Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Mice deficient in fractalkine are less susceptible to cerebral ischemia-reperfusion injury.

Fractalkine (FKN), also known as neurotactin, is a CX(3)C chemokine that exists in both secreted and neuronal membrane-bound forms and is upregulated during brain inflammation. There is accumulating evidence that FKN induces chemotaxis by binding to its receptor CX(3)CR1 on leukocytes and microglia. We generated FKN-deficient mice to study the role of FKN in postischemic brain injury. After transient focal cerebral ischemia, FKN-deficient mice had a 28% reduction in infarction size and lower mortality rate, when compared to wild-type littermates. The findings of this study indicate a possible role for FKN in augmenting postischemic injury and mortality after transient focal cerebral ischemia.

Pubmed ID: 11960641

Authors

  • Soriano SG
  • Amaravadi LS
  • Wang YF
  • Zhou H
  • Yu GX
  • Tonra JR
  • Fairchild-Huntress V
  • Fang Q
  • Dunmore JH
  • Huszar D
  • Pan Y

Journal

Journal of neuroimmunology

Publication Data

April 18, 2002

Associated Grants

None

Mesh Terms

  • Animals
  • Chemokine CX3CL1
  • Chemokines, CX3C
  • Disease Susceptibility
  • Gene Expression
  • Infarction, Middle Cerebral Artery
  • Ischemic Attack, Transient
  • Membrane Proteins
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • RNA, Messenger
  • Reperfusion Injury