Cellular dewetting refers to the process of nucleation and enlargement of transendothelial cell macroaperture (TEM) tunnels in endothelial cells (Figure 1).[1] This phenomenon is analogous to the nucleation and growth of dry patches in viscous liquids spreading on a non-wettable substrate (Figure 2).[2] Cellular dewetting is triggered by several protein toxins from pathogenic bacteria, notably the EDIN-like factors from Staphylococcus aureus and from Clostridium botulinum, as well as edema toxin from Bacillus anthracis.[3][4] TEMs form in response to the rupture of cytoskeleton physical connections through the cytoplasm due to inhibition of the RhoA/ROCK pathway or to induction of the flux of cyclic-AMP (cAMP) broad signaling molecule.[4][5]
- ^ Lemichez, E. (2012). "Transcellular tunnel dynamics: Control of cellular dewetting by actomyosin contractility and I-BAR proteins". Biology of the Cell. 105 (3): 109–117. doi:10.1111/boc.201200063. PMID 23189935. S2CID 31452113.
- ^ De Gennes, P.-G. (2004). Capillarity and Wetting Phenomena. New York: Springer. ISBN 978-0387005928.
- ^ Boyer, L. (2006). "Induction of transient macroapertures in endothelial cells through RhoA inhibition by Staphylococcus aureus factors". Journal of Cell Biology. 173 (5): 809–819. doi:10.1083/jcb.200509009. PMC 2063895. PMID 16754962.
- ^ a b Maddugoda, M. P. (2011). "cAMP signaling by anthrax edema toxin induces transendothelial cell tunnels, which are resealed by MIM via Arp2/3-driven actin polymerization". Cell Host & Microbe. 10 (5): 464–474. doi:10.1016/j.chom.2011.09.014. PMID 22100162.
- ^ Cai, Y. (2010). "Cytoskeletal coherence requires myosin-IIA contractility". Journal of Cell Science. 123 (3): 413–423. doi:10.1242/jcs.058297. PMC 2816186. PMID 20067993.