Co-expression network of long non-coding RNA and mRNA reveals molecular phenotype changes in kidney development of prenatal chlorpyrifos exposure in a mouse model.

Chlorpyrifos kidney development long non-coding ribonucleic acid (lncRNA) messenger ribonucleic acid (mRNA) weighted gene co-expression network analysis (WGCNA)

Journal

Annals of translational medicine
ISSN: 2305-5839
Titre abrégé: Ann Transl Med
Pays: China
ID NLM: 101617978

Informations de publication

Date de publication:
Apr 2021
Historique:
entrez: 14 5 2021
pubmed: 15 5 2021
medline: 15 5 2021
Statut: ppublish

Résumé

Chlorpyrifos (CPF) is one of the most widely used organophosphorus pesticides globally and can accumulate in the kidney. Researchers have confirmed the regulatory functions of long non-coding ribonucleic acid (lncRNA) in the kidney. However, very few studies have examined the effects of prenatal CPF exposure or lncRNA on kidney development. High-throughput ribonucleic acid (RNA) sequencing was performed on embryonic kidneys obtained at E12.5, E14.5, E16.5, and E18.5 of prenatal CPF-exposed mice and the dimethyl sulfoxide (DMSO) control mice. A weighted gene co-expression network analysis (WGCNA) and a functional enrichment analysis were applied to construct a lncRNA-messenger ribonucleic acid (mRNA) network and screen targeted genes. These strategies were used to select the modules and genes correlated with prenatal CPF exposure in mouse kidney development. A gene ontology (GO) analysis revealed that the hub mRNAs linked to prenatal CPF exposure were mainly involved in the extracellular matrix and collagen degradation. Prss1, Prss2, and Prss3 were the most significantly upregulated mRNAs, and all had strong connections to lncRNAs Gm28760, Gm28139, and Gm26717. Additionally, we analyzed the lncRNA-mRNA network at different developmental kidney stages after prenatal CPF exposure. The results showed that kidney development was blocked at E12.5, which led to ectopic proximal tubule formation at E18.5. In summary, the RNA-sequencing and weighted gene co-expression network analyses showed that molecular phenotype changes occur in kidney development in a prenatal CPF exposure mouse model.

Sections du résumé

BACKGROUND BACKGROUND
Chlorpyrifos (CPF) is one of the most widely used organophosphorus pesticides globally and can accumulate in the kidney. Researchers have confirmed the regulatory functions of long non-coding ribonucleic acid (lncRNA) in the kidney. However, very few studies have examined the effects of prenatal CPF exposure or lncRNA on kidney development.
METHODS METHODS
High-throughput ribonucleic acid (RNA) sequencing was performed on embryonic kidneys obtained at E12.5, E14.5, E16.5, and E18.5 of prenatal CPF-exposed mice and the dimethyl sulfoxide (DMSO) control mice. A weighted gene co-expression network analysis (WGCNA) and a functional enrichment analysis were applied to construct a lncRNA-messenger ribonucleic acid (mRNA) network and screen targeted genes. These strategies were used to select the modules and genes correlated with prenatal CPF exposure in mouse kidney development.
RESULTS RESULTS
A gene ontology (GO) analysis revealed that the hub mRNAs linked to prenatal CPF exposure were mainly involved in the extracellular matrix and collagen degradation. Prss1, Prss2, and Prss3 were the most significantly upregulated mRNAs, and all had strong connections to lncRNAs Gm28760, Gm28139, and Gm26717. Additionally, we analyzed the lncRNA-mRNA network at different developmental kidney stages after prenatal CPF exposure. The results showed that kidney development was blocked at E12.5, which led to ectopic proximal tubule formation at E18.5.
CONCLUSIONS CONCLUSIONS
In summary, the RNA-sequencing and weighted gene co-expression network analyses showed that molecular phenotype changes occur in kidney development in a prenatal CPF exposure mouse model.

Identifiants

DOI: 10.21037/atm-20-6632 PMID: 33987351 PMC: PMC8106112
pubmed: 33987351
doi: 10.21037/atm-20-6632
pii: atm-09-08-653
pmc: PMC8106112
doi:

Types de publication

Journal Article

Langues

eng

Pagination

653

Informations de copyright

2021 Annals of Translational Medicine. All rights reserved.

Déclaration de conflit d'intérêts

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-6632). The authors have no conflicts of interest to declare.

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Auteurs

Bingjue Li (B)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Wenyu Xiang (W)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Jing Qin (J)

School of Pharmaceutical Science (Shenzhen), Sun Yat-sen University, Guangzhou, China.

Qiannan Xu (Q)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Shi Feng (S)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Yucheng Wang (Y)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Jianghua Chen (J)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Hong Jiang (H)

Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Key Laboratory of Nephropathy, Hangzhou, China.
Kidney Disease Immunology Laboratory, the Third-Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China.
Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China.
Institute of Nephropathy, Zhejiang University, Hangzhou, China.

Classifications MeSH