Proliferating Keratinocytes Are Putative Sources of the Psoriasis Susceptibility-Related EDA+(Extra Domain A of Fibronectin) Oncofetal Fibronectin
| Autor: | Zsuzsanna Bata-Csörgő, Csilla Szeg, Márta Széll, A. Dobozy, Andor Pivarcsi, Magdolna Gaál, Lajos Kemény, Andrea Koreck, Hilda Polyánka |
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| Rok vydání: | 2004 |
| Předmět: |
Keratinocytes
T cell Population Dermatology Biochemistry Flow cytometry Cell Adhesion medicine Humans Psoriasis RNA Messenger education Molecular Biology Cells Cultured education.field_of_study integumentary system biology medicine.diagnostic_test Epidermis (botany) Lymphokine Cell Differentiation Dermis Cell Biology Molecular biology Fibronectins Protein Structure Tertiary Fibronectin Alternative Splicing HaCaT medicine.anatomical_structure Epidermal Cells Immunology biology.protein Keratinocyte Cell Division |
| Zdroj: | Journal of Investigative Dermatology. 123:537-546 |
| ISSN: | 0022-202X |
| DOI: | 10.1111/j.0022-202x.2004.23224.x |
| Popis: | The extra domain A of fibronectin (EDA) + oncofetal isoform of fibronectin was recently reported to be overexpressed in psoriatic uninvolved epidermis. It has been proposed that the abnormal presence of EDA + oncofetal protein at the dermal–epidermal junction in the uninvolved skin may provide the "psoriatic" environment in which keratinocytes are in a preactivated state with regard to mitogenic signals (e.g., T cell lymphokines). To determine the possible sources of cellular fibronectin in the non-lesional psoriatic skin, we aimed to investigate whether keratinocytes could produce the EDA + oncofetal form of fibronectin. RT-PCR studies revealed that both cultured normal keratinocytes and HaCaT cells express the EDA + splice variant of fibronectin mRNA, and in HaCaT cells the EDA + /EDA − transcript ratio was elevated compared with normal keratinocytes. Cultured keratinocytes and HaCaT cells showed intracytoplasmic staining with an EDA + fibronectin-specific antibody and among the positively stained cells many showed mitosis. Using RT-PCR, western blot analysis, and flow cytometry, we showed that in synchronized HaCaT cells the amount of both total fibronectin and its EDA + isoform change with the proliferation/differentiation state of HaCaT cells and peak in highly proliferating cells. We show that in short-term ex vivo cultures, a small population of EDA + fibronectin containing cell population appear among psoriatic uninvolved, but not normal epidermal cells. We also demonstrate that cell attachment has a strong influence on the expression of both total and EDA + fibronectin. Our results suggest that proliferating keratinocytes could be the sources of the psoriasis susceptibility-related EDA + oncofetal fibronectin in the epidermis. |
| Databáze: | OpenAIRE |
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