Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Decoupling the Biochemical and Mechanical Effects of Muscle Exercise on Motor Neurons with 2.5D Actuating Matrices [230828Ram_RNA-seq]

ABSTRACT: Muscles’ function as an endocrine organ is still poorly understood, but an emerging body of literature has provided evidence that myokines may aid in the development of surrounding tissues. Another outcome of muscle contraction in vivo is the localized mechanical forces produced. Current experimental techniques are not equipped to isolate and study the two effects independently. We have developed a system to culture contractile 2D optogenetic muscle long-term to provide a source for myokine secretion. We supplement our neuron monoculture with myokine secreted media and saw a 3X increase in total neurite length magnitude and a 3.2X increase in the rate of growth. As for mechanical stimulation, we optimize our Magnetic Matrix Actuation (MagMA) to provide localized stressors on the growing neurites. The mechanical stimulation regime results in a ~2.7X increase in both magnitude and rate of total neurite length. We validate our morphological findings with bulk RNA-sequencing analysis, the results show a large number of differentially expressed genes between the biochemical stimulation group and control. On the other hand, there was minimal difference between the mechanical stimulation group and control. Our study mechanistically unravels how repeated muscle contraction, or exercise, regulates motor neuron growth and maturation.

ORGANISM(S): Mus musculus

PROVIDER: GSE257540 | GEO | 2024/02/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mechanical loading and gene expression - Microarray study

Project description:Skeletal integrity in humans and animals is maintained by daily mechanical loading. It has been widely accepted that osteocytes function as mechanosensors. Many biochemical signaling molecules are involved in the response of osteocytes to mechanical stimulation. The aim of this study was to identify genes involved in the translation of mechanical stimuli into bone formation. The four-point bending model was used to induce a single period of mechanical loading (comprising 300 cycles (2 Hz) using a peak magnitude of 60 N) on the right tibia, while the contra lateral left tibia served as control. Six hours after loading, the effects of mechanical loading on gene-expression were determined with microarray analysis. Protein expression of differentially regulated genes was evaluated with immunohistochemistry. Nine genes were found to exhibit a significant differential gene expression in LOAD compared to control. MEPE, Garnl1, V2R2B, and QFG TN1 olfactory receptor were up-regulated, and creatine kinase (muscle form), fibrinogen-B beta-polypeptide, monoamine oxidase A, troponin-C and kinesin light chain-C were down-regulated. Validation with real-time RT-PCR analysis confirmed the up regulation of MEPE and the down-regulation of creatine kinase (muscle form) and troponin-C in the loaded tibia. Immunohistochemistry showed that the increase of MEPE protein expression was already detectable six hours after mechanical loading. In conclusion, these genes probably play a role during translation of mechanical stimuli six hours after mechanical loading. The modulation of MEPE expression may indicate a connection between bone mineralization and bone formation after mechanical stimulation. Two groups: LOAD vs contralateral control and SHAM vs contralateral control (n=5/group)

2013-11-21 | E-GEOD-50707 | biostudies-arrayexpress

Whole worm transcriptomics after optogenetically induced mechanical muscle stress (OptIMMuS)

Project description:Mechanical stress during muscle contraction is a constant threat to proteome integrity. Experimental systems are needed to identify proteostasis regulators that are critical under mechanical stress conditions. Although Caenorhabditis elegans combines the advantages of existing organismal and cell culture models, an inducible method to stimulate muscle contraction in large populations has been lacking. Here, we present a versatile technique called OptIMMuS (Optogenetic Induction of Mechanical Muscle Stress) to study changes in the proteostasis network associated with mechanical forces. Repeated blue light exposure of a muscle-expressed Chlamydomonas rheinhardii channelrhodopsin-2 variant leads to sustained muscle contraction and mechanical stress. OptIMMuS combined with proximity labeling and mass spectrometry identified regulators that cooperate with the myosin-directed chaperone UNC-45 in muscle proteostasis. We show in genetic epistasis and co-immunoprecipitation experiments that the E3 ligase NHL-1 interacts with UNC-45 and muscle myosin, and we provide evidence that this TRIM32 orthologue affects myosin protein levels and function.

2024-07-16 | GSE241906 | GEO

ZAKb is a cellular compression sensor that mediates hypertrophic signaling in skeletal muscle

Project description:Mechanosensing is required for the senses of touch and hearing, and impacts on cellular processes such as cell differentiation, migration, invasion and tissue homeostasis. Mechanical inputs give rise to p38- and JNK-signaling, which mediates adaptive physiological responses in various tissues. In muscle, fiber contraction-induced p38 and JNK signaling ensures adaptation to exercise, muscle repair and hypertrophy. However, the mechanism by which muscle fibers sense mechanical load to activate this signaling, as well as the physiological roles of mechanical stress sensing more broadly, have remained elusive. Here, we show that the upstream MAP3K ZAK is a sensor of cellular compression induced by osmotic shock and cyclic compression in vitro, and muscle contraction in vivo. This function relies on ZAK’s ability to recognize stress fibers in cells and the corresponding Z-discs in muscle fibers, when under tension. Consequently, ZAK-deficient mice present with skeletal muscle defects characterized by fibers with centralized nuclei and progressive adaptation towards a slower myosin profile. Our results highlight how cells in general sense mechanical compressive load, and how mechanical forces generated during muscle contraction are translated into MAP kinase signaling.

