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GROWTH HORMONES.
Term Paper ID:24511
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Essay Subject:
Analyzes research into technical effects of hormones on skeletal muscle cells of animals.... More...
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6 Pages / 1350 Words
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Paper Abstract:
Analyzes research into technical effects of hormones on skeletal muscle cells of animals.
Paper Introduction:
GROWTH HORMONES/FACTORS & MUSCLE CELLS
Abstract
Skeletal muscle contains cells that are critical for growth and regeneration of the muscle; this is of particular importance after injury. Growth hormones and growth factors are studied for their effects on skeletal muscle satellite cells. Different studies demonstrate mediated aspects and combined effects. Findings show that GH and IGF-I affect satellite cell proliferation and FGF signals are mediated through several alternatively spliced variants of FGFR1.
Introduction
Skeletal muscle contains myogenic precursor cells that are critical for muscle growth and regeneration. Growth hormone (GH) has been shown to play a role in the promotion of growth of
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The effects of growthhormone on avian skeletal muscle satellite cell proliferation anddifferentiation. It is concluded that in avian skeletal muscle satellite cells,some of the GH actions are independent of IGF-I. Hodik, Mett, and Halevy state that chicken satellite cells aresensitive to low concentrations of bFGF and maxima mitogenic response isachieved at .5-1. FGFs have been shown tohave varied actions within primary and permanent skeletal myoblastpopulations. Whichmembers of the fibroblast growth factor receptor (FGFR) family are involvedin skeletal muscle development and in myoblast-mediated regeneration ofmuscle following injury, is now known. This study presented descriptive and experimental baselinefor the FGF receptor types with their behavior during skeletal musclegrowth and terminal differentiation, at the level of RNA transcripts. Genomic PCR clones were isolated. Methodology Halevy, Hodik, and Mett studied the expression of chicken GH-R mRNAin muscle and cultured satellite cells, and effects of recombinant cGH onchicken skeletal muscle satellite cell proliferation and differentiation.Materials included male broiler chicks, chicken skeletal muscle satellitecells were cultured from pectoral muscle. Also studied was theinteractions of chicken GH (cGH) with basic fibroblast growth factor (bFGF)and insulin-like growth factor I (IGF-I) (Hodik, Mett, & Halevy, 1997).Templeton and Hauschka (1992) studied FGFR transcripts in a mouse skeletalmyoblast cell line during growth and terminal differentiation. Attempts to study of these factorsincludes investigation of growth hormone receptor (GH-R) mRNA in avianskeletal muscle tissue and satellite cells in culture and its capability ofbinding cGH (Halevy, Hodik, & Mett, 1996). Although it has been shown that GH affect skeletal muscle satellitecell proliferation and differentiation, and it is known that FGFs and FGFreceptors play major roles in control of skeletal muscle growth anddifferentiation, more understanding is needed for their roles. They analyzed effects ofvarious concentrations and found that the addition of a very lowconcentration of bFGF ( .1 ng/ml) increased mRNA expression levels of cGH-Rby almost a twofold compared to untreated controls. DifferentiatedMM14 myocytes and quiescent DD-1 cells were from switching cell cultures tolow serum medium lacking bFGF. GH inducedinsulin-like growth factor I (IGF-I) mRNA which is a potential factor forsatellite cell proliferation and differentiation; it inhibited geneexpression of myogenin and expression of muscle-specific proteins. Cells were treated with variousfactors. Effects on the expression of theirreceptors' genes and satellite cell proliferation were studied. ng/ml of the growth factor. DNA synthesis was assessed bythymidine incorporation. Heparin-binding FGFs show aconstellation of physiological actions which include skeletal muscleregeneration and repression of skeletal myoblast differentiation. (1992). Binding to its receptor, FGFtriggers a cascade of events (Hodik, Mett, & Halevy, 1997; & Templeton &Hauschka, 1992). Duringthe process of muscle cell differentiation, FGF receptors disappear fromthe cell surface and gene transcription is decreased. Each study adds a new piece to the puzzle, however,comprehensive understanding of the problem has not been reached. Different studies demonstrate mediatedaspects and combined effects. DNA synthesis wasassessed by thymidine incorporation. Hodik, V., Mett, A., & Halevy, O. GROWTH HORMONES/FACTORS & MUSCLE CELLS Abstract Skeletal muscle contains cells that are critical for growth andregeneration of the muscle; this is of particular importance after injury.Growth hormones and growth factors are studied for their effects onskeletal muscle satellite cells. The authors state that inhibitory effects of cGH onproliferation and differentiation of satellite cells can't be due to IGF-Iaction because of the latter's role in enhancing muscle satellite cellproliferation in turkey, chicken, and rat. Enzyme activity was determined with a commercialkit; for creatine kinase assay, satellite cells were seeded in 6 -mmculture dishes and sonicated at the end of the incubation period.Sarcomeric myosin expression was performed. Developmental Biology, 154, 169-181.