Fraire-Zamora Juan J, Simons Matias
Center for Systems Biology (ZBSA), University of Freiburg, Freiburg, Germany.
Renal Division, University Hospital Freiburg, Freiburg, Germany.
Wound Repair Regen. 2018 Jan;26(1):102-107. doi: 10.1111/wrr.12617. Epub 2018 Mar 7.
Epithelia have the ability to repair injuries through an evolutionary conserved wound healing mechanism. Wound healing events can be classified into the transcription-independent signals involving mobilization of ionic currents and cytoskeletal rearrangements or the transcription-dependent response with activation of repair genes. The vacuolar H -ATPase (V-ATPase) has been implicated in the regeneration of vertebrate structures, but the underlying cellular mechanisms remain unclear. Here, we use wounding assays on the epidermis of Drosophila embryos to assess the role of the V-ATPase in the healing response. We show that a deficient V-ATPase induces a defective wound healing response by delaying re-epithelialization and preventing the ERK-dependent transcriptional activation of repair around the wound site. Our data suggests that the V-ATPase plays an evolutionary conserved role in the activation of genes necessary for the wound healing response.
上皮细胞具有通过进化保守的伤口愈合机制修复损伤的能力。伤口愈合事件可分为涉及离子电流动员和细胞骨架重排的转录非依赖信号，或伴随修复基因激活的转录依赖反应。液泡H⁺ -ATP酶（V-ATP酶）与脊椎动物结构的再生有关，但其潜在的细胞机制仍不清楚。在这里，我们利用果蝇胚胎表皮的创伤试验来评估V-ATP酶在愈合反应中的作用。我们发现，V-ATP酶缺陷会通过延迟重新上皮化和阻止伤口部位周围修复的ERK依赖转录激活，从而诱导有缺陷的伤口愈合反应。我们的数据表明，V-ATP酶在激活伤口愈合反应所需基因方面发挥着进化保守的作用。
