Epidermal JunB represses G-CSF transcription and affects haematopoiesis and bone formation
| Autor: | Lukas Kenner, Helia B. Schonthaler, Harald Scheuch, Erwin F. Wagner, Rainer Zenz, Josef M. Penninger, Arabella Meixner |
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| Rok vydání: | 2008 |
| Předmět: |
Transcription
Genetic integumentary system Epidermis (botany) Proto-Oncogene Proteins c-jun JUNB Hyperkeratosis Repressor Cell Biology Biology medicine.disease Mice Mutant Strains In vitro Hematopoiesis Cell biology Repressor Proteins Mice Haematopoiesis Osteogenesis Transcription (biology) In vivo hemic and lymphatic diseases Granulocyte Colony-Stimulating Factor medicine Animals Epidermis |
| Zdroj: | Nature Cell Biology. 10:1003-1011 |
| ISSN: | 1476-4679 1465-7392 |
| DOI: | 10.1038/ncb1761 |
| Popis: | Mice that lack JunB in epidermal cells are born with normal skin; however, keratinocytes hyperproliferate in vitro and on TPA treatment in vivo. Loss of JunB expression in the epidermis of adult mice affects the skin, the proliferation of haematopoietic cells and bone formation. G-CSF is a direct transcriptional target of JunB and mutant epidermis releases large amounts of G-CSF that reach high systemic levels and cause skin ulcerations, myeloproliferative disease and low bone mass. The absence of G-CSF significantly improves hyperkeratosis and prevents the development of myeloproliferative disease, but does not affect bone loss. This study describes a mechanism by which the absence of JunB in epithelial cells causes multi-organ disease, suggesting that the epidermis can act as an endocrine-like organ. |
| Databáze: | OpenAIRE |
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