scholarly journals Growth factors improve the proliferation of Jeju black pig muscle cells by regulating MyoD and growth-related genes

2020 ◽  
Author(s):  
Jinryong Park ◽  
Jeongeun Lee ◽  
Ki-Duk Song ◽  
Sung-Jo Kim ◽  
Dae Cheol Kim ◽  
...  
Keyword(s):  
Growth Factors ◽  
Muscle Cells ◽  
Pig Muscle

scholarly journals Growth factors improve the proliferation of Jeju black pig muscle cells by regulating MyoD and growth-related genes

2020 ◽  
Author(s):  
Jinryong Park ◽  
Jeongeun Lee ◽  
Ki-Duk Song ◽  
Sung-Jo Kim ◽  
Hyun Woo Choi ◽  
...  
Keyword(s):  
Growth Factors ◽  
Culture Media ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Culture Conditions ◽  
Concurrent Use ◽  
Korean Native Pig ◽  
Pig Muscle ◽  
Differentiation And Proliferation ◽  
Relationship Of

Abstract Background Jeju black pig (JBP), one of Korean native pig breeds, has excellent meat quality but grow slowly. The growth rate of pigs is related to differentiation and proliferation of muscle cells regulated by growth factors and expression of growth-related genes. However, few studies have determined the effect of growth factors on the proliferation of porcine muscle cells. Thus, the objective of this study was to establish optimal culture conditions of JBP muscle cells and determine the relationship of various factors involved in muscle growth with the proliferation of JBP muscle cells. Results We established a muscle cell line from JBP embryos and optimized its culture conditions. These muscle cells were positive for MyoD, but not Pax7. The proliferation rate of these muscle cells was significantly higher in a culture medium containing bFGF and EGF + bFGF than that without a growth factor or containing EGF alone. Treatment with EGF and bFGF significantly induced the expression of MyoD protein, an important transcription factor in muscle cells. Moreover, we checked changes of the expression of growth-related genes in JBP muscle cells by presence or absence of growth factors. Expression level of COL21A1 gene was changed only when EGF and bFGF were both added to culture media for JBP muscle cells. Conclusions Concurrent use of EGF and bFGF increased the expression of MyoD protein, thus regulating the proliferation of JBP muscle cells and the expression of growth-related genes.

Independence of growth factor induced plasminogen activator inhibitor type-1 (PAI-1) expression from the 4G/5G polymorphism of the PAI-1 gene

2003 ◽  
Vol 90 (07) ◽  
pp. 36-42 ◽  
Author(s):  
Esther Eschenfelder ◽  
Karlheinz Peter ◽  
Burton Sobel ◽  
Christoph Bode ◽  
Thomas Nordt
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Smooth Muscle Cells ◽  
Genetic Factors ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Gene And Protein Expression ◽  
Arterial Smooth Muscle Cells ◽  
Pai 1

SummaryIncreased PAI-1 expression has been implicated in accelerating atherogenesis. Increases under some conditions are modulated by growth factors. Genetic factors such as the 4G/5G poly-morphism in the promoter of the PAI-1 gene play a role under certain circumstances. The present study was designed to delineate for the first time interactions between growth factors and the 4G/5G polymorphism with respect to PAI-1 expression in human arterial smooth muscle cells (HASMC).HASMC were genotyped and exposed to growth factors. PAI-1 gene and protein expression were induced consistently by TGF-β (up to 4.0-fold), PDGF (2.1-fold),TNF-α (1.7-fold), and thrombin (2.3-fold). Results were similar regardless of which genotype (4G/4G [n=9], 4G/5G [n=13], and 5G/5G [n=7]) was present.The induction of increased PAI-1 expression in human arterial smooth muscle cells by growth factors implicated in accelerated atherogenesis is independent of the PAI-1 4G/5G polymorphism. Accordingly, modulation of PAI-1 expression is likely to be influenced predominantly by environmental factors acting on, rather than genetic factors intrinsic to the PAI-1 promoter.

