from the International Consortium on Brain and Behavior in 22q11.2 deletion syndrome. Am J Psychiatry. 2014;171(6):627–39.
pubmed: 24577245 pmcid: 4285461 doi: 10.1176/appi.ajp.2013.13070864
Fukata Y, Fukata M. Protein palmitoylation in neuronal development and synaptic plasticity. Nat Rev Neurosci. 2010;11(3):161–75.
pubmed: 20168314 doi: 10.1038/nrn2788
Mukai J, Liu H, Burt RA, Swor DE, Lai WS, Karayiorgou M, et al. Evidence that the gene encoding ZDHHC8 contributes to the risk of schizophrenia. Nat Genet. 2004;36(7):725–31.
pubmed: 15184899 doi: 10.1038/ng1375
Chen WY, Shi YY, Zheng YL, Zhao XZ, Zhang GJ, Chen SQ, et al. Case–control study and transmission disequilibrium test provide consistent evidence for association between schizophrenia and genetic variation in the 22q11 gene ZDHHC8. Hum Mol Genet. 2004;13(23):2991–5.
pubmed: 15489219 doi: 10.1093/hmg/ddh322
Ota VK, Gadelha A, Assunção IB, Santoro ML, Christofolini DM, Bellucco FT, et al. ZDHHC8 gene may play a role in cortical volumes of patients with schizophrenia. Schizophr Res. 2013;145(1–3):33–5.
pubmed: 23403413 doi: 10.1016/j.schres.2013.01.011
Shashi V, Francis A, Hooper SR, Kranz PG, Zapadka M, Schoch K, et al. Increased corpus callosum volume in children with chromosome 22q11.2 deletion syndrome is associated with neurocognitive deficits and genetic polymorphisms. Eur J Hum Genet. 2012;20(10):1051–7.
pubmed: 22763378 pmcid: 3449066 doi: 10.1038/ejhg.2012.138
Choi WY, Giraldez AJ, Schier AF. Target protectors reveal dampening and balancing of nodal agonist and antagonist by miR-430. Sci (1979). 2007;318(5848):271–4.
Johnston RJ, Hobert O. A microRNA controlling left/right neuronal asymmetry in Caenorhabditis elegans. Nature. 2003;426(6968):845–9.
pubmed: 14685240 doi: 10.1038/nature02255
Forstner AJ, Degenhardt F, Schratt G, Nöthen MM. MicroRNAs as the cause of schizophrenia in 22q11.2 deletion carriers, and possible implications for idiopathic disease: a mini-review. Front Mol Neurosci. 2013;6.
Saunders MA, Liang H, Li WH. Human polymorphism at microRNAs and microRNA target sites. Proc Natl Acad Sci U S A. 2007;104(9):3300–5.
pubmed: 17360642 pmcid: 1805605 doi: 10.1073/pnas.0611347104
Zhao D, Wu K, Sharma S, Xing F, Wu SY, Tyagi A, et al. Exosomal mir-1304-3p promotes breast cancer progression in African americans by activating cancer-associated adipocytes. Nat Commun. 2022;13(1):7734.
pubmed: 36517516 pmcid: 9751138 doi: 10.1038/s41467-022-35305-2

Auteurs

Anelisa Gollo Dantas (AG)

Genetics Division, Department of Morphology and Genetics, Universidade Federal de São Paulo, São Paulo, Brazil.

Beatriz Carvalho Nunes (BC)

Genetics Division, Department of Morphology and Genetics, Universidade Federal de São Paulo, São Paulo, Brazil.

Natália Nunes (N)

Genetics Division, Department of Morphology and Genetics, Universidade Federal de São Paulo, São Paulo, Brazil.
Department of Biosciences and Medical Biology, University of Salzburg, Salzburg, Austria.

Pedro Galante (P)

Molecular Oncology Center, Hospital Sírio-Libanês, São Paulo, SP, Brazil.

Paula Fontes Asprino (PF)

Molecular Oncology Center, Hospital Sírio-Libanês, São Paulo, SP, Brazil.

Vanessa Kiyomi Ota (VK)

Genetics Division, Department of Morphology and Genetics, Universidade Federal de São Paulo, São Paulo, Brazil.

Maria Isabel Melaragno (MI)

Genetics Division, Department of Morphology and Genetics, Universidade Federal de São Paulo, São Paulo, Brazil. melaragno.maria@unifesp.br.

Articles similaires

Genome, Chloroplast Phylogeny Genetic Markers Base Composition High-Throughput Nucleotide Sequencing

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C

Classifications MeSH