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XB-ART-47242
Proc Natl Acad Sci U S A July 2, 2013; 110 (27): 11029-34.

Inositol kinase and its product accelerate wound healing by modulating calcium levels, Rho GTPases, and F-actin assembly.



Abstract
Wound healing is essential for survival. We took advantage of the Xenopus embryo, which exhibits remarkable capacities to repair wounds quickly and efficiently, to investigate the mechanisms responsible for wound healing. Previous work has shown that injury triggers a rapid calcium response, followed by the activation of Ras homolog (Rho) family guanosine triphosphatases (GTPases), which regulate the formation and contraction of an F-actin purse string around the wound margin. How these processes are coordinated following wounding remained unclear. Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzymatic product inositol 1,3,4,5-tetrakisphosphate (InsP4) plays an essential role during wound healing by modulating the activity of Rho family GTPases and F-actin ring assembly. Furthermore, we show that Itpkb and InsP4 modulate the speed of the calcium wave, which propagates from the site of injury into neighboring uninjured cells. Strikingly, both overexpression of itpkb and exogenous application of InsP4 accelerate the speed of wound closure, a finding that has potential implications in our quest to find treatments that improve wound healing in patients with acute or chronic wounds.

PubMed ID: 23776233
PMC ID: PMC3704016
Article link: Proc Natl Acad Sci U S A
Grant support: [+]
Genes referenced: actl6a akt1 cdc42 ctrl gem gnl3 itpkb myc noct pak1 prl.1 rac1 rho rho.2 rhoa rpl8 sox3
Antibodies: Cdc42 Ab1 Itpkb Ab1 Rac1 Ab2 Rhoa Ab1
Morpholinos: itpkb MO1


Article Images: [+] show captions
References:
Abreu-Blanco, 2011, Pubmed [+]


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