Nanogenerators are interesting for biomedical applications, with a great potential for electrical stimulation of excitable cells. Piezoelectric ZnO nanosheets present unique properties for tissue engineering. In this study, nanogenerator arrays based on ZnO nanosheets are fabricated on transparent coverslips to analyse the biocompatibility and the electromechanical interaction with two types of muscle cells, smooth and skeletal. Both cell types adhere, proliferate and differentiate on the ZnO nanogenerators. Interestingly, the amount of Zn ions released over time from the nanogenerators does not interfere with cell viability and does not trigger the associated inflammatory response, which is not triggered by the nanogenerators themselves either. The local electric field generated by the electromechanical nanogenerator-cell interaction stimulates smooth muscle cells by increasing cytosolic calcium ions, whereas no stimulation effect is observed on skeletal muscle cells. The random orientation of the ZnO nanogenerators, avoiding an overall action potential aligned along the muscle fibre, is hypothesised to be the cause of the cell-type dependent response. This demonstrates the need of optimizing the nanogenerator morphology, orientation and distribution according to the potential biomedical use. Thus, this study demonstrates the cell-scale stimulation triggered by biocompatible piezoelectric nanogenerators without using an external source on smooth muscle cells, although it remarks the cell type-dependent response.
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http://dx.doi.org/10.3390/ijms23010432 | DOI Listing |
Tissue Eng Regen Med
January 2025
College of Materials Science and Engineering, Hunan University, Changsha, 410072, People's Republic of China.
Background: Tissue engineering holds promise for vascular repair and regeneration by mimicking the extracellular matrix of blood vessels. However, achieving a functional and thick vascular wall with aligned fiber architecture by electrospinning remains a significant challenge.
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Cell Mol Life Sci
January 2025
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Unitat de Farmacologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.
Nuclear growth differentiation factor 15 (GDF15) reduces the binding of the mothers' against decapentaplegic homolog (SMAD) complex to its DNA-binding elements. However, the stimuli that control this process are unknown. Here, we examined whether saturated fatty acids (FA), particularly palmitate, regulate nuclear GDF15 levels and the activation of the SMAD3 pathway in human skeletal myotubes and mouse skeletal muscle, where most insulin-stimulated glucose use occurs in the whole organism.
View Article and Find Full Text PDFFASEB J
January 2025
National Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing, China.
Microgravity-induced cardiac remodeling and dysfunction present significant challenges to long-term spaceflight, highlighting the urgent need to elucidate the underlying molecular mechanisms and develop precise countermeasures. Previous studies have outlined the important role of miRNAs in cardiovascular disease progression, with miR-199a-3p playing a crucial role in myocardial injury repair and the maintenance of cardiac function. However, the specific role and expression pattern of miR-199a-3p in microgravity-induced cardiac remodeling remain unclear.
View Article and Find Full Text PDF() is a causative gene for genetic hydrocephalus found in hemorrhagic hydrocephalus () mice. The knockout (KO) rat has subcortical heterotopia with frequent brain hemorrhage as seen in mice. In this study, we report aberrant alpha-smooth muscle actin (α-SMA) expression in the wall of lateral ventricle of the KO rats.
View Article and Find Full Text PDFBiophys J
January 2025
Department of Pharmacology, University of California Davis, California 95616.
In every heartbeat, cardiac muscle cells perform excitation-Ca signaling-contraction (EC) coupling to pump blood against the vascular resistance. Cardiomyocytes can sense the mechanical load and activate mechano-chemo-transduction (MCT) mechanism, which provides feedback regulation of EC coupling. MCT feedback is important for the heart to upregulate contraction in response to increased load to maintain cardiac output.
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