Cadherin 11, a miR-675 Target, Induces N-Cadherin Expression and Epithelial–Mesenchymal Transition in Melasma

Kim, Nan-Hyung; Choi, Soo-Hyun; Lee, Tae Ryong; Lee, Chang‐Hoon; Lee, Ai-Young

doi:10.1038/jid.2014.257

Cited by 41 publications

(29 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although melanogenesis occurs in melanocytes, miR‐675 is released from keratinocytes. Exosomes, which are small membrane vesicles of endocytic origin and released into the extracellular environment, contain intact and functional miR‐675 as reported (Valadi et al., ) as a means of cell–cell communication between keratinocytes and melanocytes (Kim et al., ,b,c). MiRNAs exert action through targets, and we identified MITF as a target of miR‐675, with a potential role of miR‐675 reduction in MITF upregulation in melasma patients (Kim et al., ).…”

Section: Newly Discovered Factors In Melasma Pathogenesismentioning

confidence: 88%

“…Our understanding of the mechanism concerning the effect of estrogen on skin pigmentation and/or melasma has also been updated (Kim et al., ; Kippenberger et al., ; McLeod et al., ). Recently, novel cellular and molecular mechanisms for skin pigmentation including melasma have been identified in the context of cell‐to‐cell interaction between melanocytes and dermal fibroblasts (Cardinali et al., ; Choi et al., ; Kang et al., ; Kim et al., ,b; Poon et al., ; Shin et al., ; Yamaguchi et al., ) and microRNAs (Dynoodt et al., ; Kim et al., ,b,c).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Recent progress in melasma pathogenesis

Lee

2015

Pigment Cell Melanoma Res

Self Cite

156

131

View full text Add to dashboard Cite

Summary Melasma is a common skin pigmentation condition. Given therapeutic difficulty as one of the biggest concerns, understanding of the etiology and pathogenesis of melasma becomes essential. UV irradiation, female sex hormones, and inflammatory processes are addressed as triggering factors with genetic predisposition. The mechanism of UV‐induced melanogenesis has been extensively investigated as a model system to study melasma pathogenesis. Hitherto, treatment modalities for melasma are similar to other hyperpigmentation disorders. However, individual triggering factors induce a separate pigmentation disease, whose pathogenic mechanisms and clinical phenotypes are different from the ones encountered in melasma. Fortunately, there have been ongoing updates on melasma pathogenesis with regard to major triggering factors. Presence of certain factors working independently of UV exposure and role of dermal factors and microRNAs are being identified as novel discoveries about melasma pathogenesis. In this review, the melasma pathogenesis is reviewed in association with updated and new findings.

show abstract

Section: Newly Discovered Factors In Melasma Pathogenesismentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Recent progress in melasma pathogenesis

Lee

2015

Pigment Cell Melanoma Res

Self Cite

156

131

View full text Add to dashboard Cite

show abstract

“…For example, cadherin-11 has been shown to interact directly with fibroblast growth factor receptor and trigger downstream signaling to promote neurite outgrowth (44). Moreover, forcedexpression of cadherin-11 has been shown to induce the up-regulation of proinvasive genes, including N-cadherin and TWIST (45). In addition to being expressed by EVT cells, cadherin-11 is expressed in syncytiotrophoblasts and decidualizing stromal cells (46,47).…”

Section: Discussionmentioning

confidence: 99%

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Peng

Zhu

et al. 2015

Endocrinology

View full text Add to dashboard Cite

GnRH is expressed in first-trimester human placenta and increases cell invasion in extravillous cytotrophoblasts (EVTs). Invasive phenotypes have been reported to be regulated by transcription factor activator protein 1 (AP-1) and mesenchymal cadherin-11. The aim of our study was to investigate the roles of AP-1 components (c-FOS/c-JUN) and cadherin-11 in GnRH-induced cell invasion in human EVT cells. Phosphorylated c-FOS and phosphorylated c-JUN were detected in the cell column regions of human first-trimester placental villi by immunohistochemistry. GnRH treatment increased c-FOS, c-JUN, and cadherin-11 mRNA and protein levels in immortalized EVT (HTR-8/SVneo) cells. Moreover, GnRH treatment induced c-FOS and c-JUN protein phosphorylation and nuclear accumulation. Pretreatment with antide, a GnRH antagonist, attenuated GnRH-induced cadherin-11 expression. Importantly, basal and GnRH-induced cadherin-11 expression and cell invasion were reduced by small interfering RNA-mediated knockdown of c-FOS, c-JUN, and cadherin-11 in HTR-8/SVneo cells. Our results suggest that GnRH induces the expression and phosphorylation of the AP-1 transcription factors c-FOS and c-JUN in trophoblast cells, which contributes to GnRH-induced elevation of cadherin-11 expression and cell invasion.

show abstract

“…Similarly, blocking OB-cadherin or N-cadherin engagement reduces the expression of MyoFB markers in diseased dermal fibroblasts, which express higher basal levels of OB-cadherin and α-SMA compared with healthy fibroblasts (Verhoekx et al, 2013). Overexpression of OB-cadherin in fibroblasts has also been shown to increase expression of Wnt and β-catenin, increase activation of ERK1/2 and Akt, and promote expression of N-cadherin (Kim et al, 2014). These studies indicate that expression and engagement of OB-cadherin promotes differentiation of MyoFBs and increases α-SMA expression.…”

Section: Cadherins Sense Intercellular Forcesmentioning

confidence: 99%

Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease

Schroer

Merryman

2015

Journal of Cell Science

117

View full text Add to dashboard Cite

Fibrotic cardiac disease, a leading cause of death worldwide, manifests as substantial loss of function following maladaptive tissue remodeling. Fibrosis can affect both the heart valves and the myocardium and is characterized by the activation of fibroblasts and accumulation of extracellular matrix. Valvular interstitial cells and cardiac fibroblasts, the cell types responsible for maintenance of cardiac extracellular matrix, are sensitive to changing mechanical environments, and their ability to sense and respond to mechanical forces determines both normal development and the progression of disease. Recent studies have uncovered specific adhesion proteins and mechano-sensitive signaling pathways that contribute to the progression of fibrosis. Integrins form adhesions with the extracellular matrix, and respond to changes in substrate stiffness and extracellular matrix composition. Cadherins mechanically link neighboring cells and are likely to contribute to fibrotic disease propagation. Finally, transition to the active myofibroblast phenotype leads to maladaptive tissue remodeling and enhanced mechanotransductive signaling, forming a positive feedback loop that contributes to heart failure. This Commentary summarizes recent findings on the role of mechanotransduction through integrins and cadherins to perpetuate mechanically induced differentiation and fibrosis in the context of cardiac disease.

show abstract

Cadherin 11, a miR-675 Target, Induces N-Cadherin Expression and Epithelial–Mesenchymal Transition in Melasma

Cited by 41 publications

References 35 publications

Recent progress in melasma pathogenesis

Recent progress in melasma pathogenesis

AP-1 Transcription Factors c-FOS and c-JUN Mediate GnRH-Induced Cadherin-11 Expression and Trophoblast Cell Invasion

Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease

Contact Info

Product

Resources

About