Whole-transcriptome brain expression and exon-usage profiling in major depression and suicide: evidence for altered glial, endothelial and ATPase activity
Open accessAbstract
Brain gene expression profiling studies of suicide and depression using oligonucleotide microarrays have often failed to distinguish these two phenotypes. Moreover, next generation sequencing approaches are more accurate in quantifying gene expression and can detect alternative splicing. Using RNA-seq, we examined whole-exome gene and exon expression in non-psychiatric controls (CON, N=29), DSM-IV major depressive disorder suicides (MDD-S, N=21) and MDD non-suicides (MDD, N=9) in the dorsal lateral prefrontal cortex (Brodmann Area 9) of sudden death medication-free individuals post mortem. Using small RNA-seq, we also examined miRNA expression (nine samples per group). DeSeq2 identified 35 genes differentially expressed between groups and surviving adjustment for false discovery rate (adjusted P<0.1). In depression, altered genes include humanin-like-8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, clade H (SERPINH1) and chemokine ligand 4 (CCL4), while exploratory gene ontology (GO) analyses revealed lower expression of immune-related pathways such as chemokine receptor activity, chemotaxis and cytokine biosynthesis, and angiogenesis and vascular development in (adjusted P<0.1). Hypothesis-driven GO analysis suggests lower expression of genes involved in oligodendrocyte differentiation, regulation of glutamatergic neurotransmission, and oxytocin receptor expression in both suicide and depression, and provisional evidence for altered DNA-dependent ATPase expression in suicide only. DEXSEq analysis identified differential exon usage in ATPase, class II, type 9B (adjusted P<0.1) in depression. Differences in miRNA expression or structural gene variants were not detected. Results lend further support for models in which deficits in microglial, endothelial (blood-brain barrier), ATPase activity and astrocytic cell functions contribute to MDD and suicide, and identify putative pathways and mechanisms for further study in these disorders.
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SERPINH1, IL-8, MTRNRL8, and CCL4 are among the genes whose expression is altered in MDD.
“Serpin Family H Member 1 (SERPINH1), IL-8, humanin like-8 (MTRNRL8), and chemokine ligand 4 (CCL4) are among the genes whose expression is altered in MDD. 460 , 461”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [461]
RNA-sequencing analyses of postmortem DLPFC from MDD patients revealed downregulation of genes related to glutamatergic transmission.
“RNA-sequencing analyses of postmortem DLPFC from MDD patients similarly revealed the downregulation of genes related to glutamatergic transmission 211.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [211]
Combining GWAS with transcriptome data indicates that suicide-related genes are associated with inflammation, the HPA axis, GABA and glutamate neurotransmission, and neurogenesis.
“Combining GWASs with transcriptome data indicates that suicide-related genes are associated with inflammation, the hypothalamic-pituitary-adrenal (HPA) axis, γ-aminobutyric acid (GABA) and glutamate neurotransmission, and neurogenesis (51-56).”
From A brain-centric model of suicidal behavior (2020) · cites this paper as [52]
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- Authors
- Pantazatos, S. P., Huang, Y.-Y., Rosoklija, G. B., Dwork, A. J., Arango, V, & Mann, J. J.
- Affiliations
- New York State Psychiatric Institute (US)
- Columbia University (US)
- Corresponding author
- Pantazatos, S P
- Mann, J J
- Venue
- Molecular Psychiatry
- Published
- 2016-08-16
- Volume
- 22
- Issue
- 5
- Pages
- 760-773
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC5313378
- OpenAlex
- W2509761723
- Cited by
- 229
- References
- 91
- Citations by year
- 2026: 21 · 2025: 29 · 2024: 23 · 2023: 30 · 2022: 31 · 2021: 32 · 2020: 25 · 2019: 17 · 2018: 12 · 2017: 8
- FWCI
- 9.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (P50MH090964, R01MH064168, R01MH082041, K01MH108721, R01MH040210, P50MH062185)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Social Sciences › Psychology › Clinical Psychology › Suicide and Self-Harm Studies
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- major depressive disorder, suicide, brain gene expression, exon usage, alternative splicing, dorsolateral prefrontal cortex, microRNA expression, oligodendrocyte differentiation, microglia, blood-brain barrier, ATPase activity, astrocytes, glutamatergic neurotransmission, oxytocin receptor, interleukin-8, HSP47, carbon tetrachloride, immune pathways, angiogenesis
- MeSH terms
- Adenosine Triphosphatases, Adult, Aged, Brain, Major Depressive Disorder, Exons, Female, gamma-Aminobutyric Acid, Humans, Male, Middle Aged, Neuroglia, RNA, Messenger, Suicide, Case-Control Studies, Prefrontal Cortex, Sequence Analysis, RNA, MicroRNAs, Endothelial Cells, High-Throughput Nucleotide Sequencing, Transcriptome
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