- 0.1 The Science Behind Satellite Cell Functions!
- 0.1.0.1 Sources.
- 0.1.0.2 Mauro Satellite cells of skeletal muscle fibres
- 0.1.0.3 Biophys. Biochem. Cytol., 9 (1961), pp. 493–496Kitamura T, Kitamura YI, Funahashi Y, Shawber CJ, Castrillon DH, Kollipara R, DePinho RA, Kitajewski J, Accili D. J Clin Invest. 2007 Sep;117(9):2477-85.
- 0.1.0.4 Maroto M, Reshef R, Münsterberg AE, Koester S, Goulding M, Lassar AB. Cell. 1997 Apr 4;89(1):139-48.
- 0.1.0.5 Laclef C, Hamard G, Demignon J, Souil E, Houbron C, Maire P. Development. 2003 May;130(10):2239-52.
- 0.1.0.6 Zakaria S, Mao Y, Kuta A, Ferreira de Sousa C, Gaufo GO, McNeill H, Hindges R, Guthrie S, Irvine KD, Francis-West PH. Curr Biol. 2014 Jul 21;24(14):1620-7. doi: 10.1016/j.cub.2014.05.067. Epub 2014 Jul 3.
- 1 Know why PERFORMANCE PROBIOTIC gets our GOLDEN DUMBELL OF APPROVAL seal
The Science Behind Satellite Cell Functions!
Author: Ivan Solis
There is more to muscle than meets the eye the science behind muscular development is a complex one composed of a multiple mechanism and interconnecting networks working toward our simple daily function. This Article is to inform the audience of satellite cells and its correlation to the regeneration and reproduction process along with an illustration of the mechanism of satellite cells and it’s seven determinants functioning as the Delamination, Migration, Proliferation including Determination and Differentiation, next to specific muscle formation and satellite cells as well as a brief summary of Myonuclei following injury or micro trauma and it’s correlation to the regenerative machismo.
Before we commence I know what you might be thinking not this science again however I suggest you continue with the article there is actually some useful information here now let’s jump into business.
(Mauro, 1961) explains (Satellite cell) are dormant harbingering forming culture under the (basal lamina) the lateral walls of the (neural tube) dorsal tubular structure in the vertebrate embryo that develops into the brain and spinal cord when myofibers have contraction the skeletal muscle generates a large storage of (syncytial cell) a multinucleated cells that can result from multiple cell fusions of uninuclear cells, each cell containing hundreds of (Mammalian Myonuclei) the exterior film outside the myofibers however they are different they cannot regenerate themselves like syncytial cells myofibrils are usually stable as a tissue after injury regeneration via activation and reproduction of satellite cells through the immune system this process is understood as (Myogenesis) it’s myoblast acting as a fuse that signals the myonuclei to repair injured muscle tissue. (Bischoff 1990) Contributes the regeneration of Damaged Muscle – Satellite cell are involved in the regeneration of damaged muscle fibers when muscle fiber undergo trauma injured myofibers regress and diminish SC related to diminishing myofibres and myofibres are activated to return to the cell cycle and proliferate and differentiate thus causing the regeneration of the muscles even the slightest damage can induce the proliferation of SC. (Orimo 1991) shares the proximal activating signal for SC activation is not known however and interesting observation has been made that hepatocyte growth factor (HGF) the ligand for the c-met receptor tyrosine kinase is a the strongest candidate because it is sequestered in the myofibre ECM and proliferate upon injury.
This sounds like the perfect hormone I don’t if you guys missed that but (HGF) hepatocyte growth factor can induce satellite cell and we’ve now reviewed that SC is the key to regeneration of damaged muscle!!!
Moreover (Mauro, 1961) contributes regeneration and reproduction process is due to genetic factor the core of the mechanism of satellite cells if any factor is missing muscle growth wouldn’t be possible each factor play a significant role in muscle growth the mechanism is composed of seven determinates the Delamination, Migration, Proliferation in addition to Determination and Differentiation, next to specific muscle formation and satellite cells.
