To identify a cohort of rhythmically expressed genes in the murine Distal Colon,microarrays were used to measure gene expression over a 24-hour light/dark cycle.The rhythmic transcripts were classified according to expression patterns, functions and association with physiological and pathophysiological processes of the colon including motility, colorectal cancer formation and inflammatory bowel disease.
Transcriptional profiling of mRNA expression in the mouse distal colon.
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View SamplesRepair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.
Annexin A2 links poor myofiber repair with inflammation and adipogenic replacement of the injured muscle.
Age, Specimen part
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