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Authors Ma R, Gong XF, Jiang H, Lin CY, Chen YQ, Xu XM, Zhang CT, Wang J, Lu WJ, Zhong NS
Received 25 March 2016
Accepted for publication 5 September 2016
Published 20 February 2017 Volume 2017:12 Pages 581—587
DOI https://doi.org/10.2147/COPD.S109243
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 3
Editor who approved publication: Dr Richard Russell
Abstract: Skeletal muscle atrophy and dysfunction are common complications in the
chronic obstructive pulmonary disease (COPD). However, the underlying molecular
mechanism remains elusive. Serum response factor (SRF) is a transcription
factor which is critical in myocyte differentiation and growth. In this study,
we established a mouse COPD model induced by cigarette smoking (CS) exposure
for 24 weeks, with apparent pathophysiological changes, including increased
airway resistance, enlarged alveoli, and skeletal muscle atrophy. Levels of
upstream regulators of SRF, striated muscle activator of Rho signaling (STARS),
and ras homolog gene family, member A (RhoA) were decreased in quadriceps muscle
of COPD mice. Meanwhile, the nucleic location of SRF was diminished along with
its cytoplasmic accumulation. There was a downregulation of the target
muscle-specific gene, Igf1 . These results suggest that
the CS is one of the major cause for COPD pathogenesis, which induces the
COPD-associated skeletal muscle atrophy which is closely related to decreasing
SRF nucleic translocation, consequently downregulating the SRF target genes
involved in muscle growth and nutrition. The STARS/RhoA signaling pathway might
contribute to this course by impacting SRF subcellular distribution.
Keywords: SRF, chronic obstructive pulmonary
disease, skeletal muscle atrophy, cigarette smoking
* 在 583 页,在左栏,最后一段,句子 “…the primer for the Igf1 gene forward: 5′-tgctgtccctctatgcttcc-3′, reverse: 5′-gaaggaatagccacgctcag-3′” 应该是:" … forward: 5′-tggatgctcttcagttcgtg-3′, reverse: 5′-cacaatgcctgtctgaggtg-3′” 。
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