The study entitled “Genome-wide mRNA expression profiling in vast us lateralis of COPD patients with low and normal fat free mass index and healthy controls,” was recently published in the journal Respiratory Research.
In addition lung affection, Chronic Obstructive Pulmonary Disease (COPD) is also associated with several extra-pulmonary effects such as muscle wasting, which contributes to exercise limitation and is a predictor of morbidity and mortality. However, the molecular mechanisms leading to skeletal muscle wasting in COPD remain unclear. Muscle wasting affects 18 to 36% of patients with COPD and can be present even in patients with normal weight.
To examine the expression of several of genes, Microarrays have been shown to be effective. In this regard, the researchers thought that an analysis of the genes that are being transcribed in the muscle, the transcriptome, could explain the molecular mechanisms responsible for muscle wasting in patients with COPD, which can identify molecular targets for the development of therapeutic strategies specifically designed to improve muscle function.
Roberto Rabinovich examined 19 patients with COPD with low fat free mass index (FFMI) (COPDL) and compared the vast us laterals transcriptome with patients with COPD and normal FFMI (COPDN) and a group of age- and sex-matched healthy controls using microarrays. To confirm the gene altered expression, the team of researchers used PCR. The levels of Protein P21 were measured with immunoblotting.
Results revealed 42 genes that were differently expressed between the COPDL and the COPDN groups. Using the PCR, the researchers found 5 genes that were associated with cell cycle arrest and growth regulation, both features related with muscle wasting and aging. The researchers also found in the COPDL group higher levels of the Protein CDKN1A, a recognized marker of premature aging/cell cycle arrest.
The authors concluded that vast us lateralis of patients with COPD and muscle wasting overexpress genes is associated to “inhibition of cell cycle and of cell growth while genes related to muscle formation and growth and energy production were down-regulated.” In this regard, the findings suggest that premature aging may play a role in muscle wasting in patients with COPD.
This pattern is similar to observations associated with aging, which suggests that premature aging may play a role in muscle atrophy in COPD. These findings are encouraging for the treatment of muscle wasting in patients with COPD.
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