We are analyzing https://link.springer.com/article/10.1007/s10974-013-9350-0.

Title:
Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy | Journal of Muscle Research and Cell Motility
Description:
Abnormal intracellular Ca2+ handling is an important factor in the progressive functional decline of dystrophic muscle. In the present study, we investigated the function of sarco(endo)plasmic reticulum (SR) Ca2+ ATPase (SERCA) in various dystrophic muscles of mouse models of Duchenne muscular dystrophy. Our studies show that the protein expression of sarcolipin, a key regulator of the SERCA pump is abnormally high and correlates with decreased maximum velocity of SR Ca2+ uptake in the soleus, diaphragm and quadriceps of mild (mdx) and severe (mdx:utr−/−) dystrophic mice. These changes are more pronounced in the muscles of mdx:utr−/− mice. We also found increased expression of SERCA2a and calsequestrin specifically in the dystrophic quadriceps. Immunostaining analysis further showed that SERCA2a expression is associated both with fibers expressing slow-type myosin and regenerating fibers expressing embryonic myosin. Together, our data suggest that sarcolipin upregulation is a common secondary alteration in all dystrophic muscles and contributes to the abnormal elevation of intracellular Ca2+ concentration via SERCA inhibition.
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Topics {✒️}

sarcoplasmic-endoplasmic-reticulum ca2+-atpase month download article/chapter store-operated ca2+ entry fast-twitch skeletal muscles sarcoplasmic reticulum ca-atpase duchenne muscular dystrophy global/temporal gene expression excitation-contraction coupling alterations serca-type pumps sr ca2+ uptake sarcoplasmic reticulum function calcium leak channels enhanced ca2+ transport related subjects full article pdf intracellular ca2+ concentration utrophin-dystrophin-deficient mice severe muscular dystrophy muscular dystrophy association increased calcium influx sarcolipin inhibits sarco fast muscle fibers found increased expression increased sarcolipin expression calcium-dependent proteolysis privacy choices/manage cookies slow skeletal muscles tupling ar dystrophin-related protein dystrophin-deficient mdx mice muscular dystrophy differential gene expression mdx muscle fibers cell motility aims calcium transport sarcolipin knockdown therapy serca pump isoforms mice lacking utrophin sarcolipin-null mice muscle cell surface ca2+ atpase mdx mouse muscle check access instant access european economic area progressive functional decline common secondary alteration hoffman ep van der poel colson-van schoor

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         headline:Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy
         description:Abnormal intracellular Ca2+ handling is an important factor in the progressive functional decline of dystrophic muscle. In the present study, we investigated the function of sarco(endo)plasmic reticulum (SR) Ca2+ ATPase (SERCA) in various dystrophic muscles of mouse models of Duchenne muscular dystrophy. Our studies show that the protein expression of sarcolipin, a key regulator of the SERCA pump is abnormally high and correlates with decreased maximum velocity of SR Ca2+ uptake in the soleus, diaphragm and quadriceps of mild (mdx) and severe (mdx:utr−/−) dystrophic mice. These changes are more pronounced in the muscles of mdx:utr−/− mice. We also found increased expression of SERCA2a and calsequestrin specifically in the dystrophic quadriceps. Immunostaining analysis further showed that SERCA2a expression is associated both with fibers expressing slow-type myosin and regenerating fibers expressing embryonic myosin. Together, our data suggest that sarcolipin upregulation is a common secondary alteration in all dystrophic muscles and contributes to the abnormal elevation of intracellular Ca2+ concentration via SERCA inhibition.
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      headline:Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy
      description:Abnormal intracellular Ca2+ handling is an important factor in the progressive functional decline of dystrophic muscle. In the present study, we investigated the function of sarco(endo)plasmic reticulum (SR) Ca2+ ATPase (SERCA) in various dystrophic muscles of mouse models of Duchenne muscular dystrophy. Our studies show that the protein expression of sarcolipin, a key regulator of the SERCA pump is abnormally high and correlates with decreased maximum velocity of SR Ca2+ uptake in the soleus, diaphragm and quadriceps of mild (mdx) and severe (mdx:utr−/−) dystrophic mice. These changes are more pronounced in the muscles of mdx:utr−/− mice. We also found increased expression of SERCA2a and calsequestrin specifically in the dystrophic quadriceps. Immunostaining analysis further showed that SERCA2a expression is associated both with fibers expressing slow-type myosin and regenerating fibers expressing embryonic myosin. Together, our data suggest that sarcolipin upregulation is a common secondary alteration in all dystrophic muscles and contributes to the abnormal elevation of intracellular Ca2+ concentration via SERCA inhibition.
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