Phenotypes Associated with This Genotype

Genotype
MGI:4881786

• Allelic Composition: Nox4^tm1.1Hwsc/Nox4^tm1.1Hwsc
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

nervous system

enhanced blood-brain barrier function ( J:166948 )

• reduced disruption of the blood-brain barrier, as shown by less extravasation of Evans blue (brain edema) 24 h after transient middle cerebral artery occlusion (tMCAO)

• almost no brain edema is seen in the brain regions where infarcts are regularly present

decreased neuron apoptosis ( J:166948 )

• significantly lower number of apoptotic neurons 24 h after tMCAO

• normal basal apoptotic turnover rate

decreased susceptibility to ischemic brain injury ( J:166948 )

• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 6- to 8-week-old homozygous mice than in wild-type controls 24 h after tMCAO and permanent middle cerebral artery occlusion (pMCAO) and cortical photothrombosis

• seven of ten mice (70%) survive until day 5 after tMCAO , and five of these are still alive after 1 wk, versus 15 of 15 wild-type mice die by day5

• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 18- to 20-week-old homozygous mice than in wild-type controls 24 h after tMCAO

decreased cerebral infarct size ( J:166948 )

• significantly smaller infarct volumes in 6- to 8-week-old and 18- to 20-week-old male and female homozygous mice than in wild-type sex-matched controls 24 h after subjected to tMCAO

• all infarcts are restricted to the basal ganglia

• neocortex is not affected

• infarct volume did not increase over time

cellular

decreased neuron apoptosis ( J:166948 )

• significantly lower number of apoptotic neurons 24 h after tMCAO

• normal basal apoptotic turnover rate

oxidative stress ( J:166948 )

• reduced oxidative stress in brains from homozygous mice 24 h after tMCAO and pMACO

• very small ischemia-induced increases in reactive oxygen species (ROS) 24 h after tMCAO and pMCAO

• tissue nitration occurs to a lesser extent in ischemic brains from homozygous mice 24 h after tMCAO

cardiovascular system

cardiovascular system phenotype ( J:166948 )

N • no abnormal vascular phenotype

N • normal systemic blood pressure, renal and pulmonary functions

N • normal cerebral blood flow, cerebral vasculature

enhanced blood-brain barrier function ( J:166948 )

• reduced disruption of the blood-brain barrier, as shown by less extravasation of Evans blue (brain edema) 24 h after transient middle cerebral artery occlusion (tMCAO)

• almost no brain edema is seen in the brain regions where infarcts are regularly present

homeostasis/metabolism

decreased susceptibility to ischemic brain injury ( J:166948 )

• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 6- to 8-week-old homozygous mice than in wild-type controls 24 h after tMCAO and permanent middle cerebral artery occlusion (pMCAO) and cortical photothrombosis

• seven of ten mice (70%) survive until day 5 after tMCAO , and five of these are still alive after 1 wk, versus 15 of 15 wild-type mice die by day5

• reduced infarct volume, better overall neurological function (lower Bederson scores) and grip strength in 18- to 20-week-old homozygous mice than in wild-type controls 24 h after tMCAO

decreased cerebral infarct size ( J:166948 )

• significantly smaller infarct volumes in 6- to 8-week-old and 18- to 20-week-old male and female homozygous mice than in wild-type sex-matched controls 24 h after subjected to tMCAO

• all infarcts are restricted to the basal ganglia

• neocortex is not affected

• infarct volume did not increase over time