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Am J Physiol Gastrointest Liver Physiol 296: G339-G347, 2009. First published December 18, 2008; doi:10.1152/ajpgi.90607.2008
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INFLAMMATION/IMMUNITY/MEDIATORS

Ischemia-mediated aggregation of the actin cytoskeleton is one of the major initial events resulting in ischemia-reperfusion injury

Tong Shi,1 Vaishali R. Moulton,1 Peter H. Lapchak,1 Guo-Min Deng,1 Jurandir J. Dalle Lucca,2 and George C. Tsokos1

1Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; and 2Walter Reed Army Institute of Research, Silver Spring, Maryland

Submitted 22 October 2008 ; accepted in final form 16 December 2008

Ischemia-reperfusion (IR) injury represents a major clinical challenge, which contributes to morbidity and mortality during surgery. The critical role of natural immunoglobulin M (IgM) and complement in tissue injury has been demonstrated. However, cellular mechanisms that result in the deposition of natural IgM and the activation of complement are still unclear. In this report, using a murine intestinal IR injury model, we demonstrated that the β-actin protein in the small intestine was cleaved and actin filaments in the columnar epithelial cells were aggregated after a transient disruption during 30 min of ischemia. Ischemia also led to deposition of natural IgM and complement 3 (C3). A low dose of cytochalasin D, a depolymerization reagent of the actin cytoskeleton, attenuated this deposition and also attenuated intestinal tissue injury in a dose-dependent manner. In contrast, high doses of cytochalasin D failed to worsen the injury. These data indicate that ischemia-mediated aggregation of the actin cytoskeleton, rather than its disruption, results directly in the deposition of natural IgM and C3. We conclude that ischemia-mediated aggregation of the actin cytoskeleton leads to the deposition of natural IgM and the activation of complement, as well as tissue injury.

cytochalasin D; complement; deposition


Address for reprint requests and other correspondence: T. Shi or G. C. Tsokos, Division of Rheumatology, Beth Israel Deaconess Medical Center, 330 Brookline Ave. CLS 928, Boston, MA 02215 (e-mail: tshi{at}bidmc.harvard.edu or gtsokos{at}bidmc.harvard.edu)






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