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Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
Published on: August 6, 2014
Dysregulation of long noncoding RNAs in mouse testes and spermatozoa after exposure to cadmium
Fengxin Gao1, Peng Zhang1, Hongyan Zhang1
1Institute of Life Science and School of Life Science, Nanchang University, Nanchang 330031, PR China.
Abstract:
There is increasing evidence that cadmium (Cd) exposure can cause male subfertility and even complete infertility in mammals. Long noncoding (lnc) RNAs are critical for spermatogenesis, and their dysregulation might lead to male infertility. However, whether they are involved in Cd-induced subfertility is unknown. Here we found that intraperitoneal exposure to Cd in mice led to male subfertility indicated by reductions in testicular sperm production and motility, and by abnormal morphology. Testicular and sperm RNAs were used to investigate lncRNA expression profiles by strand-specific RNA sequencing at the transcriptome level to help determine any RNA-related mechanisms in Cd-induced subfertility. The Cd-treated testes and spermatozoa exhibited aberrant expression profiles for lncRNAs and mRNAs. Of the lncRNAs, there were 139 with upregulated expression and 174 with downregulated expression in testes; in contrast, 685 were upregulated and 375 were downregulated in spermatozoa. For mRNA expression, 214 were upregulated and 226 were downregulated in testes; 272 were upregulated and 111 were downregulated in spermatozoa. Gene ontology and pathway analyses showed that the functions of differentially expressed lncRNA targets and mRNAs were closely linked with many processes involved in spermatogenesis. Additionally, many newly identified lncRNAs showed inducible expression, suggesting that they might be good candidate markers for Cd-induced male reproductive toxicity. This study provides a preliminary database for further exploring lncRNA-related mechnisms in male infertility induced by Cd.
Insights
Cadmium exposure causes male infertility by disrupting sperm production and motility. This study identifies changes in long noncoding RNAs (lncRNAs) in testes and sperm, revealing potential mechanisms for cadmium-induced reproductive toxicity.
Area of Science:
- Reproductive Biology
- Environmental Toxicology
- Molecular Biology
Background:
- Cadmium (Cd) exposure is linked to male subfertility and infertility in mammals.
- Long noncoding RNAs (lncRNAs) play crucial roles in spermatogenesis.
- The involvement of lncRNAs in Cd-induced male subfertility remains unclear.
Purpose of the Study:
- To investigate the role of lncRNAs in cadmium-induced male subfertility.
- To identify lncRNA expression profiles in testes and sperm following Cd exposure.
- To explore RNA-related mechanisms underlying Cd-induced reproductive toxicity.
Main Methods:
- Mice were exposed to cadmium via intraperitoneal injection.
- Testicular sperm production, motility, and morphology were assessed.
- Strand-specific RNA sequencing was performed on testicular and sperm RNA to analyze lncRNA and mRNA expression profiles.
- Gene ontology and pathway analyses were conducted on differentially expressed gene targets.
Main Results:
- Cadmium exposure led to reduced sperm production, motility, and abnormal sperm morphology in mice.
- Significant alterations in lncRNA and mRNA expression were observed in both testes and spermatozoa of Cd-treated mice.
- Differentially expressed lncRNAs and mRNAs were functionally associated with spermatogenesis processes.
- Numerous novel lncRNAs exhibited inducible expression patterns.
Conclusions:
- Cadmium exposure induces male subfertility through mechanisms involving dysregulated lncRNA and mRNA expression.
- lncRNAs are implicated in the pathogenesis of Cd-induced male reproductive toxicity.
- Newly identified lncRNAs may serve as potential biomarkers for detecting Cd-induced male reproductive damage.

