Psoriasis – What′s Up ?

Ståhle, Mona; Schön, Michael P.

doi:10.1111/exd.13324

Cited by 3 publications

(1 citation statement)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Psoriasis is an autoimmune skin condition, characterized by increased keratinocyte (KC) proliferation and chronic inflammation . A key feature of psoriasis is increased levels of serum and skin expression of proinflammatory cytokines especially tumor necrosis factor (TNF), interleukin (IL)‐1β, IL‐6, IL‐17, IL‐22, IL‐23 and IL‐33, as well as angiogenic mediators, including vascular endothelial growth factor (VEGF) .…”

Section: Introductionmentioning

confidence: 99%

TNF stimulates IL‐6, CXCL8 and VEGF secretion from human keratinocytes via activation of mTOR, inhibited by tetramethoxyluteolin

Patel

Tsilioni

Weng

et al. 2018

Experimental Dermatology

View full text Add to dashboard Cite

Psoriasis is an autoimmune skin disease characterized by keratinocyte hyperproliferation and chronic inflammation. The pathogenesis of psoriasis involves proinflammatory cytokines, such as tumor necrosis factor (TNF), but the mechanism of keratinocyte activation is not well understood. Here, we show that TNF (10 or 50 ng/mL) stimulates a significant (P < .0001) gene expression and secretion of proinflammatory IL-6, CXCL8 and VEGF from both cultured human HaCaT and normal epidermal human keratinocytes (NHEKs). This effect occurs via activation of the mammalian target of rapamycin (mTOR) signalling complex as shown by Western blot analysis and phospho-ELISAs. Pretreatment with the novel natural flavonoid tetramethoxyluteolin (10-100 μmol L ) significantly (P < .0001) inhibits gene expression and secretion (P < .0001) of all 3 mediators in a concentration-dependent manner. Moreover, tetramethoxyluteolin (50 μmol L ) appears to be a potent inhibitor of the phosphorylated mTOR substrates (pmTOR , pp70S6K and p4EBP1 ) as compared to known mTOR inhibitors in keratinocytes. The present findings indicate that TNF stimulates skin inflammation via mTOR signalling. Inhibition by tetramethoxyluteolin may be used in the treatment for psoriasis.

show abstract

Section: Introductionmentioning

confidence: 99%

TNF stimulates IL‐6, CXCL8 and VEGF secretion from human keratinocytes via activation of mTOR, inhibited by tetramethoxyluteolin

Patel

Tsilioni

Weng

et al. 2018

Experimental Dermatology

View full text Add to dashboard Cite

show abstract

Where does psoriasis hold out in the era of biologics?

Belinchón

2019

Br J Dermatol

View full text Add to dashboard Cite

Reduced Serum Levels of Bone Formation Marker P1NP in Psoriasis

Mentzel¹,

Kynast²,

Kohlmann³

et al. 2021

Front. Med.

View full text Add to dashboard Cite

Psoriasis is a chronic inflammatory disease of the skin and joints. More recent data emphasize an association with dysregulated glucose and fatty acid metabolism, obesity, elevated blood pressure and cardiac disease, summarized as metabolic syndrome. TNF-α and IL-17, central players in the pathogenesis of psoriasis, are known to impair bone formation. Therefore, the relation between psoriasis and bone metabolism parameters was investigated. Two serum markers of either bone formation—N-terminal propeptide of type I procollagen (P1NP) or bone resorption—C-terminal telopeptide of type I collagen (CTX-I)—were analyzed in a cohort of patients with psoriasis vulgaris. In patients with psoriasis, P1NP serum levels were reduced compared to gender-, age-, and body mass index-matched healthy controls. CTX-I levels were indistinguishable between patients with psoriasis and controls. Consistently, induction of psoriasis-like skin inflammation in mice decreases bone volume and activity of osteoblasts. Moreover, efficient anti-psoriatic treatment improved psoriasis severity, but did not reverse decreased P1NP level suggesting that independent of efficient skin treatment psoriasis did affect bone metabolism and might favor the development of osteoporosis. Taken together, evidence is provided that bone metabolism might be affected by psoriatic inflammation, which may have consequences for future patient counseling and disease monitoring.

show abstract

Psoriasis – What′s Up ?

Cited by 3 publications

References 30 publications

TNF stimulates IL‐6, CXCL8 and VEGF secretion from human keratinocytes via activation of mTOR, inhibited by tetramethoxyluteolin

TNF stimulates IL‐6, CXCL8 and VEGF secretion from human keratinocytes via activation of mTOR, inhibited by tetramethoxyluteolin

Where does psoriasis hold out in the era of biologics?

Reduced Serum Levels of Bone Formation Marker P1NP in Psoriasis

Contact Info

Product

Resources

About