scholarly journals Manganese influx and expression of ZIP8 is essential in primary myoblasts and contributes to activation of SOD2

2018 ◽  
Author(s):  
Shellaina J. V. Gordon ◽  
Daniel E. Fenker ◽  
Katherine E. Vest ◽  
Teresita Padilla-Benavides
Keyword(s):  
Skeletal Muscle ◽  
Trace Elements ◽  
Second Messengers ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Metal Transporters ◽  
Primary Myoblasts ◽  
Zip Family ◽  
Enzyme Cofactors ◽  
Functional Relevance

ABSTRACTTrace elements such as copper (Cu), zinc (Zn), iron (Fe), and manganese (Mn) are enzyme cofactors and second messengers in cell signaling. Trace elements are emerging as key regulators of differentiation and development of mammalian tissues including blood, brain, and skeletal muscle. We previously reported an influx of Cu and dynamic expression of various metal transporters during differentiation of skeletal muscle cells. Here, we demonstrate that during differentiation of skeletal myoblasts an increase of additional trace elements such as Mn, Fe and Zn occurs. Interestingly the Mn increase is concomitant with increased Mn-dependent SOD2 levels. To better understand the Mn import pathway in skeletal muscle cells, we probed the functional relevance of the closely related proteins ZIP8 and ZIP14, which are implicated in Zn, Mn, and Fe transport. Partial depletion of ZIP8 severely impaired growth of myoblasts and led to cell death under differentiation conditions, indicating that ZIP8-mediated metal transport is essential in skeletal muscle cells. Moreover, knockdown of Zip8 impaired activity of the Mn-dependent SOD2. Growth defects were partially rescued by Mn supplementation to the medium, suggesting additional functions for ZIP8 in the skeletal muscle lineage. Knockdown of Zip14, on the other hand, had only a mild effect on myotube size, consistent with a role for ZIP14 in muscle hypertrophy. This is the first report on the functional relevance of two members of the ZIP family of metal transporters in the skeletal muscle lineage, and further supports the paradigm that trace metal transporters are critical modulators of mammalian tissue development.

scholarly journals Manganese influx and expression of ZIP8 is essential in primary myoblasts and contributes to activation of SOD2

Metallomics ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1140-1153 ◽  
Author(s):  
Shellaina J. V. Gordon ◽  
Daniel E. Fenker ◽  
Katherine E. Vest ◽  
Teresita Padilla-Benavides
Keyword(s):  
Trace Elements ◽  
Cell Signaling ◽  
Second Messengers ◽  
Primary Myoblasts ◽  
Enzyme Cofactors

Trace elements such as copper (Cu), zinc (Zn), iron (Fe), and manganese (Mn) function as enzyme cofactors and second messengers in cell signaling.

scholarly journals Aldosterone- and testosterone-mediated intracellular calcium response in skeletal muscle cell cultures

2000 ◽  
Vol 279 (1) ◽  
pp. E132-E139 ◽  
Author(s):  
Manuel Estrada ◽  
José Luis Liberona ◽  
Manuel Miranda ◽  
Enrique Jaimovich
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Second Messengers ◽  
Calcium Transient ◽  
Muscle Cells ◽  
Cell Types ◽  
Skeletal Muscle Cells ◽  
Calcium Signal ◽  
Cell Nuclei ◽  
Acetoxymethyl Ester

Fast nongenomic steroid actions in several cell types seem to be mediated by second messengers such as intracellular calcium ([Ca2+]i) and inositol 1,4,5-trisphosphate (IP3). We have shown the presence of both slow calcium transients and IP3 receptors associated with cell nuclei in cultured skeletal muscle cells. The effect of steroids on [Ca2+]i was monitored in Fluo 3-acetoxymethyl ester-loaded myotubes by either confocal microscopy or fluorescence microscopy, with the use of out-of-focus fluorescence elimination. The mass of IP3 was determined by radioreceptor displacement assay. [Ca2+]ichanges after either aldosterone (10–100 nM) or testosterone (50–100 nM) were observed; a relatively fast (<2 min) calcium transient, frequently accompanied by oscillations, was evident with both hormones. A slow rise in [Ca2+]i that reached its maximum after a 30-min exposure to aldosterone was also observed. Calcium responses seem to be fairly specific for aldosterone and testosterone, because several other steroid hormones do not induce detectable changes in fluorescence, even at 100-fold higher concentrations. The mass of IP3 increased transiently to reach two- to threefold the basal level 45 s after addition of either aldosterone or testosterone, and the IP3transient was more rapid than the fast calcium signal. Spironolactone, an inhibitor of the intracellular aldosterone receptor, or cyproterone acetate, an inhibitor of the testosterone receptor, had no effect on the fast [Ca2+]i signal or in the increase in IP3 mass. These signals could mean that there are distinct nongenomic pathways for the action of these two steroids in skeletal muscle cells.

Extracts of Hymenocardia acida ameliorate insulin resistance in skeletal muscle cells

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
II Ezeigbo ◽  
C Wheeler-Jones ◽  
S Gibbons ◽  
ME Cleasby
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Ameliorate Insulin Resistance

TGFß regulates metabolism of human skeletal muscle cells by miRNAs

2018 ◽  
Author(s):  
S Höckele ◽  
P Huypens ◽  
C Hoffmann ◽  
T Jeske ◽  
M Hastreiter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells

scholarly journals Annexins and Membrane Repair Dysfunctions in Muscular Dystrophies

2021 ◽  
Vol 22 (10) ◽  
pp. 5276
Author(s):  
Coralie Croissant ◽  
Romain Carmeille ◽  
Charlotte Brévart ◽  
Anthony Bouter
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Genetic Disorders ◽  
Muscle Cells ◽  
Cell Types ◽  
Clinical Severity ◽  
Skeletal Muscle Cells ◽  
Muscular Dystrophies ◽  
Membrane Repair ◽  
Human Skeletal Muscle Cells

Muscular dystrophies constitute a group of genetic disorders that cause weakness and progressive loss of skeletal muscle mass. Among them, Miyoshi muscular dystrophy 1 (MMD1), limb girdle muscular dystrophy type R2 (LGMDR2/2B), and LGMDR12 (2L) are characterized by mutation in gene encoding key membrane-repair protein, which leads to severe dysfunctions in sarcolemma repair. Cell membrane disruption is a physiological event induced by mechanical stress, such as muscle contraction and stretching. Like many eukaryotic cells, muscle fibers possess a protein machinery ensuring fast resealing of damaged plasma membrane. Members of the annexins A (ANXA) family belong to this protein machinery. ANXA are small soluble proteins, twelve in number in humans, which share the property of binding to membranes exposing negatively-charged phospholipids in the presence of calcium (Ca2+). Many ANXA have been reported to participate in membrane repair of varied cell types and species, including human skeletal muscle cells in which they may play a collective role in protection and repair of the sarcolemma. Here, we discuss the participation of ANXA in membrane repair of healthy skeletal muscle cells and how dysregulation of ANXA expression may impact the clinical severity of muscular dystrophies.

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