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    Online Resource
    Online Resource
    Indomethacin Inhibits Cell Growth of Medullary Thyroid Carcinoma by Reducing Cell Cycle Progression into S Phase
    SAGE Publications ; 2008
    In:  Experimental Biology and Medicine Vol. 233, No. 11 ( 2008-11), p. 1433-1440
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    In: Experimental Biology and Medicine, SAGE Publications, Vol. 233, No. 11 ( 2008-11), p. 1433-1440
    Abstract: Indomethacin, a non-steroidal anti-inflammatory drug (NSAID), has been reported to inhibit the growth of medullary thyroid carcinoma (MTC) cells in vitro. However, the mechanism of inhibition of MTC cell growth by indomethacin and its potency have yet to be revealed. We examined the effect of indomethacin on three different MTC cell lines (TT cells, DRO 81–1 cells and HRO 85–1 cells) and two non-MTC cells. The mechanism of indomethacin action in MTC cells was investigated by analyzing intracellular prostaglandin level, apoptosis, and cell cycle in TT cells. Indomethacin inhibited cell growth of all three MTC cell lines but not normal thyroid cells or anaplastic thyroid carcinoma cells. Indomethacin at 10 μM or greater showed a dose response inhibition of cell growth. Indomethacin at 25 μM, a putative therapeutic serum indomethacin level, showed potency similar to 100 to 200 nM sunitinib, a receptor tyrosine kinase inhibitor. To examine whether prostaglandin depletion might determine the inhibition of MTC cell growth, we created different prostaglandin E2 (PGE2) levels in TT cells using three different NSAIDs. A profound PGE2 depletion by indomethacin-ester, a potent cyclooxygenase (COX) II inhibitor, showed the least inhibition of cell growth. Indomethacin did not increase apoptosis of TT cells. Indomethacin, but not naproxen or indomethacin-ester, reduced cell cycle progression into S phase; this was unrelated to the degree of PGE2 depletion. The expression of phosphorylated retinoblastoma (pRb) protein that shifts cells from G 1 to S phase was reduced after exposure to indomethacin. In conclusion, indomethacin has specific anti-tumor effect on MTC cells, probably by reducing cell cycle progression into S phase rather than by prostaglandin depletion. Since no drug therapy is currently available for MTC, indomethacin may be one of the therapeutic candidates.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    URL: Article
    DOI: 10.3181/0804-RM-127
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2008
    detail.hit.zdb_id: 2020856-X
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  • 2
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    Online Resource
    Role of TGF-β Signaling in Remodeling of Noncoronary Artery Aneurysms in Kawasaki Disease
    SAGE Publications ; 2015
    In:  Pediatric and Developmental Pathology Vol. 18, No. 4 ( 2015-07), p. 310-317
    Details
    In: Pediatric and Developmental Pathology, SAGE Publications, Vol. 18, No. 4 ( 2015-07), p. 310-317
    Abstract: Coronary artery aneurysms (CAA) remain an important complication of Kawasaki disease (KD), the most common form of pediatric acquired heart disease in developed countries. Potentially life-threatening CAA develop in 25% of untreated children and 5% of children treated with highdose intravenous immunoglobulin during the acute phase of the self-limited vasculitis. Noncoronary artery aneurysms (NCAA) in extraparenchymal, muscular arteries occur in a minority of patients with KD who also have CAA, yet little is understood about their formation and remodeling. We postulated that activation of the transforming growth factor-β (TGF-β) pathway in KD may influence formation and remodeling of aneurysms in iliac, femoral, and axillary arteries, the most common sites for NCAA. We studied a resected axillary artery from one adult and endarterectomy tissue from the femoral artery from a second adult, both with a history of CAA and NCAA following KD in infancy. Histology of the axillary artery aneurysm revealed destruction of the internal elastic lamina and recanalization of organized thrombus, while the endarterectomy specimen showed dense calcification and luminal myofibroblastic proliferation. Immunohistochemistry for molecules in the TGF-β signaling pathway revealed increased expression of TGF-β2, TGF-β receptor 2, and phosphorylated SMAD3. These findings suggest ongoing tissue remodeling of the aneurysms decades after the acute injury and demonstrate the importance of the TGF-β signaling pathway in this process.
    Type of Medium: Online Resource
    ISSN: 1093-5266 , 1615-5742
    URL: Article
    DOI: 10.2350/14-12-1588-OA.1
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2015
    detail.hit.zdb_id: 1480654-X
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