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10.1038/nphys3040 http://scihub22266oqcxt.onion/10.1038/nphys3040 C4915550!4915550 !27340423     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27340423 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27340423 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Phys 2014 ; 10 (9 ): 683-690 Nephropedia Template TP {{tp|p=27340423 |t=2014. Forces driving epithelial wound healing |pdf=|usr=}}{{27340423 }} gab.com Text Forces driving epithelial wound healing JO: Nat Phys http://www.kidney.de/pget.php?&tw=1&pmid=27340423 #FOAvip A fundamental feature of multicellular organisms is their ability to self-repair wounds through the movement of epithelial cells into the damaged area. This collective cellular movement is commonly attributed to a combination of cell crawling and "purse-string" contraction of a supracellular actomyosin ring. Here we show by direct experimental measurement that these two mechanisms are insufficient to explain force patterns observed during wound closure. At early stages of the process, leading actin protrusions generate traction forces that point away from the wound, showing that wound closure is initially driven by cell crawling. At later stages, we observed unanticipated patterns of traction forces pointing towards the wound. Such patterns have strong force components that are both radial and tangential to the wound. We show that these force components arise from tensions transmitted by a heterogeneous actomyosin ring to the underlying substrate through focal adhesions. The structural and mechanical organization reported here provides cells with a mechanism to close the wound by cooperatively compressing the underlying substrate. Twit Text FOAVip Forces driving epithelial wound healing ????Nat Phys http://www.kidney.de/pget.php?&tw=1&pmid=27340423 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27340423 #FOAvip English Wikipedia <ref>{{Cite pmid|27340423 }}</ref> Forces driving epithelial wound healing #MMPMID27340423 Brugués A ; Anon E ; Conte V ; Veldhuis JH ; Gupta M ; Colombelli J ; Muñoz JJ ; Brodland GW ; Ladoux B ; Trepat X Nat Phys 2014[Sep]; 10 (9 ): 683-690 PMID27340423 show ga A fundamental feature of multicellular organisms is their ability to self-repair wounds through the movement of epithelial cells into the damaged area. This collective cellular movement is commonly attributed to a combination of cell crawling and "purse-string" contraction of a supracellular actomyosin ring. Here we show by direct experimental measurement that these two mechanisms are insufficient to explain force patterns observed during wound closure. At early stages of the process, leading actin protrusions generate traction forces that point away from the wound, showing that wound closure is initially driven by cell crawling. At later stages, we observed unanticipated patterns of traction forces pointing towards the wound. Such patterns have strong force components that are both radial and tangential to the wound. We show that these force components arise from tensions transmitted by a heterogeneous actomyosin ring to the underlying substrate through focal adhesions. The structural and mechanical organization reported here provides cells with a mechanism to close the wound by cooperatively compressing the underlying substrate. äForces driving epithelial wound healing (epmc).pdf DeepDyve Pubget Overpricing