Effective biomarkers and therapeutic targets of nerve-immunity interaction in the treatment of depression: an integrated investigation of the miRNA-mRNA regulatory networks.


Journal

Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617

Informations de publication

Date de publication:
25 04 2022
Historique:
received: 28 12 2021
accepted: 11 04 2022
pubmed: 26 4 2022
medline: 7 5 2022
entrez: 25 4 2022
Statut: ppublish

Résumé

Major depressive disorder (MDD) is an emotional condition that interferes with sufferers' work and daily life. Numerous studies have found that miRNAs play a significant role in the development of MDD and can be utilized as a biomarker for its diagnosis and therapy. However, there have been few studies on nerve-immunity interaction treatment for the brains of MMD patients. The work is performed on microarray data. We analyzed the differences of miRNAs (GSE58105, GSE81152, GSE152267, and GSE182194) and mRNA (GSE19738, GSE32280, GSE44593, GSE53987, and GSE98793) in MDD and healthy samples from GEO datasets. FunRich was used to predict the transcription factors and target genes of the miRNAs, and TF and GO enrichment analyses were performed. Then, by comparing the differential expression of the anticipated target genes and five mRNAs, intersecting mRNAs were discovered. The intersecting genes were submitted to GO and KEGG analyses to determine their functions. These intersecting potential genes and pathways that linked to MDD in neurological and immunological aspects have been identified for future investigation. We discovered five hub genes: KCND2, MYT1L, GJA1, CHL1, and SNAP25, which were all up-regulated genes. However, in MMD, the equivalent miRNAs, hsa-miR-206 and hsa-miR-338-3p, were both down-regulated. These miRNAs can activate or inhibit the T cell receptor signal pathway, JAK-STAT and other signal pathways, govern immune-inflammatory response, neuronal remodeling, and mediate the onset and development of MMD Conclusions: The results of a thorough bioinformatics investigation of miRNAs and mRNAs in MDD showed that miR-338-3P and miR-206 might be effective biomarkers and possible therapeutic targets for the treatment of MDD via nerve-immunity interaction.

Sections du résumé

BACKGROUND
Major depressive disorder (MDD) is an emotional condition that interferes with sufferers' work and daily life. Numerous studies have found that miRNAs play a significant role in the development of MDD and can be utilized as a biomarker for its diagnosis and therapy. However, there have been few studies on nerve-immunity interaction treatment for the brains of MMD patients.
METHODS
The work is performed on microarray data. We analyzed the differences of miRNAs (GSE58105, GSE81152, GSE152267, and GSE182194) and mRNA (GSE19738, GSE32280, GSE44593, GSE53987, and GSE98793) in MDD and healthy samples from GEO datasets. FunRich was used to predict the transcription factors and target genes of the miRNAs, and TF and GO enrichment analyses were performed. Then, by comparing the differential expression of the anticipated target genes and five mRNAs, intersecting mRNAs were discovered. The intersecting genes were submitted to GO and KEGG analyses to determine their functions. These intersecting potential genes and pathways that linked to MDD in neurological and immunological aspects have been identified for future investigation.
RESULTS
We discovered five hub genes: KCND2, MYT1L, GJA1, CHL1, and SNAP25, which were all up-regulated genes. However, in MMD, the equivalent miRNAs, hsa-miR-206 and hsa-miR-338-3p, were both down-regulated. These miRNAs can activate or inhibit the T cell receptor signal pathway, JAK-STAT and other signal pathways, govern immune-inflammatory response, neuronal remodeling, and mediate the onset and development of MMD Conclusions: The results of a thorough bioinformatics investigation of miRNAs and mRNAs in MDD showed that miR-338-3P and miR-206 might be effective biomarkers and possible therapeutic targets for the treatment of MDD via nerve-immunity interaction.

Identifiants

pubmed: 35468096
pii: 204030
doi: 10.18632/aging.204030
pmc: PMC9085226
doi:

Substances chimiques

Biomarkers 0
MIRN206 microRNA, human 0
MIRN338 microRNA, human 0
MicroRNAs 0
RNA, Messenger 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3569-3596

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Auteurs

Zixuan Wu (Z)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.

Zhixiang Cai (Z)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.

Hongshuo Shi (H)

Shandong University of Traditional Chinese Medicine, Jinan 250355, Shandong Province, China.

Xuyan Huang (X)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.

Minjie Cai (M)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.
Shantou Health School, Shantou 515061, Guangdong Province, China.

Kai Yuan (K)

Yunnan University of Chinese Medicine, Kunming 650500, Yunnan Province, China.

Peidong Huang (P)

Yunnan University of Chinese Medicine, Kunming 650500, Yunnan Province, China.

Guoqi Shi (G)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.

Tao Yan (T)

Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong Province, China.
Department of Cardiovascular Surgery, General Hospital of Southern Theater Command, PLA 510010, Guangdong Province, China.

Zhichao Li (Z)

The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250355, Shandong Province, China.

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