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Full-Text Articles in Medical Anatomy
Oligodendrocyte Ablation As A Tool To Study Demyelinating Diseases, Ahdeah Pajoohesh-Ganji, Robert H. Miller
Oligodendrocyte Ablation As A Tool To Study Demyelinating Diseases, Ahdeah Pajoohesh-Ganji, Robert H. Miller
Anatomy and Regenerative Biology Faculty Publications
Multiple sclerosis (MS) is an autoimmune mediated neurodegenerative disease characterized by demyelination and oligodendrocyte (OL) loss in the central nervous system and accompanied by local inflammation and infiltration of peripheral immune cells. Although many risk factors and symptoms have been identified in MS, the pathology is complicated and the cause remains unknown. It is also unclear whether OL apoptosis precedes the inflammation or whether the local inflammation is the cause of OL death and demyelination. This review briefly discusses several models that have been developed to specifically ablate oligodendrocytes in an effort to separate the effects of demyelination from inflammation.
Il-15 Mediates Mitochondrial Activity Through A Pparšæ-Dependent-Pparš¼-Independent Mechanism In Skeletal Muscle Cells, ShantaĆ© M. Thornton, James E. Krolopp, Marcia J. Abbott
Il-15 Mediates Mitochondrial Activity Through A Pparšæ-Dependent-Pparš¼-Independent Mechanism In Skeletal Muscle Cells, ShantaĆ© M. Thornton, James E. Krolopp, Marcia J. Abbott
Health Sciences and Kinesiology Faculty Articles
Molecular mediators of metabolic processes, to increase energy expenditure, have become a focus for therapies of obesity. The discovery of cytokines secreted from the skeletal muscle (SKM), termed āmyokines,ā has garnered attention due to their positive effects on metabolic processes. Interleukin-15 (IL-15) is a myokine that has numerous positive metabolic effects and is linked to the PPAR family of mitochondrial regulators. Here, we aimed to determine the importance of PPARš¼ and/or PPARšæ as targets of IL-15 signaling. C2C12 SKM cells were differentiated for 6 days and treated every other day with IL-15 (100 ng/mL), a PPARš¼ inhibitor (GW-6471), a PPARšæ ā¦