EDIL3, AMOT and ECM1 is altered in DMSCs in psoriasis

[Fred]

This small study suggests EDIL3  (epidermal growth factor-like repeats and discoidin I-like domains 3), AMOT (angiomotin) and ECM1 (extracellular matrix protein 1) is altered in DMSCs (dermal mesenchymal stem cells) in psoriasis.

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Background:
Dermal microvasculature expansion and angiogenesis are prominent in psoriasis. Our previous microarray study showed that the angiogenesis-related genes EDIL3 (epidermal growth factor-like repeats and discoidin I-like domains 3), AMOT (angiomotin) and ECM1 (extracellular matrix protein 1), had high expression levels in dermal mesenchymal stem cells (DMSCs) from psoriatic skin lesions.

Aim:
To investigate the mRNA and protein expressions of EDIL3, AMOT and ECM1 in DMSCs derived from psoriatic skin in order to better determine the molecular mechanisms of angiogenesis in the skin.

Methods:
DMSCs from 12 patients with psoriasis and 14 healthy controls (HCs) were cultured to passage 3, and identified by morphology, immunophenotype and multipotential differentiation. The mRNA and protein expressions of EDIL3, AMOT, and ECM1 in the DMSCs were determined using real-time reverse transcription PCR and western blotting.

Results:
DMSCs displayed spindle-like morphology and surface protein expression, and were able to differentiate into osteoblasts, chondrocytes and adipocytes. mRNA expression analysis showed that EDIL3, AMOT and ECM1 were expressed at 2.54-fold, 2.11-fold, and 1.90-fold higher levels, respectively, in psoriatic DMSCs compared with HC DMSCs (all P < 0.05). Protein analysis showed significantly (all P < 0.01) higher concentrations of EDIL3, AMOT and ECM1in the psoriasis group than in the HC group.

Conclusions:
Our data demonstrate for the first time that expression of EDIL3, AMOT and ECM1 is altered in DMSCs in psoriasis, suggesting that EDIL3, AMOT and ECM1 are involved in the excessive angiogenesis and vasodilation observed in psoriasis.

Source: onlinelibrary.wiley.com

*Funding: National Nature Science Foundation of China.