Open AccessSirt3 deficiency impairs neurovascular recovery in ischemic stroke
Author(s) -
Yang Xiao,
Geng KeYi,
Zhang YanShuang,
Zhang JinFan,
Yang Ke,
Shao JiaXiang,
Xia WeiLiang
Publication year - 2018
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12853
Subject(s) - sirt3 , angiogenesis , neun , neurogenesis , stroke (engine) , ischemia , medicine , protein kinase b , biology , endocrinology , signal transduction , neuroscience , sirtuin , microbiology and biotechnology , nad+ kinase , biochemistry , immunohistochemistry , mechanical engineering , engineering , enzyme
Summary Aims Sirt3 is one member of the NAD + ‐dependent protein deacetylase family and plays crucial roles in diverse aspects of mammalian biological function. Then the role of Sirt3 on ischemia stroke is unknown. Methods To examine the effect of Sirt3 on ischemic stroke, we performed transient middle cerebral artery occlusion ( tMCAO ) in adult male Sirt3 knockout ( KO ) and wild‐type ( WT ) mice. Results The level of Sirt3 in infarct region is decreased after ischemic stroke. In addition, we found that Sirt3 KO mice showed worse neurobehavioral outcome compared with WT mice, accompanied by decreased neurogenesis and angiogenesis as shown by the reduction in number of DCX + /BrdU + cells, NeuN + /BrdU + cells, and CD 31 + /BrdU + cells in the perifocal region during recovery phase after ischemic stroke. Furthermore, Sirt3 deficiency reduced the activation of vascular endothelial growth factor ( VEGF ), AKT , and extracellular signal‐regulated kinases ( ERK ) signaling pathways. Conclusion Our results indicated that Sirt3 is beneficial to neurovascular and functional recovery following chronic ischemic stroke.