Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153509 | ENA |
REPOSITORIES: ENA
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Project description:The goal of this experiment was to profile macrophages from mammary glands isolated from transgenic mice that express inducible FGFR1 in mammary epithelial cells (MMTV-iFGFR1 transgenic mice). The mice were treated with with dimerizer to activates iFGFR1 for 48 hours and 4 weeks to induce mammary hyperplasias. Control mice included non-transgenic littermates treated with dimerizer for the same amount of time. Macrophages were sorted from mammary glands of MMTV-iFGFR1 transgenic mice and non-transgenic mice following dimerizer treatment using Cd11b-PE. Macrophages from 3 mice were pooled for each sample. RNA was extracted and analyzed using the Affymetrix Mouse 2.0 chip.
2012-05-31 | E-GEOD-36477 | biostudies-arrayexpress
Project description:The goal of this experiment was to profile macrophages from mammary glands isolated from transgenic mice that express inducible FGFR1 in mammary epithelial cells (MMTV-iFGFR1 transgenic mice). The mice were treated with with dimerizer to activates iFGFR1 for 48 hours and 4 weeks to induce mammary hyperplasias. Control mice included non-transgenic littermates treated with dimerizer for the same amount of time.
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Project description:Cancer is considered as a disease of a specific organ, but its effects are felt throughout the body. The systemic effects of cancer can lead to weakness in muscles and heart, which hastens cancer-associated death. miR-486 is a myogenic microRNA and its reduced expression in skeletal muscle is observed in muscular dystrophy. Muscle-specific transgenic expression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues skeletal muscle defects in muscular dystrophy animal models. We had previously demonstrated reduced circulating and skeletal muscle levels of miR-486 in several cancer types and lower miR-486 levels correlated with skeletal muscle defects and functional limitations in mammary tumor models. Therefore, skeletal muscle defects induced by cancer could resemble defects observed in various dystrophies, which could be reversed through skeletal muscle expression of miR-486. We performed functional limitations studies and biochemical analysis of skeletal muscles of MMTV-Neu transgenic mice that mimic HER2+ breast cancer and MMTV-PyMT transgenic mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 transgenic mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu, but not in MMTV-PyMT mice. In MMTV-Neu model, miR-486 reversed several of the cancer-induced changes in skeletal muscle including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of phosphorylation of the pre-mRNA processing factor hnRNPA0 and the splicing factor SRSF10. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss-of-function mutation is associated with congenital muscular dystrophy. Thus, similar to muscular dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden in select cancer types.
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