Sustained muscle contraction induced by agonists, growth factors, and Ca2+ mediated by distinct PKC isozymes

2000 ◽  
Vol 279 (1) ◽  
pp. G201-G210 ◽  
Author(s):  
K. S. Murthy ◽  
J. R. Grider ◽  
J. F. Kuemmerle ◽  
G. M. Makhlouf
Keyword(s):  
Growth Factors ◽  
G Protein ◽  
Muscle Cells ◽  
Sustained Contraction ◽  
Calphostin C ◽  
Epidermal Growth ◽  
Pkc Isozymes ◽  
G Protein Coupled ◽  
Pkc Activation

The role of protein kinase C (PKC) in sustained contraction was examined in intestinal circular and longitudinal muscle cells. Initial contraction induced by agonists (CCK-8 and neuromedin C) was abolished by 1) inhibitors of Ca2+ mobilization (neomycin and dimethyleicosadienoic acid), 2) calmidazolium, and 3) myosin light chain (MLC) kinase (MLCK) inhibitor KT-5926. In contrast, sustained contraction was not affected by these inhibitors but was abolished by 1) the PKC inhibitors chelerythrine and calphostin C, 2) PKC-ε antibody, and 3) a pseudosubstrate PKC-ε inhibitor. GDPβS abolished both initial and sustained contraction, whereas a Gαq/11 antibody inhibited only initial contraction, implying that sustained contraction was dependent on activation of a distinct G protein. Sustained contraction induced by epidermal growth factor was inhibited by calphostin C, PKC-α,β,γ antibody, and a pseudosubstrate PKC-α inhibitor. Ca2+ (0.4 μM) induced an initial contraction in permeabilized muscle cells that was blocked by calmodulin and MLCK inhibitors and a sustained contraction that was blocked by calphostin C and a PKC-α,β,γ antibody. Thus initial contraction induced by Ca2+, agonists, and growth factors is mediated by MLCK, whereas sustained contraction is mediated by specific Ca2+-dependent and -independent PKC isozymes. G protein-coupled receptors are linked to PKC activation via distinct G proteins.

Effects of smooth muscle cell derived growth factor (SDGF) in combination with other growth factors on smooth muscle cells

1989 ◽  
Vol 78 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Nobuhiro Morisaki ◽  
Noriyuki Koyama ◽  
Seijiro Mori ◽  
Tetsuto Kanzaki ◽  
Tomoko Koshikawa ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Muscle Cells

scholarly journals Divergent regulation by growth factors and cytokines of 95 kDa and 72 kDa gelatinases and tissue inhibitors or metalloproteinases-1, -2, and -3 in rabbit aortic smooth muscle cells

1996 ◽  
Vol 315 (1) ◽  
pp. 335-342 ◽  
Author(s):  
Rosalind P. FABUNMI ◽  
Andrew H. BAKER ◽  
Edward J. MURRAY ◽  
Robert F. G. BOOTH ◽  
Andrew C. NEWBY
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Growth Factors ◽  
Growth Factor ◽  
Protein Kinase ◽  
Basement Membrane ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tissue Inhibitors ◽  
Kinase C

The migration and proliferation of vascular smooth muscle cells (SMCs) during neointima formation in atherosclerosis and angioplasty restenosis is mediated by certain growth factors and cytokines, one action of which may be to promote basement-membrane degradation. To test this hypothesis further, the effects of such growth factors and cytokines on the synthesis of two basement-membrane-degrading metalloproteinases, namely the 72 kDa gelatinase (MMP-2, gelatinase A) and the 95 kDa gelatinase (MMP-9, gelatinase B) and three tissue inhibitors of metalloproteinases (TIMPs) was studied in primary cultured rabbit aortic SMCs. Expression of the 95 kDa gelatinase was increased by phorbol myristate acetate, foetal calf serum, thrombin and interleukin-1α (IL-1α); platelet-derived growth factor (PDGF) BB alone had no effect but acted synergistically with IL-1α. A selective protein kinase C inhibitor, Ro 31-8220, abolished induction of the 95 kDa gelatinase. In contrast, none of the agents tested modulated the synthesis of the 72 kDa gelatinase. We conclude that maximal up-regulation of 95 kDa gelatinase expression requires the concerted action of growth factors and inflammatory cytokines mediated, in part, by a protein kinase C-dependent pathway. TIMP-1 and TIMP-2 were highly expressed, and their synthesis was not affected by growth factors or cytokines. Expression of TIMP-3 mRNAs was, however, increased by PDGF and transforming growth factor β, especially in combination. Divergent regulation of gelatinase and TIMP expression implies that either net synthesis or net degradation of basement membrane can be mediated by appropriate combinations of growth factors and cytokines.

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