Open AccessTelocyte dynamics in psoriasis
Author(s) -
Manole C.G.,
Gherghiceanu Mihaela,
Simionescu Olga
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12601
Subject(s) - psoriasis , dynamics (music) , dermatology , medicine , computational biology , biology , physics , acoustics
The presence of telocytes ( TC s) as distinct interstitial cells was previously documented in human dermis. TC s are interstitial cells completely different than dermal fibroblasts. TC s are interconnected in normal dermis in a 3D network and may be involved in skin homeostasis, remodelling, regeneration and repair. The number, distribution and ultrastructure of TC s were recently shown to be affected in systemic scleroderma. Psoriasis is a common inflammatory skin condition (estimated to affect about 0.1–11.8% of population), a keratinization disorder on a genetic background. In psoriasis, the dermis contribution to pathogenesis is frequently eclipsed by remarkable epidermal phenomena. Because of the particular distribution of TC s around blood vessels, we have investigated TC s in the dermis of patients with psoriasis vulgaris using immunohistochemistry ( IHC ), immunofluorescence ( IF ), and transmission electron microscopy ( TEM ). IHC and IF revealed that CD 34/ PDGFR α‐positive TC s are present in human papillary dermis. More TC s were present in the dermis of uninvolved skin and treated skin than in psoriatic dermis. In uninvolved skin, TEM revealed TC s with typical ultrastructural features being involved in a 3D interstitial network in close vicinity to blood vessels in contact with immunoreactive cells in normal and treated skin. In contrast, the number of TC s was significantly decreased in psoriatic plaque. The remaining TC s demonstrated multiple degenerative features: apoptosis, membrane disintegration, cytoplasm fragmentation and nuclear extrusion. We also found changes in the phenotype of vascular smooth muscle cells in small blood vessels that lost the protective envelope formed by TC s. Therefore, impaired TC s could be a ‘missed’ trigger for the characteristic vascular pathology in psoriasis. Our data explain the mechanism of Auspitz's sign, the most pathognomonic clinical sign of psoriasis vulgaris. This study offers new insights on the cellularity of psoriatic lesions and we suggest that TC s should be considered new cellular targets in forthcoming therapies.