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Myostatin genotype regulates muscle-specific miRNA expression in mouse pectoralis muscle.

Rachagani S, Cheng Y, Reecy JM - BMC Res Notes (2010)

Bottom Line: Loss of functional Myostatin results in a dramatic increase in skeletal muscle mass.Loss of functional Myostatin resulted in a significant increase (p < .001) in miR-1, miR-133a, miR-133b, and miR-206 expression.Myostatin may regulates the expression of miRNAs such as miR-133a, miR-133b, miR-1, and miR-206 in skeletal muscle as it has been observed that the expression of those miRNAs are significantly higher in myostatin mice compared to wild type and heterozygous mice.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Animal Science, Iowa State University, Ames, Iowa, USA. jreecy@iastate.edu.

ABSTRACT

Background: Loss of functional Myostatin results in a dramatic increase in skeletal muscle mass. It is unknown what role miRNAs play in Myostatin mediated repression of skeletal muscle mass. We hypothesized that Myostatin genotype would be associated with the differential expression of miRNAs in skeletal muscle.

Findings: Loss of functional Myostatin resulted in a significant increase (p < .001) in miR-1, miR-133a, miR-133b, and miR-206 expression. In contrast, Myostatin genotype had no effect (P > .2) on miR-24 expression level. Myostatin genotype did not affect the expression level of MyoD or Myogenin (P > 0.5).

Conclusions: Myostatin may regulates the expression of miRNAs such as miR-133a, miR-133b, miR-1, and miR-206 in skeletal muscle as it has been observed that the expression of those miRNAs are significantly higher in myostatin mice compared to wild type and heterozygous mice. In contrast, expression of myogenic factors such as MyoD or Myogenin has not been affected by myostatin in the muscle tissue.

No MeSH data available.


Relative expression of myogenic factors in the mouse pectoralis muscle. Real-time PCR expression values were normalized to β-actin and are reported relative to MSTN+/+ levels. The graph represents the mean (± SE) fold change in gene expression.
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Figure 2: Relative expression of myogenic factors in the mouse pectoralis muscle. Real-time PCR expression values were normalized to β-actin and are reported relative to MSTN+/+ levels. The graph represents the mean (± SE) fold change in gene expression.

Mentions: The expression level of miR-133a (p < 0.0001), miR-133b (p < 0.001), miR-1 (p < 0.001), and miR-206 (p < .0001) was greater in Myostatin- animals as compared to wild type and heterozygous animal (Figure 1). In all cases, the expression level of miRNAs was equivalent in MSTN+/- and MSTN+/+ muscle. In contrast, miR-24 expression level was not affected by Myostatin genotype (data not shown). Myostatin genotype had no significant effect on the expression level of MyoD or Myogenin (Figure 2).


Myostatin genotype regulates muscle-specific miRNA expression in mouse pectoralis muscle.

Rachagani S, Cheng Y, Reecy JM - BMC Res Notes (2010)

Relative expression of myogenic factors in the mouse pectoralis muscle. Real-time PCR expression values were normalized to β-actin and are reported relative to MSTN+/+ levels. The graph represents the mean (± SE) fold change in gene expression.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2992544&req=5

Figure 2: Relative expression of myogenic factors in the mouse pectoralis muscle. Real-time PCR expression values were normalized to β-actin and are reported relative to MSTN+/+ levels. The graph represents the mean (± SE) fold change in gene expression.
Mentions: The expression level of miR-133a (p < 0.0001), miR-133b (p < 0.001), miR-1 (p < 0.001), and miR-206 (p < .0001) was greater in Myostatin- animals as compared to wild type and heterozygous animal (Figure 1). In all cases, the expression level of miRNAs was equivalent in MSTN+/- and MSTN+/+ muscle. In contrast, miR-24 expression level was not affected by Myostatin genotype (data not shown). Myostatin genotype had no significant effect on the expression level of MyoD or Myogenin (Figure 2).

Bottom Line: Loss of functional Myostatin results in a dramatic increase in skeletal muscle mass.Loss of functional Myostatin resulted in a significant increase (p < .001) in miR-1, miR-133a, miR-133b, and miR-206 expression.Myostatin may regulates the expression of miRNAs such as miR-133a, miR-133b, miR-1, and miR-206 in skeletal muscle as it has been observed that the expression of those miRNAs are significantly higher in myostatin mice compared to wild type and heterozygous mice.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Animal Science, Iowa State University, Ames, Iowa, USA. jreecy@iastate.edu.

ABSTRACT

Background: Loss of functional Myostatin results in a dramatic increase in skeletal muscle mass. It is unknown what role miRNAs play in Myostatin mediated repression of skeletal muscle mass. We hypothesized that Myostatin genotype would be associated with the differential expression of miRNAs in skeletal muscle.

Findings: Loss of functional Myostatin resulted in a significant increase (p < .001) in miR-1, miR-133a, miR-133b, and miR-206 expression. In contrast, Myostatin genotype had no effect (P > .2) on miR-24 expression level. Myostatin genotype did not affect the expression level of MyoD or Myogenin (P > 0.5).

Conclusions: Myostatin may regulates the expression of miRNAs such as miR-133a, miR-133b, miR-1, and miR-206 in skeletal muscle as it has been observed that the expression of those miRNAs are significantly higher in myostatin mice compared to wild type and heterozygous mice. In contrast, expression of myogenic factors such as MyoD or Myogenin has not been affected by myostatin in the muscle tissue.

No MeSH data available.