2022-05-31 | PXD028548 | Pride

Mechanical loading and gene expression - Microarray study

2013-11-21 | GSE50707 | GEO

Transmural pressure is a master regulator of airway branching morphogenesis

Project description:Mechanical forces are increasingly recognized to regulate morphogenesis, but how this is accomplished in the context of the multiple tissues present within a developing organ remains unclear. Here we use bioengineered “microfluidic chest cavities” to precisely control the mechanical environment of the fetal lung. We show that transmural pressure controls airway branching morphogenesis and regulates the frequency of airway smooth muscle contraction. Next-generation sequencing analysis shows that lungs held at higher pressure are more mature than lungs held at lower pressure. Timelapse imaging reveals that branching events are synchronized across distant locations within the lung, and are preceded by long-duration waves of airway smooth muscle contraction. Higher transmural pressure decreases the interval between systemic smooth muscle contractions and increases the rate of morphogenesis of the airway epithelium. These data reveal that the mechanical properties of the microenvironment instruct crosstalk between tissues to control the rate of development of the embryonic lung.

2017-11-07 | GSE90148 | GEO

Phosphoproteomics of rodent exercise models

Project description:Exercise stimulates systemic and tissue-specific adaptations that protect against lifestyle related diseases including obesity and type 2 diabetes. Exercise places high mechanical and energetic demands on contracting skeletal muscle, which require finely-tuned protein post-translational modifications involving signal transduction (e.g. phosphorylation) to elicit appropriate short- and long-term adaptive responses. To uncover the breadth of protein phosphorylation events underlying the adaptive responses to endurance exercise and skeletal muscle contraction, we performed global, unbiased mass spectrometry-based phosphoproteomic analyses of skeletal muscle from two rodent models, in situ muscle contraction in rats and treadmill-based endurance exercise in mice.

2019-07-22 | PXD010452 | Pride

RNA-Seq of Myf6-knockout versus Wild-type satellite cells

Project description:In metazoans, skeletal muscle evolved to contract and produce force. Recent experimental evidence, however, suggests that skeletal muscle has also acquired endocrine functions and produces a vast array of muscle-derived cytokines and growth factors, collectively called myokines. The mechanisms that regulate myokine production and their effect on the resident stem cell population inskeletal muscle remain unknown. Here, we report that in adult skeletal muscle, Myf6/MRF4 is a major regulator of myokine expression. Genetic deletion of Myf6 in skeletal muscle leads to reduction of the muscle stem cell (MuSCs) pool in adult mice in a myokine-dependent manner but, surprisingly, does not disrupt muscle differentiation. Using ChIP-Seq and gene expression analyses of myogenic factors, we show that Myf6/MRF4 is a direct regulator of many myokines and muscle-secreted proteins, including ligands for canonical signaling pathways such as EGFR and VEGFR. Consequently, in Myf6-deficient animals,MuSCs increasingly break quiescence, but can nevertheless undergo differentiation. Lastly, we show that Myf6 and its gene network rapidly respondto aerobic and anaerobic exercise. Together, these findings indicate that control of myokine signaling by Myf6 is critical to maintain muscle stem cell pool and skeletal muscle function via myokine signaling.

2020-10-02 | GSE133505 | GEO

Myf6/MRF4 Mediated Myokine Signaling is Required for the Maintenance of the Adult Skeletal Muscle Stem Cell Pool

Project description:In metazoans, skeletal muscle evolved to contract and to produce force. Recent experimental evidence suggests, however, that skeletal muscle has also acquired endocrine functions and produces a vast array of myokines, but how myokine production is regulated and how they affect the resident stem cell population of the skeletal muscle is unknown. Here, we show that in adult skeletal muscle, Myf6/MRF4 is a major regulator of myokine expression. Genetic deletion of Myf6 in skeletal muscles leads to exhaustion of the muscle stem cell (MuSCs) pool in adult mice in a myokine-dependent manner but, surprisingly, does not disrupt muscle differentiation. Using ChIP-Seq and gene expression analyses of myogenic factors, we show that Myf6/MRF4 is essential for the transcriptional activation of many myokines and muscle-secreted proteins, including ligands for canonical signaling pathways such as EGFR, VEGFR and STAT3. Consequently, MuSCs from Myf6 knockout animals show impaired activation of those signaling pathways and exhibit impaired quiescence, defective self-renewal, but nevertheless undergo differentiation. Lastly, we show that induction of myokine expression during aerobic and anaerobic exercise closely correlates with Myf6 expression. Together, these findings indicate that control of myokine signaling by Myf6 is critical to maintain muscle stem cell pool in adult skeletal muscle.

2020-09-18 | GSE123836 | GEO

Quantitative LC-MSMS of human muscle cells after electrical pulse stimulation

Project description:We hypothesized that muscle contraction produces a cellular stress signal capable to increase lipolysis to sustain fuel availability during exercise. The aim of the present study was to identify novel exercise-regulated myokines, aka exerkines, able to promote lipolysis in human adipocytes. To this end, human primary myotubes from lean healthy volunteers were submitted to electrical pulse stimulation to mimic either acute intense or chronic moderate exercise. Conditioned media experiments with hMADS adipocytes were performed. Unbiased proteomic and ELISA analyses were applied in conditioned media and human plasma samples. Real-time qPCR was performed in cultured myotubes and muscle biopsy samples.

2020-05-26 | PXD014126 | Pride

MLX transcriptional regulation in muscle cells

Project description:This study set out to identify MLX transcriptional targets in muscle cells. C2C12 Myoblasts were virally transduced to increase MLX activity, by overexpression of the wild-type protein; and to decrease MLX activity by overexpression of a dominant negative MLX protein and by shRNA induced knockdown of MLX. Transcripts that were significantly and consistently regulated by the different modes of MLX modulation were identified. The largest proportion of these were genes encoding secreted proteins including growth factors, cytokines and extracellular proteins. We therefore conclude that MLX can regulate myokine transcripts. mRNA profiles from C2C12 muscle cells with increased and decreased MLX activity were examined.

2016-01-04 | E-GEOD-70028 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data