Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Global gene expression profile of small intestine from wild-type and CFTR-knockout mice.

ABSTRACT: The objective of this study was to identify changes in gene expression levels between wild-type and CFTR-knockout small intestine. CFTR-knockout mice (provided by Dr. Lane Clarke of the University of Missouri) were maintained on colyte. Keywords: gene expression comparison Four wild-type and four CFTR-knockout small intestinal RNA samples were compared. To facilitate statistical analysis and reduce affects of Cy3 and Cy5 labeling, comparison of two WT and two KO were repeated with a dye flip.

ORGANISM(S): Mus musculus

SUBMITTER: Gary Shull

PROVIDER: E-GEOD-8763 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Reduced NHE3-mediated Na+ absorption increases survival and decreases the incidence of intestinal obstructions in cystic fibrosis mice.

Bradford Emily M EM Sartor Maureen A MA Gawenis Lara R LR Clarke Lane L LL Shull Gary E GE

American journal of physiology. Gastrointestinal and liver physiology 20090122 4

In cystic fibrosis, impaired secretion resulting from loss of activity of the cystic fibrosis transmembrane conductance regulator (CFTR) causes dehydration of intestinal contents and life-threatening obstructions. Conversely, impaired absorption resulting from loss of the NHE3 Na+/H+ exchanger causes increased fluidity of the intestinal contents and diarrhea. To test the hypothesis that reduced NHE3-mediated absorption could increase survival and prevent some of the intestinal pathologies of cys ...[more]

PMID: 19164484

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Project description:ABSTRACT Stimulating the commitment of implanted dystrophin+ muscle derived stem cells (MDSC) into myogenic, as opposed to lipofibrogenic, lineages is a promising therapeutic strategy for Duchenne muscular dystrophy (DMD). To examine whether counteracting myostatin, a negative regulator of muscle mass and a pro-lipofibrotic factor, would help this process, we compared the in vitro myogenic and fibrogenic capacity of MDSC from wild type (WT), myostatin knockout (Mst KO), and mdx (DMD model) (mdx) young mice under various modulators, the expression of key stem cell and myogenic genes, and the capacity of these MDSC to repair the injured gastrocnemius in aged mdx mice with exacerbated lipofibrosis. Surprisingly, the potent in vitro myotube formation by WT MDSC was refractory to modulators of myostatin expression or activity, and the Mst KO and mdx MDSC failed to form myotubes under any condition, despite all MDSC expressed Oct-4 and various stem cell genes and differentiated into other lineages. The genetic inactivation of myostatin or dystrophin in MDSC was associated with silencing of critical genes for early myogenesis (Actc1, Acta1, and MyoD). WT MDSC implanted into the injured gastrocnemius of old mdx mice significantly improved myofiber repair and reduced fat deposition and, to a lesser extent, fibrosis. In contrast to their in vitro behavior, Mst KO MDSC in vivo also significantly improved myofiber repair, but had no significant effects on lipofibrotic degeneration. In conclusion, while WT MDSC are considerably myogenic in culture and stimulate muscle repair after injury in the aged mdx mouse, myostatin genetic inactivation blocks myotube formation in vitro but the myogenic capacity is recovered in vivo under the influence of the host tissue environment, presumably by reactivation of key genes originally silenced in the Mst KO MDSC. Key words: dystrophin, mdx mouse, Duchenne, fibrosis, dystrophy One sample each of mouse wild type (WT), myostatin knockout (KO), muscular dystrophy model mdx, and the transgenic OCT4 promoter plus reporter were grown, RNA was isolated, and subjected to the SABiosciences mouse stem cell oligo array.

Dataset Information

Global gene expression profile of small intestine from wild-type and CFTR-knockout mice.

Publications

Reduced NHE3-mediated Na+ absorption increases survival and decreases the incidence of intestinal obstructions in cystic fibrosis mice.

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