IL-1β stimulation of CCD-18co myofibroblasts enhances repair of epithelial monolayers through Wnt-5a

Raymond, Meera; Marchbank, Tania; Moyer, Mary Pat; Sanderson, Ian R.; Kruidenier, Laurens

doi:10.1152/ajpgi.00458.2011

Cited by 9 publications

(7 citation statements)

References 39 publications

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“…In the future, we will examine if abnormal occlusion (causing mechanical changes in TMJ tissue) will induce β-catemn signalling activation in TMJ tissue. In addition to mechanical loading, growth factors involved in inflammation, such as tumour necrosis factor-α (TNF-α) and mterleukin 1β (IL-1β) could be potentially important upstream regulators for β-catenin signalling in TMJ tissues.It has been reported that TNF-α and IL-1β regulate β-catenin signalling in other tissues (Kitazawa et al ., 2011; Raymond et al ., 2012; Gong et al ., 2014). Regarding the mechamsm of β-catenin overexpression-induced defects in TMJ tissue, we propose that one of the major downstream mediators for β-catemn signalling in the TMJ tissue is Runx2.…”

Section: Discussionmentioning

confidence: 99%

Activation of β-catenin signalling leads to temporomandibular joint defects

Wang

Xie

et al. 2014

eCM

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Despite extensive research in knee and hip osteoarthritis (OA), the underlying mechanism of temporomandibular joint (TMJ) disorder remains largely unknown. The purpose of this study was to determine whether the constitutive activation of β-catenin in the middle and deep layers of the articular cartilage can compromise the homeostasis of this tissue in the TMJ. Co12CreER T2 transgenic mice were bred with Rosa mT/mG reporter mice to determine Cre recombination efficiency. Co12CreER T2 mice were then crossed with β-catenin flox (ex3)/+ mice to generate β-catenin conditional activation mice, β-catenin(ex3) Co12ER . TMJ samples were harvested when the mice were 1-, 3-or 6-month-old and evaluated using histology, histomorphometry and immunohistochemistry. β-catenin(ex3) Co12ER mice were further crossed with Mmp13 flox/flox and Adamts5 −/− mice to generate β-catenin(ex3)/Mmp13) Co12ER and β-catenin(ex3) Co12ER )/Adamts5 −/− double mutant mice to investigate the role of Mmp13 and Adamts5 in the development of TMJ disorder. High levels of Cre-recombination were seen in Co12CreER T2 ;Rosa mT/mG mice. Progressive TMJ defects developed in 1-, 3-and 6-month-old β-catenin(ex3) Co12ER mice, as revealed by histology and histomorphometry. Results further demonstrated that the defects observed in β-catenin(ex3) Co12ER mice were significantly decelerated after deletion of the Mmp13 or Adamts5 gene in (β-catenin(ex3)/Mmp13) co12ER or β-catenin(ex3) Co12ER / Adamts5 −/− double mutant mice. In summary, we found that β-catenin is a critical gene in the induction of TMJ cartilage degeneration, and over-expressing β-catenin in TMJ cartilage leads to defects assembling an OA-like phenotype. Deletion of Mmp13 and Adamts5 in β-catenin (ex3

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Section: Discussionmentioning

confidence: 99%

Activation of β-catenin signalling leads to temporomandibular joint defects

Wang

Xie

et al. 2014

eCM

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“…In primary mouse microglia cells, 300 ng/mL Wnt-5a increased proliferation [33], whereas treatment of cholangio-carcinoma cells with rWnt-5a decreased cell proliferation in vitro [34]. In the context of the initiation and coordination of intestinal epithelial repair, a human colon carcinoma cell line Caco2 and an epithelial cell line from normal colon NCM460 were treated with Wnt-5a (2.5-600 ng/mL), whereby rWnt-5a enhanced cell migration at 20-400 ng/mL but proliferation only at concentrations >100 ng/mL [35]. Yet, Wnt-5a has been reported to protect, in a dose-dependent manner, germinal centre B cells from apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Herr

Horndasch

Howe

et al. 2014

Reproductive Biology

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“…Furthermore, IL-1β induced the overexpression of Wnt5a in CCD-18Co, an essential molecule of epithelium integrity and regeneration. Conditioned media depleted from Wnt5a failed to promote epithelial migration and differentiation, indicating that IL-1β indirectly induces epithelial migration through its direct action on myofibroblasts’ ability to express Wnt5a [70]. However, increased local and systemic IL-6 levels have been mainly associated with disease activity and severity.…”

Section: From Endothelial and Epithelial Injury To Myofibroblast Actimentioning

confidence: 99%

Stromal and immune cells in gut fibrosis: the myofibroblast and the scarface

Valatas

Filidou

Drygiannakis

et al. 2017

aog

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Post-inflammatory scarring is the end-result of excessive extracellular matrix (ECM) accumulation and tissue architectural destruction. It represents a failure to effectively remodel ECM and achieve proper reinstitution and healing during chronic relapsing inflammatory processes. Scarring may affect the functionality of any organ, and in the case of inflammatory bowel disease (IBD)-associated fibrosis leads to stricture formation and often surgery to remove the affected bowel. The activated myofibroblast is the final effector cell that overproduces ECM under the influence of various mediators generated by an intense interplay of classic and non-classic immune cells. This review focuses on how proinflammatory mediators from various sources produced in different stages of intestinal inflammation can form profibrotic pathways that eventually lead to tissue scarring through sustained activation of myofibroblasts.

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IL-1β stimulation of CCD-18co myofibroblasts enhances repair of epithelial monolayers through Wnt-5a

Abstract: Raymond M, Marchbank T, Moyer MP, Playford RJ, Sanderson IR, Kruidenier L. Il-1␤ stimulation of CCD-18co myofibroblasts enhances repair of epithelial monolayers through Wnt-5a.

Cited by 9 publications

References 39 publications

Activation of β-catenin signalling leads to temporomandibular joint defects

Activation of β-catenin signalling leads to temporomandibular joint defects

Human placenta-derived Wnt-5a induces the expression of ICAM-1 and VCAM-1 in CD133+CD34+-hematopoietic progenitor cells

Stromal and immune cells in gut fibrosis: the myofibroblast and the scarface

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