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Here we show that Cd151 null mice develop smaller and fewer PyMT mammary tumors than their age matched controls.
Cx3cr1−/− Apoe−/− mice develop smaller lesions with fewer macrophages when fed either a normal chow or a high-fat diet.
In addition, Cx43I130T/+ mice develop smaller mammary glands at parturition due to reduced cell proliferation despite similar overall gland architecture.
More interestingly, HMGA2-deficient mice develop smaller ears [ 20] and in dogs, HMGA2 may be involved in differences in the size and type of ears [ 21].
Experiments carried out in TLR4-deficient mice have shown that these mice develop smaller infarcts after myocardial infarction than wild-type mice in short times of observation [ 69, 70].
When fed a high fat diet, these mice develop smaller lesions which contain more apoptotic cells than those in wild-type mice: implying a direct and pro-atherogenic effect of CX3CL1 on monocyte survival.
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As previously published (Bugge et al., 1995), Plg −/− mice develop small lesions throughout the colon mucosa.
Apc Min/+ mice develop small intestinal adenomas with a high penetrance.
These mice develop small pre-cancerous lesions in their pancreas that only arise from a small subset of the acinar cells, despite mutant Kras expression in all cells.
The majority of inbred strains of mice develop small lesions that heal spontaneously within a few weeks, leaving the host immune to reinfection; this ability to control parasite replication correlates with the expansion of CD4+ Th1 cells, characterized by the production of IFN-γ.
Nevertheless, miR-33−/− /apoE−/−-deficient mice developed smaller atherosclerotic plaques than apoE−/− mice (Horie et al, 2012).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com