scholarly journals Distributed Live Muscle Actuators Controlled by Optical Stimuli

2013 ◽  
Author(s):  
Devin Neal ◽  
Mahmut Selman Sakar ◽  
H. Harry Asada
Keyword(s):  
Skeletal Muscle ◽  
Genetically Modified ◽  
Muscle Cells ◽  
Degree Of Freedom ◽  
Optical Control ◽  
Muscle System ◽  
Muscle Actuators

A multi degree of freedom skeletal muscle system stimulated via optical control is presented. These millimeter-scale, optically excitable 3D skeletal muscle bio-actuators are created by culturing genetically modified precursory muscle cells that are activated with light: optogenetics. These muscle bio-actuators are networked together to create a distributed muscle system. Muscle systems can manipulate loads having no fixed joint. These types of loads include shoulders, the mouth, and the jaw.

Extracts of Hymenocardia acida ameliorate insulin resistance in skeletal muscle cells

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
II Ezeigbo ◽  
C Wheeler-Jones ◽  
S Gibbons ◽  
ME Cleasby
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Ameliorate Insulin Resistance

TGFß regulates metabolism of human skeletal muscle cells by miRNAs

2018 ◽  
Author(s):  
S Höckele ◽  
P Huypens ◽  
C Hoffmann ◽  
T Jeske ◽  
M Hastreiter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Human Skeletal Muscle Cells

scholarly journals Annexins and Membrane Repair Dysfunctions in Muscular Dystrophies

2021 ◽  
Vol 22 (10) ◽  
pp. 5276
Author(s):  
Coralie Croissant ◽  
Romain Carmeille ◽  
Charlotte Brévart ◽  
Anthony Bouter
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Genetic Disorders ◽  
Muscle Cells ◽  
Cell Types ◽  
Clinical Severity ◽  
Skeletal Muscle Cells ◽  
Muscular Dystrophies ◽  
Membrane Repair ◽  
Human Skeletal Muscle Cells

Muscular dystrophies constitute a group of genetic disorders that cause weakness and progressive loss of skeletal muscle mass. Among them, Miyoshi muscular dystrophy 1 (MMD1), limb girdle muscular dystrophy type R2 (LGMDR2/2B), and LGMDR12 (2L) are characterized by mutation in gene encoding key membrane-repair protein, which leads to severe dysfunctions in sarcolemma repair. Cell membrane disruption is a physiological event induced by mechanical stress, such as muscle contraction and stretching. Like many eukaryotic cells, muscle fibers possess a protein machinery ensuring fast resealing of damaged plasma membrane. Members of the annexins A (ANXA) family belong to this protein machinery. ANXA are small soluble proteins, twelve in number in humans, which share the property of binding to membranes exposing negatively-charged phospholipids in the presence of calcium (Ca2+). Many ANXA have been reported to participate in membrane repair of varied cell types and species, including human skeletal muscle cells in which they may play a collective role in protection and repair of the sarcolemma. Here, we discuss the participation of ANXA in membrane repair of healthy skeletal muscle cells and how dysregulation of ANXA expression may impact the clinical severity of muscular dystrophies.

scholarly journals 6-shogaol suppresses oxidative damage in L6 muscle cells

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Jinyoung Hur ◽  
Yeonmi Lee ◽  
Chang Jun Lee ◽  
Ho-Young Park ◽  
Sang Yoon Choi
Keyword(s):  
Skeletal Muscle ◽  
Essential Oil ◽  
Oxidative Damage ◽  
Zingiber Officinale ◽  
Muscle Cells ◽  
Skeletal Muscle Cell ◽  
Intracellular Ros ◽  
Zingiber Officinale Roscoe ◽  
Mrna And Protein Expression ◽  
L6 Muscle Cells

Abstract Ginger (Zingiber Officinale Roscoe) has been known reduce muscle pain after exercise, and 6-shogaol {(E)-1-(4-Hydroxy-3-methoxyphenyl)dec-4-en-3-one)} is the major essential oil contained in ginger. In this study, the protective effect of 6-shogaol on L6 muscle cells against oxidative damage was measured. 6-shagol inhibited the damage of L6 cell induced by H2O2, and allowed the increase in mRNA and protein expression levels of intracellular HO-1 and NRF2. 6-shogaol also reduced the production of intracellular ROS. These results suggested that 6-shagol effectively inhibits oxidative damage of skeletal muscle cell.

scholarly journals β-Sitosterol-D-Glucopyranoside Mimics Estrogenic Properties and Stimulates Glucose Utilization in Skeletal Muscle Cells

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3129
Author(s):  
Jyotsana Pandey ◽  
Kapil Dev ◽  
Sourav Chattopadhyay ◽  
Sleman Kadan ◽  
Tanuj Sharma ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Utilization ◽  
Diabetes Management ◽  
Expression System ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Cell Periphery ◽  
Glut4 Translocation ◽  
In Silico Docking

Estrogenic molecules have been reported to regulate glucose homeostasis and may be beneficial for diabetes management. Here, we investigated the estrogenic effect of β-sitosterol-3-O-D-glucopyranoside (BSD), isolated from the fruits of Cupressus sempervirens and monitored its ability to regulate glucose utilization in skeletal muscle cells. BSD stimulated ERE-mediated luciferase activity in both ERα and ERβ-ERE luc expression system with greater response through ERβ in HEK-293T cells, and induced the expression of estrogen-regulated genes in estrogen responsive MCF-7 cells. In silico docking and molecular interaction studies revealed the affinity and interaction of BSD with ERβ through hydrophobic interaction and hydrogen bond pairing. Furthermore, prolonged exposure of L6-GLUT4myc myotubes to BSD raised the glucose uptake under basal conditions without affecting the insulin-stimulated glucose uptake, the effect associated with enhanced translocation of GLUT4 to the cell periphery. The BSD-mediated biological response to increase GLUT4 translocation was obliterated by PI-3-K inhibitor wortmannin, and BSD significantly increased the phosphorylation of AKT (Ser-473). Moreover, BSD-induced GLUT4 translocation was prevented in the presence of fulvestrant. Our findings reveal the estrogenic activity of BSD to stimulate glucose utilization in skeletal muscle cells via PI-3K/AKT-dependent mechanism.

Sign in / Sign up

Export Citation Format

Share Document