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The Akt Pathway Inhibitor Degeulin Prevents Staphylococcal Enterotoxin B Induced Splenocyte Proliferation and Inflammation

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Advances in Bioscience and Biotechnology 2017年第1期8卷 1-12页

作者： Sarah Joanne Christine Whitfield Jane Elizabeth Risdall Gareth Griffiths Ethel Diane Williamson alun james carter Department of Biomedical Sciences Defence Science and Technology Laboratory Porton Down Wiltshire UK Department of Anaesthesia University of Cambridge Cambridge UK Department of Medicine Washington University St. Louis Missouri USA

Staphylococcal Enterotoxin B (SEB) is considered a potential biological weapon. It is toxic by both inhalation and ingestion. Effects of ingestion include fever, vomiting and diarrhoea, while inhalation may additionally result in chest pain, dyspnoea, pulmonary oedema and respiratory failure. Severe exposure may be fatal and treatment relies on symptomatic support. At a cellular level, SEB up-regulates T-cell proliferation leading to a pathological inflammatory response. Deguelin, a rotenoid isolated from the African plant Mundulea sericea (Leguminosae), has been shown to reduce cellular proliferation by inhibiting the phosphoinositide 3-kinase/Akt (PI3K/Akt) signalling pathway. Using isolated murine splenocytes, we have demonstrated that treatment with deguelin reduces SEB inducing T cell proliferation by 60%. Deguelin treatment also decreased IL-2 and CCL2 secretion by splenocytes exposed to SEB. We demonstrate that targeting cellular proliferation can significantly reduce inflammation after SEB exposure and suggest that anti-proliferatives may have a role as potential generic medical counter measures if superantigens are used as biological weapons.

关键词： Staphylococcal Enterotoxin B Deguelin Therapy Inflammation Biological Weapon

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Calcium signaling and T-type calcium channels in cancer cell cycling

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World Journal of Gastroenterology 2008年第32期14卷 4984-4991页

作者： james T Taylor Xiang-Bin Zeng Jonathan E Pottle Kevin Lee alun R Wang Stephenie G Yi lennifer A S Scruggs Suresh S Sikka Ming Li Department of Pharmacology Tulane University Health Sciences Center New Orleans LA 70112 United States Department of Urology Tulane University Health Sciences Center New Orleans LA 70112 United States Department of Physiology Tulane University Health Sciences Center New Orleans LA 70112 United States Department of Pathology Tulane University Health Sciences Center New Orleans LA 70112 United States

Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca2+ channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca2+ channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel isminimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca2+ channels are not expressed in epithelial cells, selective T-type Ca2+ channel blockers may be useful in the treatment of certain types of cancers.

关键词： T-type calcium channels Cancer Cellcycle Calcium

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