Extracellular Reactive Oxygen Species Drive Apoptosis-Induced Proliferation via Drosophila Macrophages

Fogarty, Caitlin E.; Diwanji, Neha; Lindblad, Jillian L.; Tare, Meghana; Amcheslavsky, Alla; Makhijani, Kalpana; Brückner, Katja; Fan, Yun; Bergmann, Andreas

doi:10.1016/j.cub.2015.12.064

Cited by 182 publications

(286 citation statements)

References 50 publications

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“…Reactive oxygen species (ROS) are produced rapidly after damage and act as chemoattractants for macrophages. This has been demonstrated in both the imaginal disc [41] and the embryo [42] and ROS are required for activation of JNK and p38 [40]. In embryonic wounds, the NADPH oxidase DUOX, which acts as a source of H 2 O 2 , is activated by calcium, and Ca 2+ flashes have been found upon damage [43].…”

Section: Wound Healing and Early Responses To Tissue Damagementioning

confidence: 99%

Imaginal disc regeneration takes flight

Hariharan

Serras

2017

Current Opinion in Cell Biology

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Drosophila imaginal discs, the larval precursors of adult structures such as the wing and leg, are capable of regenerating after damage. During the course of regeneration, discs can sometimes generate structures that are appropriate for a different type of disc, a phenomenon termed transdetermination. Until recently, these phenomena were studied by physically fragmenting discs and then transplanting them into the abdomens of adult female flies. This field has experienced a renaissance following the development of genetic ablation systems that can damage precisely defined regions of the disc without the need for surgery. Together with more traditional approaches, these newer methods have generated many novel insights into wound healing, the mechanisms that drive regenerative growth, plasticity during regeneration and systemic effects of tissue damage and regeneration.

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Section: Wound Healing and Early Responses To Tissue Damagementioning

confidence: 99%

Imaginal disc regeneration takes flight

Hariharan

Serras

2017

Current Opinion in Cell Biology

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“…Pioneering work in the Drosophila wing disc and eye has identified a requirement for JNK, Shh, EGF and TNF signaling pathways during apoptosis-induced compensatory proliferation [66][67][68][69]. In Drosophila imaginal discs, JNK activation in dying and neighboring cells depends on an inflammatory response that is triggered by Duox, which produces extracellular reactive oxygen species (ROS) [70 ]. Interestingly, hemocytes (macrophages) are required for ROS-mediated apoptosis-induced compensatory proliferation.…”

Section: Identifying New Molecules/pathways Important For Hair Cell Rmentioning

confidence: 99%

Insights into sensory hair cell regeneration from the zebrafish lateral line

Kniss

Jiang

Piotrowski

2016

Current Opinion in Genetics & Development

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“…Two recent reports, including our own, demonstrated that repair processes in imaginal discs also require ROS 9,15 . In the first report, ROS were generated in response to a short pulse of apoptosis in larval wing imaginal discs.…”

Section: Synopsis Of Our Recently Published Workmentioning

confidence: 88%

The beneficial role of extracellular reactive oxygen species in apoptosis-induced compensatory proliferation

Diwanji

Bergmann

2016

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Apoptosis-induced proliferation (AiP) maintains tissue homeostasis following massive stress-induced cell death. During this phenomenon, dying cells induce proliferation of the surviving cells to compensate for the tissue loss, and thus restore organ size. Along with wound healing and tissue regeneration, AiP also contributes to tumor repopulation following radiation or chemotherapy. There are several models of AiP. Using an “undead” AiP model that causes hyperplastic overgrowth of Drosophila epithelial tissue, we recently demonstrated that extracellular reactive oxygen species (eROS) are produced by undead epithelial cells, and are necessary for inducing AiP and overgrowth. Furthermore, hemocytes, the Drosophila blood cells, are seen adjacent to the undead epithelial tissue, and may secrete the TNF ortholog Eiger that signals through the TNF receptor to active Jun-N-terminal kinase (JNK) in the undead tissue and induce proliferation. We propose that undead epithelial tissue triggers an inflammatory response that resembles recruitment of macrophages to human epithelial tumors, and that these tumor-associated macrophages release signals for proliferation and tumor growth of the epithelium. This Extra View article summarizes these recent findings with a focus on the role of eROS for promoting regeneration and inflammation-induced tumorigenesis.

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Extracellular Reactive Oxygen Species Drive Apoptosis-Induced Proliferation via Drosophila Macrophages

Cited by 182 publications

References 50 publications

Imaginal disc regeneration takes flight

Imaginal disc regeneration takes flight

Insights into sensory hair cell regeneration from the zebrafish lateral line

The beneficial role of extracellular reactive oxygen species in apoptosis-induced compensatory proliferation

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