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Published on: September 21, 2010
Gga-let-7f-3p promotes apoptosis in selenium deficiency-induced skeletal muscle by targeting selenoprotein K
Rui-Feng Fan1, Chang-Yu Cao, Meng-Hao Chen
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China. shiwenxu@neau.edu.cn.
Abstract:
Selenoprotein K (SELENOK) is primarily observed in the endoplasmic reticulum, and serves to maintain the normal physiological functions of skeletal muscle. Skeletal muscle development and regeneration are associated with significant changes in the expression of specific microRNAs (miRNAs). Downregulated SELENOK expression is observed in chicken muscles deficient of Se. However, the mechanisms of miRNA regulation of SELENOK expression remain elusive. Here, deep sequencing was used to detect the miRNA profiles of muscle in Se deficient (-Se group) and normal (C group) chickens. A dual-luciferase reporter assay was adopted to verify the relationship between SELENOK and gga-let-7f-3p. In addition, gga-let-7f-3p was either overexpressed or knocked-down in chicken myoblasts. Furthermore, the cells were treated with N-acetyl-l-cysteine (NAC) or hydrogen peroxide (H2O2) in order to probe the factors involved in oxidative stress, endoplasmic reticulum stress (ERS) and apoptosis, respectively. Relative to the C group, there were 132 differentially expressed miRNAs (including 57 upregulated and 75 downregulated) in the muscles of the -Se group. The dual-luciferase reporter assay showed that SELENOK was a primary target of gga-let-7f-3p. It was also observed that the overexpression or knock-down of gga-let-7f-3p significantly influenced the SELENOK expression. Moreover, NAC blocked mimics of ga-let-7f-3p, thus inducing oxidative stress, ERS and apoptosis. Simultaneously, gga-let-7f-3p inhibitors blocked the stimulant effects caused by H2O2 in chicken myoblasts. Furthermore, Se deficiency downregulated the SELENOK protein expression and induced oxidative stress, ERS and apoptosis in chicken muscles. In conclusion, the gga-let-7f-3p-SELENOK pathway played a pivotal role in Se deficiency mediated muscle injuries through the induction of oxidative stress and ERS, ultimately promoting apoptosis.
Insights
Selenium deficiency in chickens impairs skeletal muscle by downregulating Selenoprotein K (SELENOK) via the gga-let-7f-3p microRNA pathway, leading to oxidative stress and apoptosis.
Area of Science:
- Biochemistry
- Molecular Biology
- Animal Science
Background:
- Selenoprotein K (SELENOK) is crucial for skeletal muscle function and is found in the endoplasmic reticulum.
- MicroRNAs (miRNAs) are implicated in skeletal muscle development and regeneration.
- Selenium (Se) deficiency in chickens leads to reduced SELENOK expression, but the regulatory mechanisms are unclear.
Purpose of the Study:
- To investigate the role of microRNAs in regulating SELENOK expression in Se-deficient chicken muscle.
- To elucidate the specific miRNA involved in the Se deficiency-mediated SELENOK regulation.
- To explore the impact of the identified miRNA-SELENOK pathway on oxidative stress, endoplasmic reticulum stress (ERS), and apoptosis in chicken myoblasts.
Main Methods:
- Deep sequencing to profile miRNA expression in Se-deficient and normal chicken muscle.
- Dual-luciferase reporter assay to confirm the interaction between SELENOK and gga-let-7f-3p.
- In vitro experiments involving overexpression and knockdown of gga-let-7f-3p in chicken myoblasts, with treatments of N-acetyl-l-cysteine (NAC) and hydrogen peroxide (H2O2).
Main Results:
- Deep sequencing identified 132 differentially expressed miRNAs between Se-deficient and normal groups.
- SELENOK was confirmed as a direct target of gga-let-7f-3p, with its expression significantly affected by gga-let-7f-3p manipulation.
- Se deficiency downregulated SELENOK protein, induced oxidative stress, ERS, and apoptosis, while gga-let-7f-3p mimics exacerbated these effects, and inhibitors counteracted H2O2-induced stress.
Conclusions:
- The gga-let-7f-3p-SELENOK pathway is a key mediator of Se deficiency-induced muscle injury in chickens.
- This pathway promotes muscle damage by inducing oxidative stress and endoplasmic reticulum stress, ultimately leading to apoptosis.
- Understanding this regulatory mechanism provides insights into preventing and treating Se deficiency-related myopathies.
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