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Programming cells to build tissues with synthetic biology
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
The engineered cells will perform patterning-installing routines to generate signaling centers for the localized production of growth factors. The aim is to replicate the 3D signaling centers that are guiding limb formation during development (Tabin and McMahon 2008) along the proximo-distal, antero-posterior, and dorso-ventral axes. This step of patterning has been problematic to achieve, even with a simple scaffold (Lin et al. 2013). Synthetic blastema cells have the potential of installing complex spatio-temporal dynamics in a self-organized fashion. For example, a cell–cell communication network of pole formation (e.g., positive feedback with lateral inhibition), a multicellular version of an intracellular polarization circuit (Chau et al. 2012), can be used to select and differentiate a group of cells to be the synthetic zone of polarizing activity (sZPA) to recapitulate the endogenous signaling center (ZPA) that patterns the developing limb along the antero-posterior axis. To do that, the polarization circuit is wired to effectors that increase homotypic cell–cell adhesion to condense the cells in a stable structure and to the secretion of sonic hedgehog (SHH), the main effector morphogen secreted by ZPA. Subsequently, non-sZPA cells will be executing a Turing pattern algorithm to generate columns of digit fields to specify the future sides of digit formation (Cooper 2015). The goal is to re-establish the signaling centers for limb patterning as they were used during development.
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Other pathways such as Sonic Hedgehog (SHH) and Notch are implicated. SHH binds to patched 1 receptor (PTCH1) which inhibits the repression of the Smoothened receptor (SMO). SMO activation stimulates the glioma family transcription receptors (Gli1) during development and cancer progression (Briscoe and Thérond 2013; Yue et al. 2014). Notch interacts with Delta-like or Jagged ligands that lead to proteolysis of Notch intracellular domain (Hori, Sen, and Artavanis-Tsakonas 2013). This domain regulates activation of SNAI1 and 2 (Lamouille, Xu, and Derynck 2014; Yuan et al. 2014).