Ca2+-independent phospholipase A2 enhances store-operated Ca2+ entry in dystrophic skeletal muscle fibers

Boittin, François-Xavier; Petermann, Olivier; Hirn, Carole; Mittaud, Peggy; Dorchies, O.M.; Roulet, E.; Rüegg, Urs T.

doi:10.1242/jcs.03184

Cited by 115 publications

(103 citation statements)

References 56 publications

(95 reference statements)

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“…These studies and others led to the hypothesis that the DAPC may control TRPC-MS/ SOC channels at the sarcolemma and that is involved in regulating subsarcolemmal calcium concentration. These channels could be regulated directly in normal cells by the presence of the DAPC, which could explain the enhanced SOCE observed in dystrophin-deficient muscles (29,30). In accordance with this idea, we recently reported that when transfected in dystrophin-deficient myotubes, recombinant mini-dystrophin or ␣1-syntrophin forms a complex with TRPC1 channels and restores normal divalent cation entry after store depletion (7).…”

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confidence: 58%

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Sabourin

Lamiche

Vandebrouck

et al. 2009

Journal of Biological Chemistry

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The dystrophin-associated protein complex (DAPC) is essential for skeletal muscle, and the lack of dystrophin in Duchenne muscular dystrophy results in a reduction of DAPC components such as syntrophins and in fiber necrosis. By anchoring various molecules, the syntrophins may confer a role in cell signaling to the DAPC. Calcium disorders and abnormally elevated cation influx in dystrophic muscle cells have suggested that the DAPC regulates some sarcolemmal cationic channels. We demonstrated previously that minidystrophin and ␣1-syntrophin restore normal cation entry in dystrophin-deficient myotubes and that sarcolemmal TRPC1 channels associate with dystrophin and the bound PDZ domain of ␣1-syntrophin. This study shows that small interfering RNA (siRNA) silencing of ␣1-syntrophin dysregulated cation influx in myotubes. Moreover, deletion of the PDZcontaining domain prevented restoration of normal cation entry by ␣1-syntrophin transfection in dystrophin-deficient myotubes. TRPC1 and TRPC4 channels are expressed at the sarcolemma of muscle cells; forced expression or siRNA silencing showed that cation influx regulated by ␣1-syntrophin is supported by TRPC1 and TRPC4. A molecular association was found between TRPC1 and TRPC4 channels and the ␣1-syntrophin-dystrophin complex. TRPC1 and TRPC4 channels may form sarcolemmal channels anchored to the DAPC, and ␣1-syntrophin is necessary to maintain the normal regulation of TRPC-supported cation entry in skeletal muscle. Cation channels with DAPC form a signaling complex that modulates cation entry and may be crucial for normal calcium homeostasis in skeletal muscles.

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mentioning

confidence: 58%

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Sabourin

Lamiche

Vandebrouck

et al. 2009

Journal of Biological Chemistry

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“…junctions (41) and growing evidence for iPLA 2 ␤ to be an equally important component for SOCE in a variety of cell types (11,32,33,(42)(43)(44)(45)(46)(47)(48)(49), strongly suggests that additional molecules, functional steps, and signaling events (in ER, at PM, and in between) may be involved in the SOCE pathway. Although direct coupling of ER-resident STIM1 to PM-resident Orai1 may be right- fully considered as the easiest possible way of signal transduction, the functional unit of SOCE is certainly a more complex phenomenon, which is far from being understood.…”

Section: Resultsmentioning

confidence: 99%

Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Csutora¹,

Peter²,

Kilic

et al. 2008

Journal of Biological Chemistry

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STIM1 has been recently identified as a Ca 2؉ sensor in endoplasmic reticulum (ER) and an initiator of the store-operated Ca 2؉ entry (SOCE) pathway, but the mechanism of SOCE activation remains controversial. Here we focus on the early ERdelimited steps of the SOCE pathway and demonstrate that STIM1 is critically involved in initiating of production of calcium influx factor (CIF), a diffusible messenger that can deliver the signal from the stores to plasma membrane and activate SOCE. We discovered that CIF production is tightly coupled with STIM1 expression and requires functional integrity of its intraluminal sterile ␣-motif (SAM) domain. We demonstrate that 1) molecular knockdown or overexpression

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“…The relationship between OS and frailty could be explained by several hypotheses. First, OS may lead to musculoskeletal system damage due to the fact that OS increase intracellular calcium promoting proteasomal activity and accelerating muscle breakdown, and ROS may trigger the apoptosis of murine skeletal muscle, and decrease myoblast proliferation (12,31). These factors may contribute to a decline in muscle function and strength.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress and frailty: A systematic review and synthesis of the best evidence

et al. 2017

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Highlights There is a lack of clarity around the relationship between oxidative stress and frailty.  Our review provides some cross sectional evidence of increased oxidative stress among frail older people.  There is some preliminary evidence of lower anti-oxidant parameters (vitamin C, E, α-tocopherol, biological anti-oxidant potential, total thiol levels) in frailty. ABSTRACT (250/250)Objective: Oxidative stress (OS) is associated with accelerated aging. Previous studies have suggested a possible relationship between OS and frailty but this association remains unclear.We conducted a systematic review to investigate potential interactions between OS and frailty.Methods: A systematic literature search of original reports providing data on 'OS and antioxidant' parameters and frailty was carried out across major electronic databases from inception until May 2016. Cross-sectional/case control and longitudinal studies reporting data on the association between frailty and anti-oxidants-OS biomarkers were considered for inclusion. Results were summarized with a best-evidence based synthesis.Results: From 1,856 hits, 8 studies (cross-sectional/case control) were included (N=6,349; mean age of 75±12 years; 56.4% females). Overall, there were 588 (=9.3%) frail, 3,036 prefrail (=47.8%), 40 (=0.6%) pre-frail/robust, and 2,685 (=42.3%) robust subjects. Six crosssectional/case control studies demonstrated that frailty was associated with an increase in peripheral OS biomarkers including lipoprotein phospholipase A2 (studies=1), isoprostanes (studies=2), Malonaldehyde (studies=2), 8-hydroxy-20-deoxyguanosine (studies=2), derivate of reactive oxygen metabolites (studies=2), oxidized Glutathione/ Glutathione (studies=1), 4-hydroxy-2,3-nonenal (studies=1), and protein carbonylation levels (study=1). In addition, preliminary evidence points to lower anti-oxidant parameters (vitamin C, E, α-tocopherol, biological anti-oxidant potential, total thiol levels) in frailty. Conclusion:Frailty and pre-frailty appear to be associated with higher OS and possibly lower anti-oxidant parameters. However, due to the cross sectional design, it is not possible to disentangle the directionality of the relationships observed. Thus, future high quality and in particular longitudinal research is required to confirm/refute these relationships and to further elucidate pathophysiological mechanisms.

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Ca2+-independent phospholipase A2 enhances store-operated Ca2+ entry in dystrophic skeletal muscle fibers

Cited by 115 publications

References 56 publications

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

Novel Role for STIM1 as a Trigger for Calcium Influx Factor Production

Oxidative stress and frailty: A systematic review and synthesis of the best evidence

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