----------------------- 8 Bothfactors increased cGH-R mRNA expression levels and further increases werenoted when both factors were added together. Stimulatory effects betweenbFGF and GH may lead to the addition of more satellite cell nuclei togrowing muscle. This may suggest themediation of FGF's effects via its receptors. General and Comparative Endocrinology, 1 1, 43-52. This was not the case with bFGF; cGH and bFGF affect eachother and have mutual effects on satellite cell proliferation. Results Halevy, Hodik, and Mett report findings that GH-R gene expression wasregulated by cGH and it correlated with GH effect on cell proliferation.Results showed that 2-1 ng/ml hormone increased GH-R mRNA and DNAsynthesis and higher concentrations decreased these effects. Combinations of cGH and bFGFwere analyzed with DNA syntheses; a correlation between thymidineincorporation to DNA and satellite cell number upon exposure to growthfactors suggested thymidine incorporation was a marker for cellproliferation. Discussion Templeton and Hauschka concluded that FGF signals involved inskeletal muscle proliferation and repression of terminal differentiationare mediated through several alternatively spliced variants of FGFR1; inthe MM14 mouse myoblast system, myoblasts expressed FGFR1 and FGFR2 mRNAwas indetectable.The authors suggest that during development distinct classes of myoblastsexist with respect to FGFRs that they express. The dominate FGFR1 transcripts contained threeimmunoglobulin-like domains in the extracellular ligand binding region.Cloning of mouse genomic DNA surrounding the region of the FGFR1 6-ntdeletion shows that the deletion is from alternative splicing of FGFR1transcripts. Templeton and Hauschka found that MM14 cells expressed transcriptsfor FGFR1 but not FGFR2. Satellite cells were cultured; binding of I-hGH to the cells wasperformed. Bothdemonstrated effects, and combinations increased effects. Results implied thatbFGF affects GH activity via modulation of its receptor expression and thefactors may function together. It appearsthat the information offered points to the conclusion that effects aremediated by their own and other peptide's receptors which are possiblyregulated at the postranscriptional level. Total RNA from tissue culture cells was isolated.Also performed were transcription reactions to generate antisenseradiolabeled RNA probe. FGF-mediated aspects ofskeletal muscle growth and differentiation are controlled by a highaffinity receptor, FGFR1. Findings show that GH and IGF-I affectsatellite cell proliferation and FGF signals are mediated through severalalternatively spliced variants of FGFR1. Observations led to theconclusion that cGH's effect on satellite cell differentiation is IGH-I-independent (shown in mammalian and avian species). (1997). Findings showed that cGH inhibited theexpression and activity of muscle regulatory and specific genes in a dose-dependent manner. Fibroblast growth factor (FGF) is a factor in satellite cellmyogenesis for mammals and chickens; it is found to be the most potentinhibitor of myoblast differentiation. Analysis of variance determined differences between treatments. RNA blot analysis and RNase protectionassays were included. Templeton, T., & Hauschka, S. Introduction Skeletal muscle contains myogenic precursor cells that are criticalfor muscle growth and regeneration. It has also been shownthat GH involvement in rat muscle regeneration was independent of local IGF-I levels; opposite effects of GH and IGF-I have been found in other aviantissues. GHadministrated to pigs, ruminants, and humans has been found to increaseskeletal muscle growth. Mutual effects of growthhormone and growth factors on avian skeletal muscle satellite cells.General and Comparative Endocrinology, 1 8, 161-17 . Earlier studies showed that cGH affects chicken skeletal musclesatellite cell proliferation and differentiation, the study by Hodik, Mett,and Halevy described interactions of cGH with bFGF and IGF-I. Templeton and Hauschka used murine 3T3-D1 cells for their study. In chicken satellite cells, IGF-I mRNA expressionlevels were found to be induced by cGH; this agrees with findings in ratskeletal muscle cells. Satellite cells are found beneath the basallamina; when activated by signals which are not completely understood, theyundergo proliferation and terminal differentiation to form new myofibers orfuse into others (Halevy, Hodik, & Mett, 1996; & Hodik, Mett, & Halevy,1997). References Halevy, O., Hodik, V., & Mett, A. Allcell lines were grown on gelatin-coated culture dishes. Hodik, Mett, and Halevy used male broiler chicks; skeletal musclesatellite cells were cultured from the pectoral muscle. (1996). The later study by Halevy, Hodik, and Mett reported further on theeffects of growth hormone on avian skeletal muscle satellite cellproliferation and differentiation. Addition of IGF-I to satellite cells did not affect cGH-RmRNA expression levels compared to controls; however levels of IGF-I weremitogenic to cells dose-dependently. Total RNA was isolated withguanidinium thiocyanate-phenol technique; hybridization was performed over-night. This suggested an inhibitory role in chicken satellitecell differentiation. Growth hormone (GH) has been shown toplay a role in the promotion of growth of skeletal muscle in mammals. Total RNA was isolated with guanidinium-thiocyanate-phenoltechnique. These resultsshow that cGH may act independently of IGF-I in chicken skeletal musclesatellite cells. This study showed GH-Rgene expression decreased during satellite cell differentiation; it wasassumed that GH-R mRNA expression in whole muscle is represented byproliferating satellite cell fraction.
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