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Dedifferentiation as a cell source for organ regeneration
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Summarizing, we observe that dedifferentiation is an important process to form the cells that are needed for organ regeneration. This dedifferentiation can give rise to precursor cells of the organ directly or to organ stem cells that eventually give rise to the organ’s cellular component. It is thus plausible that, by activating the dedifferentiation process, organ regeneration can be achieved. In fact, induced dedifferentiation with particular genes is a potential therapy for organ regeneration. One of the best examples of this was shown by inducing dedifferentiation and proliferation in adult mice cardiomyocytes with a constitutively active ERBB2 receptor for neuregulin-1 (D’Uva et al. 2015). The partial dedifferentiation allowed the cells to re-enter the cell cycle and proliferate, producing new cardiomyocytes, a process that does not occur in mature cardiac muscle cells.
Self-assembled monolayers of phosphonates promote primary chondrocyte adhesion to silicon dioxide and polyvinyl alcohol materials
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Patrick E. Donnelly, Laurianne Imbert, Kirsty L. Culley, Russell F. Warren, Tony Chen, Suzanne A. Maher
There was an observed difference in chondrocyte morphology between chondrocytes cultured on 4-terminated SiO2 and PVA surfaces. These differences can be attributed to several factors: the studies were conducted on flat surfaces at low-seeding densities, and not three-dimensional gels, scaffolds, or in micromass that chondrocytes are typically cultured in [61–63] and as such, changes in morphology away from the more typical rounded shape are not surprising. The spindle-like morphology and the spreading of cells on the modified SiO2 surfaces suggested a fibroblast-like phenotypic shift of the cells respectively. To assess whether such a changes occurred, real-time quantitative RT-PCR (RT-qPCR) analysis was completed to assess the gene expression of chondrocytes cultured on standard tissue culture plastic (TCP), 4-terminated SiO2 and unmodified SiO2 surfaces after 3 days of culture. The genes analyzed (type I collagen (Col1a2), type II collagen (Col2a1), Aggrecan (Acan), Runx2, and Sox9) represent those that delineate the transition of normal chondrocytes to hypertrophic chondrocytes or dedifferentiation to fibroblast-like cells due to either their decrease or increased expression. We found no significant differences in chondrogenic or hypertrophic gene expression between chondrocytes cultured on TCP and 4-terminated SiO2 but a difference of the dedifferentiation marker Col1a2 between chondrocytes cultured on unmodified SiO2 and the other 2 conditions. These results suggest that bisphosphonic acid SAMP modification does not induce phenotypic change of chondrocytes any more than tissue culture plastic, and that the morphological differences are likely due to dedifferentiation of the chondrocytes into a more fibroblast-like cell when cultured on a cell-adherent stiff substrate [64,65]. This finding is further noted by the morphological differences noted between modified SiO2 and modified PVA – where chondrocytes cultured on SiO2 have a more fibroblastic morphology, that is not seen for chondrocytes cultured on modified PVA which has a much lower stiffness – PVA films have a Young’s modulus ranging from 1.50-3.75 GPa, while that of silicon ranges from 130 to 188 GPa [66,67].