Progenies Derived from Males under Chronic Stress have Downregulated miR-29a

Jamal Al-Farsi^*
*Correspondence: Jamal Al-Farsi, Department of Physiology, University of Tabuk, Tabuk, Saudi Arabia, Email:

Keywords

Chronic stress • miR-29a • Progenies • Inheritance

Introduction

The impact of parental stress on offspring development has long been a topic of interest in scientific research. It is well established that environmental factors experienced by parents can influence the health and well-being of their progenies. One intriguing aspect of this phenomenon is the role of microRNAs (miRNAs) in mediating the effects of parental stress on offspring. MiRNAs are small non-coding RNAs that play crucial roles in post-transcriptional gene regulation. They can modulate gene expression by binding to the 3' Untranslated Region (UTR) of target mRNAs, leading to mRNA degradation or translational repression. Among the various miRNAs implicated in stress responses, miR-29a has garnered significant attention due to its diverse functions in cellular processes and its potential involvement in mediating the effects of stress on offspring [1].

In this review, we delve into the current understanding of how chronic stress in males can lead to the downregulation of miR-29a in their progenies. We examine the molecular mechanisms underlying this phenomenon and discuss its implications for inheritance patterns and offspring health [2].

Literature Review

The regulation of miR-29a expression under conditions of chronic stress has been a subject of investigation in recent years. Studies in animal models have provided compelling evidence that stressors such as social isolation, predator exposure, and chronic unpredictable stress can lead to dysregulation of miR-29a levels in various tissues, including the brain, liver, and reproductive organs. One study demonstrated that male mice subjected to chronic social defeat stress exhibited decreased expression of miR-29a in the hippocampus, a brain region crucial for stress responses and cognitive function. This downregulation was associated with alterations in the expression of target genes involved in synaptic plasticity and neurodevelopment, suggesting a potential link between miR-29a dysregulation and stress-related phenotypes in offspring [3].

Further investigations have revealed that the effects of paternal stress on miR-29a expression in progenies are not limited to the brain. For instance, studies in rat models have shown that chronic stressors such as exposure to high-fat diet-induced obesity or chronic unpredictable stress can lead to reduced miR-29a levels in the spermatozoa of male rats. Remarkably, these changes in sperm miRNA content were transmitted to the next generation and associated with metabolic alterations and altered stress responses in offspring. The mechanisms underlying the transmission of stress-induced miRNA alterations to progenies are not fully elucidated but may involve epigenetic modifications such as DNA methylation and histone modifications in the germline. For example, recent studies have suggested that stress-induced changes in DNA methylation patterns at miRNA loci in sperm cells could contribute to the downregulation of miR-29a and other stress-responsive miRNAs in offspring [4].

Discussion

The findings discussed above underscore the complex interplay between parental stress, miRNA regulation, and offspring health. The downregulation of miR-29a in progenies derived from males under chronic stress represents a potential mechanism by which environmental factors can influence gene expression and phenotypic outcomes across generations. One of the key questions raised by these studies is how miR-29a dysregulation in sperm cells translates into phenotypic changes in offspring. While the exact mechanisms remain to be fully elucidated, several hypotheses have been proposed. First, miR-29a is known to target genes involved in pathways related to development, metabolism, and stress responses. Thus, alterations in miR-29a levels could lead to dysregulation of these pathways in offspring, contributing to phenotypic changes such as altered metabolic homeostasis, stress resilience, and neurobehavioral traits [5].

Second, the transmission of stress-induced miRNA alterations from sperm to embryos could occur through epigenetic mechanisms during early development. Studies have shown that miRNAs packaged in spermatozoa can be delivered to oocytes upon fertilization and influence gene expression in the developing embryo. Therefore, changes in miRNA content in sperm cells due to paternal stress may have lasting effects on gene regulation in offspring tissues. Furthermore, the role of miR-29a in mediating the effects of stress on specific tissues and organs warrants further investigation. For instance, studies have highlighted the importance of miR-29a in regulating immune responses, fibrosis, and cardiac function [6].

Understanding how stress-induced changes in miR-29a expression impact these processes in progenies could have implications for the development of therapeutic strategies targeting miRNA pathways. It is also essential to consider the potential transgenerational effects of stress-induced miRNA alterations. While most studies have focused on the F1 generation (offspring of stressed males), there is growing evidence that such changes can persist across multiple generations. This raises important questions about the stability of stress-induced epigenetic modifications and their cumulative effects on offspring health over time.

Conclusion

In conclusion, the downregulation of miR-29a in progenies derived from males under chronic stress represents a fascinating area of research with significant implications for our understanding of parental effects on offspring development. The molecular mechanisms linking paternal stress to miRNA dysregulation in progenies, the phenotypic consequences of altered miR-29a expression, and the potential transgenerational effects of these changes warrant further investigation.

By elucidating the complex interplay between environmental factors, epigenetic regulation, and miRNA-mediated gene expression, we can gain valuable insights into how parental experiences shape offspring health and disease risk. This knowledge may pave the way for novel interventions aimed at mitigating the adverse effects of parental stress on future generations and promoting healthier outcomes across the lifespan.

Acknowledgement

None.

Conflict of Interest

None.

References

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