It remains elusive whether oligodendroglial αSYN exerts a deleterious effect on transplanted MSCs, however in a recent study addressing the fate of embryonic striatal grafts in presence of oligodendroglial αSYN inclusions, disturbed dopaminergic re-innervation and reduced p-zone volume of the grafts in the MSA mouse model has been attributed to effects of host αSYN pathology [48].
SnCl2 is a potent inductor of heme oxygenase-1 [ 15, 35] and the protective role of SnCl2 in this experimental model has been attributed, at least in part, to the heme oxygenase-1 preinduction [ 15, 34].
This likely contributed to the extreme virulence of the 1918 pandemic strain, wherein a large part of the virulence in animal models has been attributed to the HA and NA [ 31].
GH induces acute insulin resistance in skeletal muscle in vivo, which in rodent models has been attributed to crosstalk between GH and insulin signaling pathways.
All of this evidence after MD lesion damage in rodent models has been attributed to impaired executive functioning and changes in cognitive control.
N-methyl-D-aspartate acid (NMDAs) toxic effect in HD mice and cellular models has been attributed to cytosolic calcium overload or to increased mitochondrial depolarization (Browne, 2008; Fernandes et al, 2007).
Further complicating the interpretation of the data is that differentiation events in animal models have been attributed to differentiation, transdifferentiation, cell fusion or surface antigen transfer (trogocytosis), depending on the donor cells and the animal model being used.
Skeletal muscle is responsible for 30 40% of resting metabolic rate (Zurlo et al, 1990), and consequently, lean phenotypes of many mouse models have been attributed to enhanced muscle metabolism (Reitman, 2002; Gilliam & Neufer, 2012).
Resistance to the anti-proliferation effects of TGF-β in several cell line models, including breast cancer, has been attributed to overexpression of Smad co-repressor proteins [ 75] such as ski [ 76, 77], sno [ 78] and evi-1 [ 79].
It has successfully been used to prevent restenosis after coronary angioplasty (Tardif et al, 1997) and also prevents atherosclerosis and related cardiovascular diseases associated with increased oxidative stress and inflammation in several animal models, where its efficacy has been attributed to induction of heme oxygenase (Wu et al, 2006).
In the collagen-induced arthritis (CIA) model, mouse anti-LTα efficacy has been attributed to depletion of Th1 and Th17 cells, which are T-cell subsets that express LTα and are pathogenic drivers of disease.
