Felthaus, Oliver and Schoen, Teresa and Schiltz, Daniel and Aung, Thiha and Kuehlmann, Britta and Jung, Friedrich and Anker, Alexandra and Klein, Silvan and Prantl, Lukas (2018) Adipose tissue-derived stem cells from affected and unaffected areas in patients with multiple symmetric lipomatosis show differential regulation of mTOR pathway genes. CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, 69 (1-2). pp. 141-151. ISSN 1386-0291, 1875-8622
Full text not available from this repository. (Request a copy)Abstract
BACKGROUND: Multiple symmetric lipomatosis is a rare disease characterized by the excessive growth of uncapsulated masses of adipose tissue. Although the etiology has yet to be elucidated, a connection to brown adipose tissue has been proposed recently. The mTOR pathway which is found to be regulated in lipomatous tissue as well as associated with brown adipose tissue can be inhibited by a compound called rapamycin. METHODS: We isolated adipose tissue derived stem cells from both affected and unaffected tissue and treated these cells with different concentrations of rapamycin. RESULTS: The differences in both proliferation and differentiation between adipose tissue derived stem cells (ASCs) from lipomatous and normal tissue decreased after mTOR pathway inhibition. In some patients regulation of mTOR genes was opposed in the ASCs from the two different tissues. CONCLUSIONS: Treatment with rapamycin might be a novel therapeutical approach for patients suffering from multiple symmetric lipomatosis.
Item Type: | Article |
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Uncontrolled Keywords: | INSULIN-RESISTANCE; CLINICAL ASPECTS; DISEASE; MUTATION; ABNORMALITIES; MANIFESTATION; DENERVATION; SIROLIMUS; DIAGNOSIS; Multiple symmetric lipomatosis; rare disease; mTOR pathway; rapamycin |
Subjects: | 600 Technology > 610 Medical sciences Medicine |
Divisions: | Medicine > Lehrstuhl für Mund-, Kiefer- und Gesichtschirurgie |
Depositing User: | Dr. Gernot Deinzer |
Date Deposited: | 20 Mar 2020 13:37 |
Last Modified: | 20 Mar 2020 13:37 |
URI: | https://pred.uni-regensburg.de/id/eprint/15372 |
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