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Selective neutrophil targeting in infected mice caused enhanced mortality (Tate et al. 2009).
As little as 5 min of UV exposure in nude mice caused enhanced deposition of HA, indicating that UV radiation induced skin damage is an extremely rapid event.
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In vehicle-treated SERT+ mice, hypoxia caused enhanced pulmonary vascular remodelling relative to hypoxic wild-type vehicle-treated mice and this was also markedly reduced by MPP.
Deficiency of OPG in mice induces osteoporosis caused enhanced bone resorption.
In addition, TSA treatment caused enhanced Nrf2 and histone 3 acetylation in mouse joints (Fig. 4f).
Furthermore, iNOS-/ caused enhanced pulmonary inflammation after instillation of lipopolysaccharide into the lung [ 7], whereas wild-type controls and mice lacking endothelial NO synthase (eNOS-/) presented with similar less pronounced inflammatory responses.
These gene knockdowns caused enhanced neurodegeneration.
Studies of mouse brain and zebrafish retina indicate that perturbation of INM by downregulation of centrosomal and microtubule motor-associated proteins, respectively, caused enhanced neurogenesis at the expense of neural progenitor cells (Xie et al, 2007; Del Bene et al, 2008).
For example, specific truncated forms of mouse p53 can cause enhanced cancer resistance and accelerated aging phenotypes, generally interpreted as a state of p53 hyperactivation [ 12].
Administration of leptin to neural cell-specific SOCS3 conditional KO mice greatly reduces their food intake and causes enhanced body weight loss compared with wild-type mice, indicating that SOCS3 in the brain negatively regulates leptin signaling [ 49].
An overnight fast causes enhanced metabolic stress in mice associated with a significant reduction of liver weight.
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