Requirement of the NF-κB pathway for induction of Wnt-5A by interleukin-1β in condylar chondrocytes of the temporomandibular joint: functional crosstalk between the Wnt-5A and NF-κB signaling pathways

Abstract

These results clarify the molecular mechanism underlying up-regulation of Wnt-5A by IL-1β in chondrocytes, suggesting an important functional crosstalk between Wnt-5A and NF-κB signaling pathways. This finding provides new insights into the involvement of Wnt signaling in the cartilage destruction caused by arthritis.

Interleukin-1β-Induced Wnt5a Enhances Human Corneal Endothelial Cell Migration through Regulation of Cdc42 and RhoA

“…1A) strongly suggested the presence of another signaling pathway downstream of IL-1␤ that could enhance migration in human CECs. Several reports linking IL-1␤ with Wnt5a signaling led us to investigate its potential as a candidate (44,54,55). Expression of Wnt5a has been reported in fetal but not adult corneal endothelium in humans (34), and this is consistent with our Western blot analysis results, where Wnt5a could not be detected in differentiated human CECs in vitro (Fig.…”

“…It has been reported that IL-1␤ can induce Wnt5a expression through NF-B in chondrocytes (44). Moreover, NF-B has been reported to bind and activate the human Wnt5a promoter (45).…”

Microglia-Induced Activation of Noncanonical Wnt Signaling Aggravates Neurodegeneration in Demyelinating Disorders

“…2), proinflammatory microglia might provoke Ror2 expression in spinal neurons of the gray matter. Although it remains unclear how inflammatory cytokines elicit Ror2 expression in the spinal neurons, previous reports have demonstrated that IL-1␤ induces noncanonical Wnt5a expression via NF-B in chondrocytes and that NF-B can bind to the human Wnt5a promoter (54,55). It is possible that inflammatory cytokines recruit transcription factors, such as NF-B or AP-1, to induce Wnt11 or Ror2 expression in spinal neurons.…”

Progranulin deficiency induces overactivation of WNT5A expression via TNF-α/NF-κB pathway in peripheral cells from frontotemporal dementia-linked granulin mutation carriers

“…Because it has been reported that WNT5A expression could be regulated by NF-κB, 27 we were interested in assessing whether PGRN deficiency influences NF-κB activity. Fig.…”

“…27 In this sense, 2 promoter regions have been identified in the human WNT5A gene (promoter A and B), which contains putative NF-κB binding sites. 28 NF-κB mediates the expression of many genes involved in inflammation and it is known to be upregulated in some neurodegenerative disorders such as Alzheimer disease, 29,30 Parkinson disease 31 or amyotrophic lateral sclerosis (ALS).…”