作者
Faith H Brennan, Trisha Jogia, Ellen R Gillespie, Linda V Blomster, Xaria X Li, Bianca Nowlan, Gail M Williams, Esther Jacobson, Geoff W Osborne, Frederic A Meunier, Stephen M Taylor, Kate E Campbell, Kelli PA MacDonald, Jean-Pierre Levesque, Trent M Woodruff, Marc J Ruitenberg
发表日期
2019/5/5
期刊
JCI insight
卷号
4
期号
9
出版商
American Society for Clinical Investigation
简介
Traumatic spinal cord injury (SCI) triggers an acute-phase response that leads to systemic inflammation and rapid mobilization of bone marrow (BM) neutrophils into the blood. These mobilized neutrophils then accumulate in visceral organs and the injured spinal cord where they cause inflammatory tissue damage. The receptor for complement activation product 3a, C3aR1, has been implicated in negatively regulating the BM neutrophil response to tissue injury. However, the mechanism via which C3aR1 controls BM neutrophil mobilization, and also its influence over SCI outcomes, are unknown. Here, we show that the C3a/C3aR1 axis exerts neuroprotection in SCI by acting as a physiological antagonist against neutrophil chemotactic signals. We show that C3aR1 engages phosphatase and tensin homolog (PTEN), a negative regulator of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway, to restrain CXC …
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FH Brennan, T Jogia, ER Gillespie, LV Blomster, XX Li… - JCI insight, 2019