China
Africa
Explore chapters and articles related to this topic
Environmental factors contribute to skeletal muscle and spinal cord regeneration
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Ophelia Ehrlich, Yona Goldshmit, Peter Currie
Integrin-α7 also reliably marks Pax7+ quiescent satellite cells in mice (Gnocchi et al. 2009), and in vitro experiments where integrin-α7 was inhibited identified integrin-α7 as a pivotal protein for cell adhesion and cell motility, with laminin-α1 and -α2 as its ligand (Yao et al. 1996). These studies support the theory that on activation, muscle stem cells use the laminin basement membrane to migrate and then regenerate the damaged area (Hughes and Blau 1990; Stoiber and Sanger 1996). Recently, the ability to undertake intervital imaging within living mouse muscle has been developed (Webster et al. 2016). This significant technical breakthrough has documented that activated muscle stem and progenitor cells use the remaining ECM of ghost fibers that degenerate after injury, again highlighting the central role that muscle cell matrix plays in guiding and controlling the activated stem cell during the regenerative process (Webster et al. 2016). Extracellular ligands can also activate integrins, changing the intracellular conformation and allowing proteins, such as focal adhesion kinase (FAK) and integrin-linked kinase (ILK), to engage with integrin (Sage 1982; Giancotti and Ruoslahti 1999; Postel et al. 2008). On activation, integrins can either induce downstream signaling cascades or form protein complexes that will in turn interact with actin filaments, maintaining the cell structure (Otey et al. 1990; Guan 1997; Giancotti and Ruoslahti 1999; Parsons 2003; Hannigan et al. 2005; Wegener et al. 2007; Postel et al. 2008; Janoštiak et al. 2014).
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Hexachlorobenzene (HCB) is a non-genotoxic hepatocarcinogenic chemical thought to induce cancer via inhibition of GJIC (Mally and Chipman 2002). The compound was mainly used as a fungicide to protect seeds and wheat until it was banned in 1965 (Pohanish 2015). HCB effects on connexins, mainly Cx32, were examined both in vitro and in vivo (Plante, Charbonneau, and Cyr 2002, 2006; Plante, Cyr, and Charbonneau 2007). Noteworthy is the sexual dimorphism. Because of the occurrence of ovarian hormones, HCB produces liver tumors in female rats, but not in males. Upon HCB administration, GJIC is inhibited, and mRNA levels of Cx26 and Cx32 are significantly reduced (Plante, Charbonneau, and Cyr 2002). In vitro studies linked this decrease to activation of the integrin-linked kinase pathway, which induced and translocated Akt that subsequently triggered transcription factors changing Cx32 expression, such as specificity protein 1 and hepatocyte nuclear factor 1α (Plante, Charbonneau, and Cyr 2006). This observation was confirmed in vivo, where HCB administration produced decreased binding of transcriptional complexes Fr26 and Fr110, known to be controlled by Akt, to the Cx32 gene promotor in female, but not in male rat liver (Plante, Cyr, and Charbonneau 2007).