| Autor: |
Cao, J., Boucher, W., Donelan, J. M., Theoharides, T. C. |
| Předmět: |
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| Zdroj: |
Clinical Pharmacology & Therapeutics; Feb2006, Vol. 79 Issue 2, pP8-P8, 1p |
| Abstrakt: |
Background/aims: Corticotropin-releasing hormone (CRH) is typically released from the hypothalamus, but has proinflammatory effects outside the brain. This action involves selective mast cell secretion of vascular endothelial growth factor (VEGF), which may be responsible for bladder glomerulations in interstitial cystitis (IC). Here we investigated the effect of CRH on VEGF release from mouse bladder explants and the role of mast cells.Methods: Bladders of C57BL/6, mast cell-deficient (W/Wv) and normal congenic (+/+) female mice were catheterized; after emptying the urine, normal saline or CRH was introduced for 45 min, the urine was removed and frozen. Mice were allowed to recover for 4h before sacrifice. The bladder was removed, minced into pieces and cultured with or without CRH overnight. Urine and media were assayed for release of histamine, IL-6 or TNF-α and VEGF.Results: CRH (100 nM) increased histamine release in the urine and VEGF release in the medium from bladder explants of C57BL/6 or +/+ mice; VEGF in the medium from bladder explants of W/Wv mice was unaffected by CRH. There was no change in histamine and IL-6 release in medium and TNF-α was under detection level in the normal or W/Wv mice. No VEGF, IL-6 or TNF-α was detected in the urine before or after stimulation.Conclusions: CRH induces mast cell-dependent VEGF release from bladder explants without IL-6 and TNF-α. This finding further implicates mast cells in the pathogenesis of IC that worsens by stress and provides for a therapeutic new target.Clinical Pharmacology & Therapeutics (2005) 79, P8–P8; doi: 10.1016/j.clpt.2005.12.026 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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