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• W2167663011 abstract "Cell surface glycans are known to play vital roles in muscle membrane stability and muscle disease, but to date, roles for glycans in muscle regeneration have been less well understood. Here, we describe a role for complex gangliosides synthesized by the Galgt1 gene in muscle regeneration. Cardiotoxin-injected wild type (WT) and Galgt1 −/− muscles, and mdx and Galgt1 −/− mdx muscles, were used to study regeneration in response to acute and chronic injury, respectively. Muscle tissue was analyzed at various time points for morphometric measurements and for gene expression changes in satellite cell and muscle differentiation markers by quantitative real-time polymerase chain reaction (qRT-PCR). Primary cell cultures were used to measure growth rate and myotube formation and to identify Galgt1 expression changes after cardiotoxin by fluorescence-activated cell sorting (FACS). Primary cell culture and tissue sections were also used to quantify satellite cell apoptosis. A query of a microarray data set of cardiotoxin-induced mouse muscle gene expression changes identified Galgt1 as the most upregulated glycosylation gene immediately after muscle injury. This was validated by qRT-PCR as a 23-fold upregulation in Galgt1 expression 1 day after cardiotoxin administration and a 16-fold upregulation in 6-week-old mdx muscles. These changes correlated with increased expression of Galgt1 protein and GM1 ganglioside in mononuclear muscle cells. In the absence of Galgt1, cardiotoxin-induced injury led to significantly reduced myofiber diameters after 14 and 28 days of regeneration. Myofiber diameters were also significantly reduced in Galgt1-deficient mdx mice compared to age-matched mdx controls, and this was coupled with a significant increase in the loss of muscle tissue. Cardiotoxin-injected Galgt1 −/− muscles showed reduced gene expression of the satellite cell marker Pax7 and increased expression of myoblast markers MyoD, Myf5, and Myogenin after injury along with a tenfold increase in apoptosis of Pax7-positive muscle cells. Cultured primary Galgt1 −/− muscle cells showed a normal growth rate but demonstrated premature fusion into myofibers, resulting in an overall impairment of myofiber formation coupled with a threefold increase in muscle cell apoptosis. These experiments demonstrate a role for Galgt1 in skeletal muscle regeneration and suggest that complex gangliosides made by Galgt1 modulate the survival and differentiation of satellite cells." @default.
• W2167663011 created "2016-06-24" @default.
• W2167663011 creator A5045451244 @default.
• W2167663011 creator A5083328627 @default.
• W2167663011 date "2015-01-01" @default.
• W2167663011 modified "2023-09-23" @default.
• W2167663011 title "A role for Galgt1 in skeletal muscle regeneration" @default.
• W2167663011 cites W1521447037 @default.
• W2167663011 cites W1586159393 @default.
• W2167663011 cites W1735329386 @default.
• W2167663011 cites W1751746490 @default.
• W2167663011 cites W1967755924 @default.
• W2167663011 cites W1969244765 @default.
• W2167663011 cites W1969981779 @default.
• W2167663011 cites W1970055257 @default.
• W2167663011 cites W1973887944 @default.
• W2167663011 cites W1974547730 @default.
• W2167663011 cites W1974732548 @default.
• W2167663011 cites W1982853790 @default.
• W2167663011 cites W1984532339 @default.
• W2167663011 cites W1987980762 @default.
• W2167663011 cites W1991108346 @default.
• W2167663011 cites W1991523935 @default.
• W2167663011 cites W1995681816 @default.
• W2167663011 cites W2003816645 @default.
• W2167663011 cites W2006073788 @default.
• W2167663011 cites W2007577289 @default.
• W2167663011 cites W2010111273 @default.
• W2167663011 cites W2015287703 @default.
• W2167663011 cites W2018600945 @default.
• W2167663011 cites W2019101092 @default.
• W2167663011 cites W2019404217 @default.
• W2167663011 cites W2019563312 @default.
• W2167663011 cites W2022223340 @default.
• W2167663011 cites W2023585072 @default.
• W2167663011 cites W2026728314 @default.
• W2167663011 cites W2029038052 @default.
• W2167663011 cites W2029914169 @default.
• W2167663011 cites W2035337456 @default.
• W2167663011 cites W2037286164 @default.
• W2167663011 cites W2043407398 @default.
• W2167663011 cites W2044677869 @default.
• W2167663011 cites W2044864736 @default.
• W2167663011 cites W2047850625 @default.
• W2167663011 cites W2048954221 @default.
• W2167663011 cites W2051183371 @default.
• W2167663011 cites W2052091909 @default.
• W2167663011 cites W2052555529 @default.
• W2167663011 cites W2053069441 @default.
• W2167663011 cites W2053820753 @default.
• W2167663011 cites W2054963293 @default.
• W2167663011 cites W2057289143 @default.
• W2167663011 cites W2058964204 @default.
• W2167663011 cites W2062593867 @default.
• W2167663011 cites W2063893684 @default.
• W2167663011 cites W2065914048 @default.
• W2167663011 cites W2070936696 @default.
• W2167663011 cites W2072784433 @default.
• W2167663011 cites W2073724408 @default.
• W2167663011 cites W2074163558 @default.
• W2167663011 cites W2077664599 @default.
• W2167663011 cites W2080384465 @default.
• W2167663011 cites W2082101394 @default.
• W2167663011 cites W2082621603 @default.
• W2167663011 cites W2085014866 @default.
• W2167663011 cites W2085979120 @default.
• W2167663011 cites W2091113651 @default.
• W2167663011 cites W2092252579 @default.
• W2167663011 cites W2094191351 @default.
• W2167663011 cites W2094723549 @default.
• W2167663011 cites W2098862614 @default.
• W2167663011 cites W2101900451 @default.
• W2167663011 cites W2105660048 @default.
• W2167663011 cites W2107277218 @default.
• W2167663011 cites W2111462809 @default.
• W2167663011 cites W2124170577 @default.
• W2167663011 cites W2129501942 @default.
• W2167663011 cites W2130630186 @default.
• W2167663011 cites W2133843400 @default.
• W2167663011 cites W2143890380 @default.
• W2167663011 cites W2146774835 @default.
• W2167663011 cites W2150107400 @default.
• W2167663011 cites W2154041187 @default.
• W2167663011 cites W2154066388 @default.
• W2167663011 cites W2156565513 @default.
• W2167663011 cites W2157735441 @default.
• W2167663011 cites W2164316354 @default.
• W2167663011 cites W2165261456 @default.
• W2167663011 cites W2165645269 @default.
• W2167663011 cites W2166371391 @default.
• W2167663011 cites W2168058510 @default.
• W2167663011 cites W2172139714 @default.
• W2167663011 cites W2192080449 @default.
• W2167663011 cites W2321280241 @default.
• W2167663011 cites W954700306 @default.
• W2167663011 doi "https://doi.org/10.1186/s13395-014-0028-0" @default.
• W2167663011 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4333175" @default.
• W2167663011 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25699169" @default.

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