G protein-mediated pathways and stem cell proliferation and differentiation
DOI:
https://doi.org/10.61173/twpaz804Keywords:
-G protein-coupled receptors, Stem cell regu-lation, Signal transduction dynamicsAbstract
The current popular targets of GPCR activate intracellular signal transduction by binding to G proteins. The drugs developed by it can inhibit the proliferation and migration of cancer cells and promote their programmed cell death. It can be linked to the proliferation and differentiation of stem cells, providing new ideas for regenerative medicine. Research progress has shown that through different Gα subunit activation pathways, these pathways can integrate multiple extracellular signals (growth factors, chemokines, hormones, mechanical forces), and determine the behavior of stem cells by regulating the core transcription factor network. However, there is a lack of detailed depiction and mechanism analysis of the dynamicity (time, space, cellular heterogeneity) and integrative (multi-dimensional signal input, especially mechanical force input in three-dimensional physical environment) of G protein signaling networks in specific stem cell environments. This article analyzed the signals and their correlations mediated by some GPCRs, and recognized their importance in regulating stem cell activities. Regulating the activities of stem cells through GPCRs not only promotes the in vitro cultivation of tissues and organs, but also provides new drug development ideas for human self-healing. However, to understand the complexity of the signals (which may function differently under different time and environmental conditions), further research and analysis are still needed.
References
[1] Kobayashi N. R., Hawes S. M., Crook J. M., and Pébay A., “G-protein coupled receptors in stem cell self-renewal and differentiation,” Stem Cell Rev. Rep., vol. 6, no. 3, pp. 351–366, 2010. Dean&Francis Yifan Li
[2] Zhang L., Noguchi Y. T., Nakayama H., et al., “The CalcR- PKA-Yap1 Axis Is Critical for Maintaining Quiescence in Muscle Stem Cells,” Cell Rep., vol. 29, no. 8, pp. 2154–2163.e5, 2019.
[3] Gomes I., Jordan B. A., Gupta A., Rios C., Trapaidze N., and Devi L. A., “G protein coupled receptor dimerization: implications in modulating receptor function,” J. Mol. Med. (Berl)., vol. 79, no. 5–6, pp. 226–242, 2001.
[4] Bernardo M. E. and Fibbe W. E., “Mesenchymal stromal cells: sensors and switchers of inflammation,” Cell Stem Cell, vol. 13, no. 4, pp. 392–402, 2013.
[5] “Advances in Regenerative Stem Cell Therapy in Androgenic Alopecia and Hair Loss: Wnt Pathway, Growth-Factor, and Mesenchymal Stem Cell Signaling Impact Analysis on Cell Growth and Hair Follicle Development.”
[6] Zhang L., Noguchi Y. T., Nakayama H., et al., “The CalcR- PKA-Yap1 Axis Is Critical for Maintaining Quiescence in Muscle Stem Cells,” Cell Rep., vol. 29, no. 8, pp. 2154–2163.e5, 2019.
[7] Apáti Á., Berecz T., and Sarkadi B., “Calcium signaling in human pluripotent stem cells,” Cell Calcium, vol. 59, no. 2–3, pp. 117–123, 2016.
[8] Wu C. I., Hoffman J. A., Shy B. R., et al., “Function of Wnt/ β-catenin in counteracting Tcf3 repression through the Tcf3-βcatenin interaction,” Development, vol. 139, no. 12, pp. 2118– 2129, 2012.
[9] Kwon Y., Mehta S., Clark M., et al., “Non-canonical β-adrenergic activation of ERK at endosomes,” Nature, vol. 611, no. 7934, pp. 173–179, 2022.
[10] Wang L. C., Liu Z. Y., Gambardella L., et al., “Regular articles: conditional disruption of hedgehog signaling pathway defines its critical role in hair development and regeneration,” J. Invest. Dermatol., vol. 114, no. 5, pp. 901–908, 2000.
[11] Abe Y. and Tanaka N., “Roles of the Hedgehog Signaling Pathway in Epidermal and Hair Follicle Development, Homeostasis, and Cancer,” J. Dev. Biol., vol. 5, no. 4, p. 12, 2017.
[12] Taylor S. S., Yang J., Wu J., Haste N. M., Radzio-Andzelm E., and Anand G., “PKA: a portrait of protein kinase dynamics,” Biochim. Biophys. Acta, vol. 1697, no. 1–2, pp. 259–269, 2004.
[13] Taelman V. F., Dobrowolski R., Plouhinec J. L., et al., “Wnt signaling requires sequestration of glycogen synthase kinase 3 inside multivesicular endosomes,” Cell, vol. 143, no. 7, pp. 1136–1148, 2010.
[14] van Biesen T., Hawes B. E., Luttrell D. K., et al., “Receptortyrosine-kinase- and G beta gamma-mediated MAP kinase activation by a common signalling pathway,” Nature, vol. 376, no. 6543, pp. 781–784, 1995.
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