3D in vitro M2 macrophage model to mimic modulation of tissue repair
Abstract Distinct anti-inflammatory macrophage (M2) subtypes, namely M2a and M2c, are reported to modulate the tissue repair process tightly and chronologically by modulating fibroblast differentiation state and functions. To establish a well-defined three-dimensional (3D) cell culture model to mimi...
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2021
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oai:doaj.org-article:df8378eacbdc424884f4426f5edffb1e2021-12-05T12:24:36Z3D in vitro M2 macrophage model to mimic modulation of tissue repair10.1038/s41536-021-00193-52057-3995https://doaj.org/article/df8378eacbdc424884f4426f5edffb1e2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41536-021-00193-5https://doaj.org/toc/2057-3995Abstract Distinct anti-inflammatory macrophage (M2) subtypes, namely M2a and M2c, are reported to modulate the tissue repair process tightly and chronologically by modulating fibroblast differentiation state and functions. To establish a well-defined three-dimensional (3D) cell culture model to mimic the tissue repair process, we utilized THP-1 human monocytic cells and a 3D collagen matrix as a biomimetic tissue model. THP-1 cells were differentiated into macrophages, and activated using IL-4/IL-13 (MIL-4/IL-13) and IL-10 (MIL-10). Both activated macrophages were characterized by both their cell surface marker expression and cytokine secretion profile. Our cell characterization suggested that MIL-4/IL-13 and MIL-10 demonstrate M2a- and M2c-like subtypes, respectively. To mimic the initial and resolution phases during the tissue repair, both activated macrophages were co-cultured with fibroblasts and myofibroblasts. We showed that MIL-4/IL-13 were able to promote matrix synthesis and remodeling by induction of myofibroblast differentiation via transforming growth factor beta-1 (TGF-β1). On the contrary, MIL-10 demonstrated the ability to resolve the tissue repair process by dedifferentiation of myofibroblast via IL-10 secretion. Overall, our study demonstrated the importance and the exact roles of M2a and M2c-like macrophage subtypes in coordinating tissue repair in a biomimetic model. The established model can be applied for high-throughput platforms for improving tissue healing and anti-fibrotic drugs testing, as well as other biomedical studies.Jiranuwat SapudomShaza KaramanWalaa K. E. MohamedAnna Garcia-SabatéBrian C. QuarteyJeremy C. M. TeoNature PortfolioarticleMedicineRENnpj Regenerative Medicine, Vol 6, Iss 1, Pp 1-13 (2021) |
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Medicine R Jiranuwat Sapudom Shaza Karaman Walaa K. E. Mohamed Anna Garcia-Sabaté Brian C. Quartey Jeremy C. M. Teo 3D in vitro M2 macrophage model to mimic modulation of tissue repair |
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Abstract Distinct anti-inflammatory macrophage (M2) subtypes, namely M2a and M2c, are reported to modulate the tissue repair process tightly and chronologically by modulating fibroblast differentiation state and functions. To establish a well-defined three-dimensional (3D) cell culture model to mimic the tissue repair process, we utilized THP-1 human monocytic cells and a 3D collagen matrix as a biomimetic tissue model. THP-1 cells were differentiated into macrophages, and activated using IL-4/IL-13 (MIL-4/IL-13) and IL-10 (MIL-10). Both activated macrophages were characterized by both their cell surface marker expression and cytokine secretion profile. Our cell characterization suggested that MIL-4/IL-13 and MIL-10 demonstrate M2a- and M2c-like subtypes, respectively. To mimic the initial and resolution phases during the tissue repair, both activated macrophages were co-cultured with fibroblasts and myofibroblasts. We showed that MIL-4/IL-13 were able to promote matrix synthesis and remodeling by induction of myofibroblast differentiation via transforming growth factor beta-1 (TGF-β1). On the contrary, MIL-10 demonstrated the ability to resolve the tissue repair process by dedifferentiation of myofibroblast via IL-10 secretion. Overall, our study demonstrated the importance and the exact roles of M2a and M2c-like macrophage subtypes in coordinating tissue repair in a biomimetic model. The established model can be applied for high-throughput platforms for improving tissue healing and anti-fibrotic drugs testing, as well as other biomedical studies. |
format |
article |
author |
Jiranuwat Sapudom Shaza Karaman Walaa K. E. Mohamed Anna Garcia-Sabaté Brian C. Quartey Jeremy C. M. Teo |
author_facet |
Jiranuwat Sapudom Shaza Karaman Walaa K. E. Mohamed Anna Garcia-Sabaté Brian C. Quartey Jeremy C. M. Teo |
author_sort |
Jiranuwat Sapudom |
title |
3D in vitro M2 macrophage model to mimic modulation of tissue repair |
title_short |
3D in vitro M2 macrophage model to mimic modulation of tissue repair |
title_full |
3D in vitro M2 macrophage model to mimic modulation of tissue repair |
title_fullStr |
3D in vitro M2 macrophage model to mimic modulation of tissue repair |
title_full_unstemmed |
3D in vitro M2 macrophage model to mimic modulation of tissue repair |
title_sort |
3d in vitro m2 macrophage model to mimic modulation of tissue repair |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/df8378eacbdc424884f4426f5edffb1e |
work_keys_str_mv |
AT jiranuwatsapudom 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair AT shazakaraman 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair AT walaakemohamed 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair AT annagarciasabate 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair AT briancquartey 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair AT jeremycmteo 3dinvitrom2macrophagemodeltomimicmodulationoftissuerepair |
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