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Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays

ABSTRACT: Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays

PROVIDER: PRJNA1312619 | ENA |

REPOSITORIES: ENA

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Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [30min]

Project description:Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [30min]

| PRJNA1312499 | ENA

Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [60min]

Project description:Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [60min]

| PRJNA1312685 | ENA

Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [30min]

Project description:Exercise has long been considered an essential part of human health and longevity. Recent physiological studies have expanded muscle’s role beyond simply acting as an actuator, revealing muscle’s exercise-mediated paracrine and endocrine relationships with other organ systems. In vitro engineered skeletal muscle models can address physiological questions about exercise adaptation with the precision of cell biology. Optogenetic tools have enabled a noninvasive approach to stimulating muscle contraction that avoids the potential off-target effects of electrical stimulation techniques. In this article we propose high-throughput culture and optical exercise protocols to generate statistically robust cellular exercise response datasets. We characterize optical rheobase for 2D muscle tissue morphology, finding that optical intensities as low as 5 μW mm-2 can trigger contraction. We then analyze bulk RNA sequencing data collected from high throughput, acute exercise protocols and find a rich display of transcriptional behavior that is consistent with experimental observations. The spontaneous contractility of our tissue constructs introduced oxygen diffusion challenges when maintained in a 24 well plate, and our analysis shows divergent myogenic and pathological transcriptional consequences of hypoxia. We believe our techniques provide a practical foundation for conducting future high-precision in vitro exercise studies of skeletal muscle.

2025-08-29 | GSE306842 | GEO

Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays [60min]

2025-08-29 | GSE306857 | GEO

Physiological and functional characterization for high-throughput optogenetic skeletal muscle exercise assays

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-29 | GSE306860 | GEO

Sensing Cardiac Electrical Activity with a Cardiomyocyte Targeted Optogenetic Voltage Indicator

Project description:Rationale: Monitoring and controlling cardiomyocyte activity with optogenetic tools offers exciting possibilities for fundamental and translational cardiovascular research. Genetically encoded voltage indicators may be particularly attractive for minimal invasive and repeated assessments of cardiac excitation from the cellular to the whole heart level. Objective: To test the hypothesis that cardiomyocyte-targeted voltage-sensitive fluorescence protein 2.3 (VSFP2.3) can be exploited as optogenetic tool for the monitoring of electrical activity in isolated cardiomyocytes and the whole heart as well as function and maturity in induced pluripotent stem cell (iPSC)-derived cardiomyocytes. Methods and Results: We first generated mice with cardiomyocyte-restricted expression of VSFP2.3 and demonstrated distinct sarcolemmal localization of VSFP2.3 without any signs for associated pathologies (assessed by echocardiography). Optically recorded VSFP2.3 signals correlated well with membrane voltage measured simultaneously by patch-clamping. The utility of VSFP2.3 for human action potential recordings was confirmed by simulation of immature and mature action potentials in murine VSFP2.3 cardiomyocytes. Optical cardiograms (OCGs) could be monitored in whole hearts ex vivo and minimally invasively in vivo via fiber optics at physiological heart rate (10 Hz) and under pacing-induced arrhythmia. Finally, we reprogrammed tail-tip fibroblasts from transgenic mice and used the VSFP2.3 sensor for benchmarking functional and structural maturation in iPSC-derived cardiomyocytes. Conclusions: We introduce a novel transgenic voltage-sensor model as a new method in cardiovascular research and provide proof-of-concept for its utility in optogenetic sensing of physiological and pathological excitation in mature and immature cardiomyocytes in vitro and in vivo. Determination of transgene (VSFP2.3) cardiotoxicity

2015-09-02 | E-GEOD-69190 | biostudies-arrayexpress

Discovering human diabetes-risk gene function with genetics and physiological assays

Project description:Discovering human diabetes-risk gene function with genetics and physiological assays

| PRJNA478311 | ENA

Physiological and molecular dissection of daily variance in exercise capacity

Project description:Physiological and molecular dissection of daily variance in exercise capacity

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Antihypertrophic Memory after Regression of Exercise-induced Physiological Myocardial Hypertrophy

Project description:Antihypertrophic Memory after Regression of Exercise-induced Physiological Myocardial Hypertrophy

| PRJNA675138 | ENA

Resistance Exercise Reverses Aging in Human Skeletal Muscle

Project description:Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training. Keywords: resistance exercise, muscle, aging

2007-07-16 | GSE8479 | GEO

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