(Maroto 1997) contributes that denomination is Pax3 this what activates MyoD expression Scatter factor and fibroblast growth factor are what control the migration of delamination. Genetic factors that are interconnected with migration function as LBX1, c-Met and Hgf. LBX1 (ladybird homeobox 1) is a key regulator of cell migration LBX1 developed the organization of the muscles in the dorsal for limbs as well as the movements of the dorsal muscles into the limb leading to delamination. Hgf (Hepatocyte growth factor) is another genetic factor that regulates cell growth and it’s cell migration through the immune system and morphogenesis the (formation of new cells that binds to the c-Met receptor) correlated to tissue regeneration.
Proliferation is Mox2 (mesenchyme homeobox 2) if disturbed it would prevent the reproduction of the myogenic precursors and would result in muscular deformation Myf5 is essential in aiding myoblast it’s the regulating gene factor in myogenesis.
Furthermore (Laclef 2003) indicates that determination is correlated to Myf-5 (myogenic factor 5) and MyoD (myogenic determination protein 1) this is one of the most important requirements myogenesis undergoes both myoD and Myf5 are members of the (Myogenic bHlh) basic helix-loop-helix a protein transcript factor if inactive there would no skeletal muscle this indicates the importance of each genetic factor for muscular development.
Moreover (Kitamura 2007) explains differentiation a genetic factor that’s interconnected with Myogenin Mcf2, Six, MyoD and Myf6 removing of these genetic factors would result in nearly complete loss of muscle fibers and an ample loss of the skeletal muscle mass geared towards the lateral and ventral walls of the body.
Myogenin (myogenic factor 4) is a genetic factor correlated to the skeletal muscle and the myogenesis process it’s essential to the fusion of myogenic and newly split cells or pre-existing myofibrils myogenin is essential in the development of functional skeletal muscle. Myogenin is required for the fusion of myogenic precursor cells to either new or previously existing fibers during the process myogenin and has been observed to induce myogenesis in non-muscle cell type as well. Mcf2 (MCF.2 cell line derived transforming sequence) is a nucleotide exchange factor proteins that stimulate the exchange bound to other proteins, (Laclef 2003) indicates Six (Transmembrane Epithelial Antigen Of Prostate 1) is a gene found in the prostate tissue, MyoD (Family inhibitor) is a transcription factor that negatively regulates myogenic family proteins it interferes with myogenic factors by masking (NLS) nuclear localization the amino acid fusion that binds to proteins that import into the cell nucleus via nuclear transport this consist of one or more short positive charges on the protein surface so MyoD’s negative regulation would prevent DNA binding also Myf6 (Herculin) Myogenic Factor 6 it’s another indispensable regulatory factor in the myogenesis process.
In Final analysis (Maroto 1997) adds Specific muscle formulation genetic factors interconnected are LBX1 and Mox2 removal of Lbx1 would result in glitching the exterior hind limbs muscles and Mox2 removal would result in unnatural patterning of limb muscles and will cause an ample reduction in myofibrils along with Satellite cells genetic factor interconnected are the Pax7 removal of these factors will prevent the formation of satellite cells and in turn hurt muscle growth. I hope the audience has gained a better understand of satellite cells and its correlation to the regeneration and reproduction process along with a clear understanding of the mechanism of satellite cells and it’s seven determinants functioning as the Delamination, Migration, Proliferation along with Determination and Differentiation, conjointly to specific muscle formation and satellite cells and it’s interaction with muscle growth.
Mauro Satellite cells of skeletal muscle fibres
Biophys. Biochem. Cytol., 9 (1961), pp. 493–496Kitamura T, Kitamura YI, Funahashi Y, Shawber CJ, Castrillon DH, Kollipara R, DePinho RA, Kitajewski J, Accili D. J Clin Invest. 2007 Sep;117(9):2477-85.
Maroto M, Reshef R, Münsterberg AE, Koester S, Goulding M, Lassar AB. Cell. 1997 Apr 4;89(1):139-48.
Laclef C, Hamard G, Demignon J, Souil E, Houbron C, Maire P. Development. 2003 May;130(10):2239-52.
Zakaria S, Mao Y, Kuta A, Ferreira de Sousa C, Gaufo GO, McNeill H, Hindges R, Guthrie S, Irvine KD, Francis-West PH. Curr Biol. 2014 Jul 21;24(14):1620-7. doi: 10.1016/j.cub.2014.05.067. Epub 2014 Jul 3.