scholarly journals Peer Review #1 of "Molecular characteristic of activin receptor IIB and its functions in growth and nutrient regulation in Eriocheir sinensis (v0.2)"

2020 ◽  
Keyword(s):  
Peer Review ◽  
Eriocheir Sinensis ◽  
Molecular Characteristic ◽  
Nutrient Regulation ◽  
Activin Receptor ◽  
Activin Receptor Iib

scholarly journals Molecular characteristic of activin receptor IIB and its functions in growth and nutrient regulation in Eriocheir sinensis

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9673
Author(s):  
Jingan Wang ◽  
Kaijun Zhang ◽  
Xin Hou ◽  
Wucheng Yue ◽  
He Yang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
Eriocheir Sinensis ◽  
Negative Regulator ◽  
Control Group ◽  
Molting Cycle ◽  
Activin Receptor ◽  
Activin Receptor Iib

Activin receptor IIB (ActRIIB) is a serine/threonine-kinase receptor binding with transforming growth factor-β (TGF-β) superfamily ligands to participate in the regulation of muscle mass in vertebrates. However, its structure and function in crustaceans remain unknown. In this study, the ActRIIB gene in Eriocheir sinensis (Es-ActRIIB) was cloned and obtained with a 1,683 bp open reading frame, which contains the characteristic domains of TGF-β type II receptor superfamily, encoding 560 amino acids. The mRNA expression of Es-ActRIIB was the highest in hepatopancreas and the lowest in muscle at each molting stage. After injection of Es-ActRIIB double-stranded RNA during one molting cycle, the RNA interference (RNAi) group showed higher weight gain rate, higher specific growth rate, and lower hepatopancreas index compared with the control group. Meanwhile, the RNAi group displayed a significantly increased content of hydrolytic amino acid in both hepatopancreas and muscle. The RNAi group also displayed slightly higher contents of saturated fatty acid and monounsaturated fatty acid but significantly decreased levels of polyunsaturated fatty acid compared with the control group. After RNAi on Es-ActRIIB, the mRNA expressions of five ActRIIB signaling pathway genes showed that ActRI and forkhead box O (FoxO) were downregulated in hepatopancreas and muscle, but no significant expression differences were found in small mother against decapentaplegic (SMAD) 3, SMAD4 and mammalian target of rapamycin. The mRNA expression s of three lipid metabolism-related genes (carnitine palmitoyltransferase 1β (CPT1β), fatty acid synthase, and fatty acid elongation) were significantly downregulated in both hepatopancreas and muscle with the exception of CPT1β in muscles. These results indicate that ActRIIB is a functionally conservative negative regulator in growth mass, and protein and lipid metabolism could be affected by inhibiting ActRIIB signaling in crustacean.

O.10 Effect of combined treatment with soluble activin receptor IIB and AAV-U7-mediated dystrophin exon skipping on muscle function in mdx mice

2011 ◽  
Vol 21 (9-10) ◽  
pp. 703
Author(s):  
W.M.H. Hoogaars ◽  
E. Mouisel ◽  
K. Relizani ◽  
A. Pasternack ◽  
C. Hourde ◽  
...  
Keyword(s):  
Muscle Function ◽  
Combined Treatment ◽  
Exon Skipping ◽  
Mdx Mice ◽  
Activin Receptor ◽  
Activin Receptor Iib ◽  
O 10

The role of myostatin and activin receptor IIB in the regulation of unloading-induced myofiber type-specific skeletal muscle atrophy

2015 ◽  
Vol 119 (6) ◽  
pp. 633-642 ◽  
Author(s):  
Lyle W. Babcock ◽  
Mark Knoblauch ◽  
Mark S. F. Clarke
Keyword(s):  
Satellite Cells ◽  
Negative Regulator ◽  
Hindlimb Suspension ◽  
Immunofluorescent Staining ◽  
Fiber Types ◽  
Specific Expression ◽  
Cytoplasmic Staining ◽  
Activin Receptor ◽  
Activin Receptor Iib ◽  
Myofiber Type

Chronic unloading induces decrements in muscle size and strength. This adaptation is governed by a number of molecular factors including myostatin, a potent negative regulator of muscle mass. Myostatin must first be secreted into the circulation and then bind to the membrane-bound activin receptor IIB (actRIIB) to exert its atrophic action. Therefore, we hypothesized that myofiber type-specific atrophy observed after hindlimb suspension (HLS) would be related to myofiber type-specific expression of myostatin and/or actRIIB. Wistar rats underwent HLS for 10 days, after which the tibialis anterior was harvested for frozen cross sectioning. Simultaneous multichannel immunofluorescent staining combined with differential interference contrast imaging was employed to analyze myofiber type-specific expression of myostatin and actRIIB and myofiber type cross-sectional area (CSA) across fiber types, myonuclei, and satellite cells. Hindlimb suspension (HLS) induced significant myofiber type-specific atrophy in myosin heavy chain (MHC) IIx ( P < 0.05) and MHC IIb myofibers ( P < 0.05). Myostatin staining associated with myonuclei was less in HLS rats compared with controls, while satellite cell staining for myostatin remained unchanged. In contrast, the total number myonuclei and satellite cells per myofiber was reduced in HLS compared with ambulatory control rats ( P < 0.01). Sarcoplasmic actRIIB staining differed between myofiber types (I < IIa < IIx < IIb) independent of loading conditions. Myofiber types exhibiting the greatest cytoplasmic staining of actRIIB corresponded to those exhibiting the greatest degree of atrophy following HLS. Our data suggest that differential expression of actRIIB may be responsible for myostatin-induced myofiber type-selective atrophy observed during chronic unloading.

scholarly journals Modified activin receptor IIB ligand trap mitigates ineffective erythropoiesis and disease complications in murine β-thalassemia

Blood ◽  
2014 ◽  
Vol 123 (25) ◽  
pp. 3864-3872 ◽  
Author(s):  
Rajasekhar N. V. S. Suragani ◽  
Sharon M. Cawley ◽  
Robert Li ◽  
Samantha Wallner ◽  
Mark J. Alexander ◽  
...  
Keyword(s):  
Iron Overload ◽  
Erythroid Differentiation ◽  
Bone Defects ◽  
Ineffective Erythropoiesis ◽  
Activin Receptor ◽  
Key Points ◽  
Terminal Erythroid Differentiation ◽  
Activin Receptor Iib

Key Points Modified ActRIIB ligand trap promotes terminal erythroid differentiation and mitigates ineffective erythropoiesis in murine β-thalassemia. This agent reduces anemia, α-globin aggregates, hemolysis, and disease complications such as iron overload, splenomegaly, and bone defects.

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