Methylation in MAD1L1 is associated with the severity of suicide attempt and phenotypes of depression

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Sokolov, Aleksandr V.Uppsala universitet,Funktionell farmakologi och neurovetenskap (författare)

Methylation in MAD1L1 is associated with the severity of suicide attempt and phenotypes of depression

Artikel/kapitelEngelska2023

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2023-01-04
BioMed Central (BMC),2023
electronicrdacarrier

Nummerbeteckningar

LIBRIS-ID:oai:DiVA.org:umu-202575
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-202575URI
https://doi.org/10.1186/s13148-022-01394-5DOI
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-495863URI
http://kipublications.ki.se/Default.aspx?queryparsed=id:151645632URI

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Språk:engelska
Sammanfattning på:engelska

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Ämneskategori:art swepub-publicationtype

Anmärkningar

Depression is a multifactorial disorder representing a significant public health burden. Previous studies have linked multiple single nucleotide polymorphisms with depressive phenotypes and suicidal behavior. MAD1L1 is a mitosis metaphase checkpoint protein that has been linked to depression in GWAS. Using a longitudinal EWAS approach in an adolescent cohort at two time points (n = 216 and n = 154), we identified differentially methylated sites that were associated with depression-related genetic variants in MAD1L1. Three methylation loci (cg02825527, cg18302629, and cg19624444) were consistently hypomethylated in the minor allele carriers, being cross-dependent on several SNPs. We further investigated whether DNA methylation at these CpGs is associated with depressive psychiatric phenotypes in independent cohorts. The first site (cg02825527) was hypomethylated in blood (exp(β) = 84.521, p value ~ 0.003) in participants with severe suicide attempts (n = 88). The same locus showed increased methylation in glial cells (exp(β) = 0.041, p value ~ 0.004) in the validation cohort, involving 29 depressed patients and 29 controls, and showed a trend for association with suicide (n = 40, p value ~ 0.089) and trend for association with depression treatment (n = 377, p value ~ 0.075). The second CpG (cg18302629) was significantly hypomethylated in depressed participants (exp(β) = 56.374, p value ~ 0.023) in glial cells, but did not show associations in the discovery cohorts. The last methylation site (cg19624444) was hypomethylated in the whole blood of severe suicide attempters; however, this association was at the borderline for statistical significance (p value ~ 0.061). This locus, however, showed a strong association with depression treatment in the validation cohort (exp(β) = 2.237, p value ~ 0.003) with 377 participants. The direction of associations between psychiatric phenotypes appeared to be different in the whole blood in comparison with brain samples for cg02825527 and cg19624444. The association analysis between methylation at cg18302629 and cg19624444 and MAD1L1 transcript levels in CD14+ cells shows a potential link between methylation at these CpGs and MAD1L1 expression. This study suggests evidence that methylation at MAD1L1 is important for psychiatric health as supported by several independent cohorts.

Ämnesord och genrebeteckningar

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Psykiatri hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Psychiatry hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Medicinsk genetik hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Medical Genetics hsv//eng
Depression
DNA methylation
MAD1L1
Suicide

Biuppslag (personer, institutioner, konferenser, titlar ...)

Manu, Diana-MariaUppsala universitet,Funktionell farmakologi och neurovetenskap (författare)
Nordberg, Didi O. T.Uppsala universitet,Funktionell farmakologi och neurovetenskap (författare)
Boström, Adrian Desai E.Umeå universitet,Psykiatri,Department of Women’s and Children’s Health/Neuropediatrics, Karolinska Institutet, Stockholm, Sweden,Umeå Univ, Dept Clin Sci Psychiat, Umeå, Sweden.;Karolinska Inst, Dept Womens & Childrens Hlth Neuropediat, Stockholm, Sweden.(Swepub:umu)adbo0015 (författare)
Jokinen, JussiKarolinska Institutet,Umeå universitet,Psykiatri,Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden,Umeå Univ, Dept Clin Sci Psychiat, Umeå, Sweden.;Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.(Swepub:umu)jujo0022 (författare)
Schiöth, Helgi B.Uppsala universitet,Funktionell farmakologi och neurovetenskap(Swepub:uu)helgschi (författare)
Uppsala universitetFunktionell farmakologi och neurovetenskap (creator_code:org_t)

Sammanhörande titlar

Ingår i:Clinical Epigenetics: BioMed Central (BMC)15:11868-7083

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Av lärosätet: Umeå universitet; Uppsala universitet; Karolinska Institutet

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