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Linking Notch signaling to ischemic stroke.

http://www.ncbi.nlm.nih.gov/pubmed/18347334

Vascular smooth muscle cells (SMCs) have been implicated in the pathophysiology of stroke, the third most common cause of death and the leading cause of long-term neurological disability in the world. However, there is little insight into the underlying cellular pathways that link SMC function to brain ischemia susceptibility. Using a hitherto uncharacterized knockout mouse model of Notch 3, a Notch signaling receptor paralogue highly expressed in vascular SMCs, we uncover a striking susceptibility to ischemic stroke upon challenge. Cellular and molecular analyses of vascular SMCs derived from these animals associate Notch 3 activity to the expression of specific gene targets, whereas genetic rescue experiments unambiguously link Notch 3 function in vessels to the ischemic phenotype.

Pubmed ID: 18347334 RIS Download

Mesh terms: Animals | Aorta | Arteries | Brain | Brain Ischemia | Cell Separation | Disease Susceptibility | Flow Cytometry | Humans | Male | Mice | Mice, Knockout | Muscle, Smooth, Vascular | Myocytes, Smooth Muscle | Receptors, Notch | Regional Blood Flow | Signal Transduction | Stroke

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Associated grants

  • Agency: NINDS NIH HHS, Id: 5 P50 NS10828-32
  • Agency: NCI NIH HHS, Id: CA098402-06
  • Agency: NHGRI NIH HHS, Id: HG003616-01A1
  • Agency: NHLBI NIH HHS, Id: HL052233
  • Agency: NINDS NIH HHS, Id: NS026084-18

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