Investigators tested the hypothesis that TMEM16A, a calcium-activated chloride channel, contributed to modifications in arterial contractility during type 2 diabetes (T2D). They indicated that T2D increased TMEM16A mRNA in arterial smooth muscle cells and total and surface TMEM16A protein in resistance-size arteries of mice.
[American Journal of Physiology-Heart and Circulatory Physiology]
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Leo, M. D., Peixoto-Neves, D., Yin, W., Raghavan, S., Muralidharan, P., Mata-Daboin, A., & Jaggar, J. H. (2021). TMEM16A channel upregulation in arterial smooth muscle cells produces vasoconstriction during diabetes. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00690.2020 Cite
Researchers investigated the mechanism by which sphingosine‐1‐phosphate contributes to age‐associated contractile dysfunction.
[Neurogastroenterology and Motility]
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Shen, X., Zhang, L., Jiang, L., Xiong, W., Tang, Y., Lin, L., & Yu, T. (n.d.). Alteration of sphingosine-1-phosphate with aging induces contractile dysfunction of colonic smooth muscle cells via Ca2+-activated K+ channel (BKCa) upregulation. Neurogastroenterology & Motility, n/a(n/a), e14052. https://doi.org/https://doi.org/10.1111/nmo.14052 Cite
Scientists report the origin and molecular mechanisms of calcium signals that control the internal anal sphincter (IAS) basal tone, using a combination approach including a novel IAS slice preparation that retains cell arrangement and architecture as in vivo, 2‐photon imaging, and cell‐specific gene‐modified mice.
[Journal of Cellular Physiology]
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Lu, P., Chen, J., Zhang, C., Saur, D., Baer, C. E., Lifshitz, L. M., Fogarty, K. E., & ZhuGe, R. (n.d.). Oscillating calcium signals in smooth muscle cells underlie the persistent basal tone of internal anal sphincter. Journal of Cellular Physiology, n/a(n/a). https://doi.org/https://doi.org/10.1002/jcp.30279 Cite
Lymphatic marker-positive cells were present in the perivascular space, the walls of small and large arteries and veins, the media of large vessels along smooth muscle cell membranes, and the vascular adventitia.
[Proceedings of the National Academy of Sciences of the United States of America]
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Researchers hypothesized in this study that an lnc-Rps4l-encoded peptide is involved in hypoxic induced pulmonary artery smooth muscle cells (PASMCs) proliferation. The presence of peptide RPS4XL encoded by lnc-Rps4l in PASMCs under hypoxic conditions were confirmed by bioinformatics, immunofluorescence and immunohistochemistry.
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The authors investigated changes of the vascular smooth muscle cell (VSMC) transcriptome by utilizing 3D human vascular organoids organized as a core of VSMCs enclosed by a monolayer of endothelial cells.
[Experimental Cell Research]
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Deconvolution analysis revealed that the proportions of alveolar type 2 cells, proliferating basal cells, goblet cells, and proliferating natural killer/T cells decreased with age, whereas alveolar fibroblasts, pericytes, airway smooth muscle cells, endothelial cells and IGSF21+ dendritic cells increased with age.
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Scientists highlighted the dynamics of mesenchymal cells in the airway niche and implications for chronic airway-injury-associated diseases.
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Moiseenko, A., Vazquez-Armendariz, A. I., Kheirollahi, V., Chu, X., Tata, A., Rivetti, S., Günther, S., Lebrigand, K., Herold, S., Braun, T., Mari, B., Langhe, S. D., Kwapiszewska, G., Günther, A., Chen, C., Seeger, W., Tata, P. R., Zhang, J.-S., Bellusci, S., & Agha, E. E. (2020). Identification of a Repair-Supportive Mesenchymal Cell Population during Airway Epithelial Regeneration. Cell Reports, 33(12). https://doi.org/10.1016/j.celrep.2020.108549 Cite
Researchers tested whether a laminin 111‐rich extracellular matrix could affect smooth muscle cells (SMCs) phenotype and differentiation status. Using time lapse microscopy, image analyses, qRT‐PCR, immunohistochemistry and immunoblotting, and transmission electron microscopy, they showed that SMC acquired a migratory behavior with a decreased expression of differentiation markers and relocation of FAK.
[Cell Biology International]
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Despite the absence of AT1A receptors in cardiomyocytes, C-SMKOs developed robust cardiac hypertrophy. By contrast, R-SMKOs developed identical levels of hypertrophy in response to pressure overload–induced by transverse aortic banding.
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The authors demonstrated that BMP9 and BMP10 acted directly on vascular smooth muscle cells for induction and maintenance of their contractile state.
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