We observed complex metabolic abnormalities in GPRC6A−/− mice involving multiple organ systems that express GPRC6A, including bone, kidney, testes, and liver.
One possibility is that mouse telomeres are substantially longer than human telomeres, and that other organ systems in mice might suffer life-limiting complications before telomeres in lung epithelial cells are sufficiently short to cause or exacerbate fibrosis in late generation telomerase-null mice.
However, Jag1dDSL/+ Notch2del1/+ mice exhibit defects in many organ systems other than the biliary tract, such as the heart and the kidney [15].
T. canis completes its life cycle in dogs, but when it infects aberrant mammalian hosts (e.g., humans or mice), larvae migrate through various organ systems including the brain, where they can remain viable and mobile for extended periods of time.
An alternative to implanting human tumours in immunodeficient mice is to generate counterpart murine tumours in situ in relevant organ systems in immunocompetent mice.
It is likely that the brain is especially sensitive to damaging conditions, and one may ask whether heterozygous Pex11β mice might also show defects in other organ systems.
It has been reported that extremely low levels of maternal peripheral 5-HT result in smaller mouse embryos that also exhibit abnormalities in many organ systems [ 60, 61].
Through systematically phenotyping organ systems in Sun1 −/− mice, we discovered that the average weight of the brains of adult Sun1 −/− (n=12, 402.0±7.2 mg) mice was significantly lower than wild-type (WT) counterparts (WT, n=10, 449.2±5.1 mg, P<0.001; supplementary material Fig. S1A,B).
Few studies have assessed the effect of the same injury stimulus in different organ systems using the same strains of mouse.
Through targeting GSK-3α in the mouse, we found accelerated development of age-related pathologies in multiple organ systems.
