Wound repair at a glance

Shaw, Tanya J.; Martin, Paul

doi:10.1242/jcs.031187

Cited by 671 publications

(633 citation statements)

References 68 publications

(65 reference statements)

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“…Reepithelialization requires not only altered adhesion of keratinocytes at the wound edge (Shaw and Martin 2009) but also diminished contacts of keratins to desmosomal proteins, along with elevated expression of KRT6/16/17 and a decrease in KRT1/10 (Patel et al 2006). In agreement, cells expressing KRT6 or KRT17 show elevated, PKCa-mediated desmosome disassembly and subsequent destabilization of epithelial sheets.…”

Section: Interdependence Of Keratins and Desmosomesmentioning

confidence: 83%

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Hatzfeld

Keil

Magin

2017

Cold Spring Harb Perspect Biol

116

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Adherens junctions (AJs) and desmosomes connect the actin and keratin filament networks of adjacent cells into a mechanical unit. Whereas AJs function in mechanosensing and in transducing mechanical forces between the plasma membrane and the actomyosin cytoskeleton, desmosomes and intermediate filaments (IFs) provide mechanical stability required to maintain tissue architecture and integrity when the tissues are exposed to mechanical stress. Desmosomes are essential for stable intercellular cohesion, whereas keratins determine cell mechanics but are not involved in generating tension. Here, we summarize the current knowledge of the role of IFs and desmosomes in tissue mechanics and discuss whether the desmosome-keratin scaffold might be actively involved in mechanosensing and in the conversion of chemical signals into mechanical strength.

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Section: Interdependence Of Keratins and Desmosomesmentioning

confidence: 83%

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Hatzfeld

Keil

Magin

2017

Cold Spring Harb Perspect Biol

116

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“…It involves three temporally overlapping phases: inflammation, new tissue formation, and remodeling. 15 Inflammation takes place immediately after tissue damage to prevent fluid loss and infection, and to remove dead cells. This first step is orchestrated by components of the coagulation cascade, inflammatory pathways, and the immune system.…”

Section: Discussionmentioning

confidence: 99%

“…2,15 These trigger specific changes in gene expression and promote the proliferation, differentiation, and migration of endothelial cells, keratinocytes, and fibroblasts, which is in concert with different types of immune cells. 15 As recovery progresses, these signaling cascades are gradually down-regulated in an orchestrated manner. Deregulation of the repair process can cause defects ranging from Figure 1.…”

Section: Discussionmentioning

confidence: 99%

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Harnessing the Electric Spark of Life to Cure Skin Wounds

Martin-Granados

McCaig

2014

Advances in Wound Care

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“…In the acute phase of inflammation, neutrophils, the first responder inflammatory cells, migrate toward wound sites to internalize and eliminate pathogens. Subsequently, macrophages preferentially infiltrate to wound sites after neutrophil recruitment, where they release cytokines, chemokines, and growth factors to control skin wound healing by stimulating the activation and proliferation of fibroblasts and keratinocytes, and by promoting wound contraction and angiogenesis [1]. Although this inflammatory response …”

mentioning

confidence: 99%

Release of TNF‐α from macrophages is mediated by small GTPase Rab37

et al. 2011

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Activated macrophages at wound sites release many cytokines which positively affect skin wound healing. However, the molecular mechanisms controlling cytokine secretion from macrophages have not been elucidated. In the present study, we performed an RT-PCR analysis and found that 19 small GTPase Rab isoforms were expressed at skin wound sites, with six of them (i.e. Rab3B, Rab27B, Rab30, Rab33A, Rab37, and Rab40C) being upregulated during the inflammation and proliferation/migration phase of skin repair. We also found that gene expression of Rab37 in murine primary and RAW264.7 macrophages was significantly induced after stimulation with LPS. Overexpression of wild type and constitutively active Rab37 in RAW264.7 cells significantly increased TNF-a secretion, whereas knockdown of Rab37 by siRNA significantly decreased it. We also identified 29 putative Rab37-interacting proteins, including the membrane fusion regulating Munc13-1, using liquid chromatography/ linear ion trap mass spectrometry (LC-MS/MS). Immunocytochemical analysis further revealed that TNF-a-containing vesicles were colocalized with both Rab37 and Munc13-1 in activated macrophages. Knockdown of Munc13-1 by siRNA significantly decreased TNF-a secretion. Taken together, these findings demonstrate that Rab37 interacts with Munc13-1 to control TNF-a secretion from activated macrophages.Key words: Macrophage . Munc13-1 . Rab37 . Skin wound healing . TNF-a Supporting Information available online IntroductionIn response to skin tissue damage, inflammatory cells rapidly infiltrate the wound site to protect against infection. In the acute phase of inflammation, neutrophils, the first responder inflammatory cells, migrate toward wound sites to internalize and eliminate pathogens. Subsequently, macrophages preferentially infiltrate to wound sites after neutrophil recruitment, where they release cytokines, chemokines, and growth factors to control skin wound healing by stimulating the activation and proliferation of fibroblasts and keratinocytes, and by promoting wound contraction and angiogenesis [1]. Although this inflammatory response 3230is part of the wound-healing process, wound models in several organisms have shown that the inflammatory response can cause fibrotic diseases (i.e. scarring) in the skin and other organs [2]. Recently, we have shown that osteopontin is secreted by activated fibroblasts in response to platelet-derived growth factor secreted from macrophages, and that silencing of osteopontin at skin wound sites reduces scarring and improves the quality of healing in vivo [3]. Therefore, the pathways controlling inflammatory mediator secretion could provide novel molecular therapeutic targets [4].One such inflammatory mediator, TNF-a, is a pleiotropic proinflammatory cytokine expressed by macrophages and neutrophils at skin wound sites [5,6]. It has been reported that signaling via TNF-a negatively regulates skin wound healing, because TNF-a receptor p55 KO mice showed rapid skin wound healing coincident with reduced inflammatory respons...

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Wound repair at a glance

Cited by 671 publications

References 68 publications

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Harnessing the Electric Spark of Life to Cure Skin Wounds

Release of TNF‐α from macrophages is mediated by small GTPase Rab37

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