| Autor: |
Kovalchin JT; Center for Immunotherapy, University of Connecticut School of Medicine, Farmington, Connecticut, USA., Wang R, Wagh MS, Azoulay J, Sanders M, Chandawarkar RY |
| Jazyk: |
angličtina |
| Zdroj: |
Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society [Wound Repair Regen] 2006 Mar-Apr; Vol. 14 (2), pp. 129-37. |
| DOI: |
10.1111/j.1743-6109.2006.00102.x |
| Abstrakt: |
Injury causes tissue breakdown, which releases large quantities of intracellular contents into the extracellular space. Some of these materials are well-established activators of the immune system and include heat shock proteins (HSPs), uric acid, nucleotides, High Mobility Group Box-1 protein (HMGB-1), and DNA. Here, we show that in vivo delivery of HSPs into BALB/cJ mice with full-thickness wounds accelerates the rate of wound closure by 60% as compared with control-treated mice. The onset is rapid and the effect is sustained, dose dependent, and protein specific. Adoptive transfer of RAW264 macrophages pretreated with HSP70 into naïve recipients with a wound transfers the HSP-mediated effect on the rate of wound closure. Further, we demonstrate that part of the mechanism by which HSP70 accelerates wound closure is through the stimulation of macrophage-mediated phagocytosis of wound debris. Disabling the HSP70-mediated enhancement of phagocytosis abrogates the HSP-mediated acceleration of the healing process. These findings create two opportunities: one, therapeutic, wherein HSP70 could be used in the clinical management of wounds; and two, pathophysiologic, to decode signals by which the host defenses recognize and respond to injury. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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