S100a8 S100a9

Overexpression

Knock-out

Knock-out Knock-out

Female specific hyperactivity, lack of habituation to novelty, reduced T-maze spontaneous alternation rate, abnormal exploratory behavior Enhanced astrocytosis and neurite proliferation Impaired learning and memory, increased dendrite density, enhanced age-related loss of dendrites Inhibitory effect on cardiac hypertrophy Increased susceptibility to hypoxia-ischemia Increased apoptosis after myocardial infarction Enhanced neuroinflammation and neuronal dysfunction induced by amyloid-( Increased synaptic plasticity, spatial memory and fear memory Chronic gliosis

Decreased susceptibility to hypoxia-ischemia Enhanced epileptogenesis Enhanced Ca2+ transients

Enhanced hypertrophy, decreased apoptosis and improved hemodynamics after myocardial infarction

Increased myocardial contractile performance Impaired cardiac contractility in response to (-adrenergic stimulation and hemodynamic stress Reduced anxiety-related responses and increased exploratory drive in male KO mice Prolonged Q-T intervals, reduced Ca2+-induced Ca2+ release upon (-adrenergic stimulation. Enhanced tumour development and metastasis Increased right ventricular systolic pressure, right ventricular hypertrophy, reduced ventricular elastance and decreased cardiac output. Tumour development and reduced apoptosis Delayed tumour uptake, decreased tumour incidences, no metastasis after transplantation of highly metastatic mammary carcinomas. Enhanced astrocyte migration after demyelination Embryonic lethal

No functional abnormalities. Absence of S100A8 protein. Myeloid cells with reduced density. No functional abnormalities in vivo. Absence of S100A8 protein. Reduced response to chemoattractant stimuli in vitro. Stimulation of myeloid cells with ATP results in a stronger increase of intracellular free Ca2+. No emigration of CD4-CD8 double-negative thymocytes upon tetrachlorodibenzo-p-dioxin exposure.

(Continued)

Table 3. (Continued)

Transgene

Mouse model

Pheontype

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