Activation of RhoA, Smad2, c-Src, PKC-βII/δ and JNK in atopic dermatitis.
Jianyun LuRong YinZhibing FuVeronica M LeeJohn Stuart NelsonWenbin TanPublished in: The Australasian journal of dermatology (2018)
Atopic dermatitis is a multifactorial skin disease characterised by chronic and relapsing inflammation whose pathogenesis is incompletely understood. We found that the expression of TGFβR1 and the activation of SMAD2, RhoA, JNK, PKC-βII/δ and c-Src were upregulated in the infiltrated inflammatory cells, fibroblasts and vasculatures in the dermis and epidermis. In addition, increases in the expression of TGFβR1 and phosphorylation levels of JNK and c-Src were positively correlated with the inflammatory progression of atopic dermatitis severity.
Keyphrases
- atopic dermatitis
- induced apoptosis
- oxidative stress
- transforming growth factor
- signaling pathway
- tyrosine kinase
- poor prognosis
- epithelial mesenchymal transition
- cell death
- endoplasmic reticulum stress
- multiple sclerosis
- cell cycle arrest
- protein kinase
- binding protein
- long non coding rna
- pi k akt
- wound healing
- rheumatoid arthritis