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The Journal of Immunology, 2006, 176: 4512.
Copyright © 2006 by The American Association of Immunologists

LETTERS TO THE EDITOR

Comment on "Cutting Edge: Extracellular High Mobility Group Box-1 Protein Is a Proangiogenic Cytokine"

Lisa Alleva

School of Biochemistry and Molecular Biology, The Australian National University, Canberra, Australia

I read with interest the recent article by Mitola et al. (1) describing the proangiogenic effects of high mobility group box 1 protein (HMGB1). A Taiwanese study in 2005 showed that when levels of serum thrombomodulin continued to increase following acute coronary syndrome, this associated with worsening outcomes for the patient, which manifested as unstable angina, myocardial infarction, or sudden cardiac death (2). This correlation between increased serum thrombomodulin and a poorer outcome after acute coronary syndrome could potentially occur via thrombomodulin impeding the proangiogenic effects of HMGB1. It is known that the N-terminal domain of thrombomodulin sequesters HMGB1, thereby preventing it from interacting with its cellular receptor RAGE, the receptor for advanced glycation end products (3). Since the work of Mitola et al. showed that the proangiogenic effects of HMGB1 are mediated through RAGE, it is certainly possible that in the presence of enough thrombomodulin these HMGB1-mediated effects might be lost, to the detriment of the patient.

References

  1. Mitola, S., M. Belleri, C. Urbinati, D. Coltrini, B. Sparatore, M. Pedrazzi, E. Melloni, M. Presta. 2006. Cutting edge: extracellular high mobility group box-1 protein is a proangiogenic cytokine. J. Immunol. 176: 12-15. [Abstract/Free Full Text]
  2. Chan, S. H., J. H. Chen, Y. H. Li, L. J. Lin, and L. M. Tsai. Increasing post-event plasma thrombomodulin level associates with worse outcome in survival of acute coronary syndrome. Int. J. Cardiol. In press.
  3. Abeyama, K., D. M. Stern, Y. Ito, K. Kawahara, Y. Yoshimoto, M. Tanaka, T. Uchimura, N. Ida, Y. Yamazaki, S. Yamada, et al 2005. The N-terminal domain of thrombomodulin sequesters high-mobility group-B1 protein, a novel antiinflammatory mechanism. J. Clin. Invest. 115: 1267-1274. [Medline]



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