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Estrogen Receptor α Drives Pro-Resilient Transcription in Mouse Models of Depression

ABSTRACT: Estrogen Receptor α Drives Pro-Resilient Transcription in Mouse Models of Depression

PROVIDER: PRJNA434438 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6743170.fastq.gz	Fastqsanger.gz
	SRR6743180.fastq.gz	Fastqsanger.gz
	SRR6743190.fastq.gz	Fastqsanger.gz
	SRR6743171.fastq.gz	Fastqsanger.gz
	SRR6743181.fastq.gz	Fastqsanger.gz

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Estrogen Receptor α Drives Pro-Resilient Transcription in Mouse Models of Depression

Project description:Most people exposed to stress do not develop depression. Animal models have shown that stress resilience is an active state that requires broad transcriptional adaptations, but how this homeostatic process is regulated remains poorly understood. In this study, we analyze upstream regulators of genes differentially expressed after chronic social defeat stress. We identify estrogen receptor α (ERα) as the top regulator of pro-resilient transcriptional changes in the nucleus accumbens (NAc), a key brain reward region implicated in depression. In accordance with these findings, nuclear ERα protein levels are altered by stress in male and female mice. Further, overexpression of ERα in the NAc promotes stress resilience in both sexes. Subsequent RNA sequencing reveals that ERα overexpression in NAc reproduces the transcriptional signature of resilience in male, but not female, mice. These results indicate that NAc ERα is an important regulator of pro-resilient transcriptional changes, but with sex-specific downstream targets.

2018-02-16 | GSE110725 | GEO

Estrogen receptor α drives pro-resilient transcription in mouse models of depression.

Project description:Most people exposed to stress do not develop depression. Animal models have shown that stress resilience is an active state that requires broad transcriptional adaptations, but how this homeostatic process is regulated remains poorly understood. In this study, we analyze upstream regulators of genes differentially expressed after chronic social defeat stress. We identify estrogen receptor α (ERα) as the top regulator of pro-resilient transcriptional changes in the nucleus accumbens (NAc), a key brain reward region implicated in depression. In accordance with these findings, nuclear ERα protein levels are altered by stress in male and female mice. Further, overexpression of ERα in the NAc promotes stress resilience in both sexes. Subsequent RNA-sequencing reveals that ERα overexpression in NAc reproduces the transcriptional signature of resilience in male, but not female, mice. These results indicate that NAc ERα is an important regulator of pro-resilient transcriptional changes, but with sex-specific downstream targets.

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Project description:Stressful circumstances are significant contributors to mental illnesses, such as major depressive disorder. Anhedonia, which is the loss of the ability to enjoy pleasure, including rewarding activities or social contexts, is considered a key symptom of depression. Although stress-induced depression is associated with anhedonia in humans and animals, the underlying molecular mechanisms of anhedonic responses remain poorly understood. In this study, we conducted RNA sequencing to profile the medial prefrontal cortex which was substantially associated with the CUS-induced anhedonic behavioral phenotypes. Employing chronic unpredictable stress (CUS), we determined two subpopulations based on sucrose preference, which was highly correlated with social reward: susceptible (SUS, anhedonic) vs. resilient (RES, non-anhedonic) groups. We identified Syt4 as a hub gene in a gene network unique to anhedonia by conducting a weighted gene co-expression network analysis of the RNA sequencing data from the mPFC of SUS and RES mice. We also confirmed that Syt4 overexpression in the mPFC was pro-susceptible, while the Syt4 knockdown was pro-resilient; the pro-susceptible effects of SYT4 were mediated through the reduction of brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signaling in the mPFC. These findings suggested that SYT4-BDNF interactions in the mPFC could be a crucial regulatory mechanism of anhedonic susceptibility to chronic stress.

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