Abstract
Diabetes is associated with increased risk and worsened outcome of stroke. Previous studies showed that male diabetic animals had greater hemorrhagic transformation (HT), profound loss of cerebral vasculature, and poor behavioral outcomes after ischemic stroke induced by suture or embolic middle cerebral artery occlusion (MCAO). Females are protected from stroke until reaching the menopause age, but young females with diabetes have a higher risk of stroke and women account for the majority of stroke mortality. The current study postulated that diabetes is associated with greater vascular injury and exacerbated sensorimotor and cognitive outcome after stroke even in young female animals. Male and female control and diabetic animals were subjected to transient MCAO and followed for 3 or 14 days to assess the neurovascular injury and repair. The vascularization indices after stroke were lower in male diabetic animals with 90-min but not 60-min ischemia/reperfusion injury, while there was no change in female groups. Cognitive deficits were exacerbated in both male and female groups regardless of the injury period, while the sensorimotor dysfunction was worsened in male diabetic animals with longer ischemia time. These results suggest that diabetes negates the protection afforded by sex in young female animals, and post-stroke vascularization pattern is influenced by the degree of injury and correlates with functional outcome in both sexes. Vasculoprotection after acute ischemic stroke may provide a novel therapeutic strategy in diabetes.
| Language | English (US) |
|---|---|
| Pages | 106-114 |
| Number of pages | 9 |
| Journal | Experimental Neurology |
| Volume | 311 |
| DOIs | |
| State | Published - Jan 1 2019 |
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Keywords
- Diabetes
- Female
- Hemorrhagic Transformation
- Ischemic Stroke
- Neurovascular Injury
- Vascular Cognitive Impairment/Dementia
ASJC Scopus subject areas
- Neurology
- Developmental Neuroscience
Cite this
Post-stroke neovascularization and functional outcomes differ in diabetes depending on severity of injury and sex : Potential link to hemorrhagic transformation. / Li, Weiguo; Valenzuela, John Paul; Ward, Rebecca; Abdelbary, Mahmoud; Dong, Guangkuo; Fagan, Susan C.; Ergul, Adviye.
In: Experimental Neurology, Vol. 311, 01.01.2019, p. 106-114.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Post-stroke neovascularization and functional outcomes differ in diabetes depending on severity of injury and sex
T2 - Experimental Neurology
AU - Li, Weiguo
AU - Valenzuela, John Paul
AU - Ward, Rebecca
AU - Abdelbary, Mahmoud
AU - Dong, Guangkuo
AU - Fagan, Susan C.
AU - Ergul, Adviye
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Diabetes is associated with increased risk and worsened outcome of stroke. Previous studies showed that male diabetic animals had greater hemorrhagic transformation (HT), profound loss of cerebral vasculature, and poor behavioral outcomes after ischemic stroke induced by suture or embolic middle cerebral artery occlusion (MCAO). Females are protected from stroke until reaching the menopause age, but young females with diabetes have a higher risk of stroke and women account for the majority of stroke mortality. The current study postulated that diabetes is associated with greater vascular injury and exacerbated sensorimotor and cognitive outcome after stroke even in young female animals. Male and female control and diabetic animals were subjected to transient MCAO and followed for 3 or 14 days to assess the neurovascular injury and repair. The vascularization indices after stroke were lower in male diabetic animals with 90-min but not 60-min ischemia/reperfusion injury, while there was no change in female groups. Cognitive deficits were exacerbated in both male and female groups regardless of the injury period, while the sensorimotor dysfunction was worsened in male diabetic animals with longer ischemia time. These results suggest that diabetes negates the protection afforded by sex in young female animals, and post-stroke vascularization pattern is influenced by the degree of injury and correlates with functional outcome in both sexes. Vasculoprotection after acute ischemic stroke may provide a novel therapeutic strategy in diabetes.
AB - Diabetes is associated with increased risk and worsened outcome of stroke. Previous studies showed that male diabetic animals had greater hemorrhagic transformation (HT), profound loss of cerebral vasculature, and poor behavioral outcomes after ischemic stroke induced by suture or embolic middle cerebral artery occlusion (MCAO). Females are protected from stroke until reaching the menopause age, but young females with diabetes have a higher risk of stroke and women account for the majority of stroke mortality. The current study postulated that diabetes is associated with greater vascular injury and exacerbated sensorimotor and cognitive outcome after stroke even in young female animals. Male and female control and diabetic animals were subjected to transient MCAO and followed for 3 or 14 days to assess the neurovascular injury and repair. The vascularization indices after stroke were lower in male diabetic animals with 90-min but not 60-min ischemia/reperfusion injury, while there was no change in female groups. Cognitive deficits were exacerbated in both male and female groups regardless of the injury period, while the sensorimotor dysfunction was worsened in male diabetic animals with longer ischemia time. These results suggest that diabetes negates the protection afforded by sex in young female animals, and post-stroke vascularization pattern is influenced by the degree of injury and correlates with functional outcome in both sexes. Vasculoprotection after acute ischemic stroke may provide a novel therapeutic strategy in diabetes.
KW - Diabetes
KW - Female
KW - Hemorrhagic Transformation
KW - Ischemic Stroke
KW - Neurovascular Injury
KW - Vascular Cognitive Impairment/Dementia
UR - http://www.scopus.com/inward/record.url?scp=85054183299&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85054183299&partnerID=8YFLogxK
U2 - 10.1016/j.expneurol.2018.09.013
DO - 10.1016/j.expneurol.2018.09.013
M3 - Article
VL - 311
SP - 106
EP - 114
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
ER -