scholarly journals A Novel Nanobody Directed against Ovine Myostatin to Enhance Muscle Growth in Mouse

Animals ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1398
Author(s):  
Kepeng Ou ◽  
Youjian Li ◽  
Peng Wu ◽  
Jixing Guo ◽  
Xiujing Hao ◽  
...  
Keyword(s):  
Transforming Growth Factor Beta ◽  
Intramuscular Injection ◽  
Transforming Growth Factor ◽  
Muscle Growth ◽  
Domestic Animals ◽  
Negative Regulator ◽  
Promising Treatment ◽  
Animal Growth ◽  
Growth Factor Beta ◽  
Diagnostics And Therapy

Myostatin (MSTN) is a member of the transforming growth factor beta superfamily and is a negative regulator of myogenesis. It has been shown to function by controlling the proliferation of myoblasts. MSTN inhibition is considered as a promising treatment for promoting animal growth in livestock. Nanobodies, a special antibody discovered in camel, have arisen as an alternative to conventional antibodies and have shown great potential when used as tools in different biotechnology fields, such as diagnostics and therapy. In this study, we examined the effect of MSTN inhibition by RMN on the muscle growth of mice. The results showed that RMN could specifically detect and bind MSTN, as well as inhibit MSTN activity. A significant increase in skeletal muscle mass was observed after intramuscular injection of RMN into mice. Enhanced muscle growth occurred because of myofiber hypertrophy. These results offer a promising approach to enhance muscle growth that warrants further investigation in domestic animals.

scholarly journals Transforming Growth Factor Beta has Dual Effects on MMP9 and uPA Expression in HTR-8/SVneo Human Trophoblastic Cell Line

2019 ◽  
Vol 24 (1) ◽  
pp. 26-37
Author(s):  
Sandra Susana Novoa Herran ◽  
Mariela Castelblanco ◽  
Myriam Sanchez-Gomez ◽  
Adriana Umaña Pérez
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
In Silico ◽  
Transforming Growth Factor ◽  
In Silico Analysis ◽  
Negative Regulator ◽  
Trophoblast Invasion ◽  
Trophoblastic Cell ◽  
Growth Factor Beta

Invasion of trophoblast into endometrium is vital for successful pregnancy development. MMP9 and uPA are key proteases in this process, but it is still not clear the regulation of its expression by Transforming Growth Factor Beta (TGF-β), known negative regulator of trophoblast invasion. We evaluated the effect of TGF-β on the transcriptional expression of uPA and MMP9 over time, in HTR- /SVneo trophoblast cells cultured with or without 0.5 % fetal bovine serum, via RT qPCR. The involved transcription factors and signaling pathways were analyzed in silico, using Proscan, Enrich, PCViz and WikiPathway. Results showed that that TGF-β regulates the expression of uPA and MMP9. Serum modified the nature of TGF-β’s effects on uPA expression, from negative without serum to positive with it, showing opposite effects on MMP9 expression. In silico analysis evidenced different transcription factors for each protease, some belonging to TGF-β ssignaling pathway, and crosstalk with MAPK and Wnt/β-catenin pathways. The TGF-β ddual role is discussed proposing that serum affects the cellular context. Transcriptional regulation of MMP9 and uPA by TGF-β is differential and depends on serum presence and evaluation time.

scholarly journals Transforming growth factor beta inhibits the proliferation of the blast cells of acute myeloblastic leukemia

Blood ◽  
1988 ◽  
Vol 72 (1) ◽  
pp. 159-164 ◽  
Author(s):  
N Tessier ◽  
T Hoang
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Acute Myeloblastic Leukemia ◽  
Negative Regulator ◽  
Thymidine Uptake ◽  
Tgf Beta ◽  
Bladder Cell ◽  
Growth Factor Beta

Abstract The effect of transforming growth factor beta (TGF beta) on proliferation and differentiation of peripheral blast precursors in acute myeloblastic leukemia (AML) was investigated. TGF beta induced a dose-dependent inhibition of blast clonogenic cells in suspension and methylcellulose cultures in the presence of optimal concentrations of stimulators provided by conditioned media from the bladder cell line HTB9 (HTB9-CM) or the recombinant granulocyte-macrophage colony- stimulating factor (GM-CSF). On removal of TGF beta, blast clonogenic cell proliferation recovers to the same level as that observed in control cultures, indicating that the effect is reversible. There was no induction of cell differentiation, as indicated by morphological and functional studies (production of superoxyde anions). Cell cycle analysis by thymidine uptake and flow cytometry with a DNA binding dye indicated that TGF beta caused a delay in progression into S and G2/M phases of the cell cycle without affecting cell viability. Thus, TGF beta appears to have a cytostatic rather than cytolytic effect on blast precursors and might therefore play a role as a negative regulator in hematopoiesis.

