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Cerebral infarct size is gender‐dependent following transient but not permanent middle cerebral artery occlusion in mice
Author(s) -
Brait Vanessa H,
Jackman Katherine A,
Mast Anja E,
Drummond Grant R,
Sobey Christopher G
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.719.7
Subject(s) - smad , medicine , ischemia , endocrinology , occlusion , middle cerebral artery , cardiology , transforming growth factor
Estrogen mediates protection of females in cerebral ischemia‐reperfusion (I‐R), and inhibits atherosclerosis via TGFβ signalling. We tested whether females are also protected during cerebral ischemia with no reperfusion (I‐NR), and whether this may be related to TGFβ activity. Stroke was induced by 0.5 h middle cerebral artery occlusion in 6–8 week old female (n=22) and male (n=30) C57Bl6J mice. After 24 h, brain infarct volume was measured in thionin‐stained coronal sections. After I‐R, females had a smaller infarct volume than males (24±6 vs 55±11 mm 3 , n=7–8; P<0.05), whereas there was no gender difference following I‐NR (88±9 vs 88±11 mm 3 , n=8–9). Preliminary data (n=1–3) indicate that expression of p‐SMAD, a marker of TGFβ signalling, is 47% higher in brains of sham‐operated females vs males. Furthermore, in females p‐SMAD expression was reduced by 37% after I‐R and by 67% after I‐NR. By contrast, neither model of stroke had any effect on p‐SMAD expression in males. Thus, cerebral infarct size is gender‐dependent following I‐R but not I‐NR in mice. The lack of protection in females in I‐NR may be related to reduced TGFβ signalling.