scholarly journals Myostatin expression during development and chronic stress in zebrafish (Danio rerio)

2003 ◽  
Vol 176 (1) ◽  
pp. 47-59 ◽  
Author(s):  
S Vianello ◽  
L Brazzoduro ◽  
L Dalla Valle ◽  
P Belvedere ◽  
L Colombo
Keyword(s):  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cultured Cells ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Muscle Growth ◽  
Negative Regulator ◽  
Small Fish ◽  
Adult Muscle ◽  
Lateral Muscle

Myostatin, a member of the transforming growth factor-beta superfamily, is a negative regulator of skeletal muscle mass in mammals. We have studied myostatin expression during embryonic and post-hatching development in zebrafish by semiquantitative RT-PCR. The transcript is present in just-fertilized eggs and declines at 8 h post-fertilization (hpf), suggesting a maternal origin. A secondary rise occurs at 16 hpf, indicating the onset of embryonic transcription at the time of muscle cell differentiation. The level of myostatin mRNA decreases slightly at 24 hpf, when somitogenesis is almost concluded, and rises again at and after hatching, during the period of limited muscle hyperplastic growth that is typical of slow-growing, small fish. In the adult muscle, we found the highest expression of myostatin mRNA and protein, which were detectable by Northern and Western blot analyses respectively. Although only the precursor protein form was revealed in the adult lateral muscle, we demonstrated that zebrafish myostatin is proteolytically processed and secreted in cultured cells, as is its mammalian counterpart. These results suggest that myostatin may play an important regulatory role during myogenesis and muscle growth in fish, as it does in mammals. In chronically stressed fish, grown from 16 days post-fertilization to adulthood in an overcrowded environment, we observed both depression of body growth and a diminished level of myostatin mRNA in the adult muscle, as compared with controls. We propose that chronic stunting in fish brings about a general depression of muscle protein synthesis which does not spare myostatin.

scholarly journals Enhanced Muscle Growth by Plasmid-Mediated Delivery of Myostatin Propeptide

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Shengwei Hu ◽  
Chuangfu Chen ◽  
Jingliang Sheng ◽  
Yufang Sun ◽  
Xudong Cao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transforming Growth Factor Beta ◽  
Muscle Development ◽  
Transforming Growth Factor ◽  
Genetic Manipulation ◽  
Muscle Growth ◽  
Negative Regulator ◽  
Dna Encoding ◽  
Single Intramuscular Injection ◽  
Myostatin Inhibition

Myostatin is a member of the transforming growth factor beta (TGF-β) superfamily that functions as a negative regulator of skeletal muscle development and growth. Myostatin blockade therefore offers a strategy for promoting muscle growth in livestock production without resorting to genetic manipulation. In this report, we examined the effect of myostatin inhibition by plasmid-mediated delivery of a mutant myostatin propeptide (MProD76A), a natural inhibitor of myostatin, on the growth performance of mice. A significant increase in skeletal muscle mass was observed after a single intramuscular injection of naked plasmid DNA encoding MProD76A into mice. Enhanced muscle growth occurred because of myofiber hypertrophy, but no cardiac muscle hypertrophy and organomegaly was observed in the mice after myostatin inhibition by plasmid-mediated MProD76A delivery. These results demonstrate a promising approach to enhancing muscle growth that warrants further investigation in domestic animals.

scholarly journals Transforming growth factor beta inhibits the proliferation of the blast cells of acute myeloblastic leukemia

Blood ◽  
1988 ◽  
Vol 72 (1) ◽  
pp. 159-164 ◽  
Author(s):  
N Tessier ◽  
T Hoang
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Acute Myeloblastic Leukemia ◽  
Negative Regulator ◽  
Thymidine Uptake ◽  
Tgf Beta ◽  
Bladder Cell ◽  
Growth Factor Beta

The effect of transforming growth factor beta (TGF beta) on proliferation and differentiation of peripheral blast precursors in acute myeloblastic leukemia (AML) was investigated. TGF beta induced a dose-dependent inhibition of blast clonogenic cells in suspension and methylcellulose cultures in the presence of optimal concentrations of stimulators provided by conditioned media from the bladder cell line HTB9 (HTB9-CM) or the recombinant granulocyte-macrophage colony- stimulating factor (GM-CSF). On removal of TGF beta, blast clonogenic cell proliferation recovers to the same level as that observed in control cultures, indicating that the effect is reversible. There was no induction of cell differentiation, as indicated by morphological and functional studies (production of superoxyde anions). Cell cycle analysis by thymidine uptake and flow cytometry with a DNA binding dye indicated that TGF beta caused a delay in progression into S and G2/M phases of the cell cycle without affecting cell viability. Thus, TGF beta appears to have a cytostatic rather than cytolytic effect on blast precursors and might therefore play a role as a negative regulator in hematopoiesis.

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