Relevant bibliographies by topics / Elocalcitolo

Academic literature on the topic 'Elocalcitolo'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Elocalcitolo"

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Morelli, Annamaria, Roberta Squecco, Paola Failli, Sandra Filippi, Linda Vignozzi, Aravinda K. Chavalmane, Benedetta Fibbi, et al. "The vitamin D receptor agonist elocalcitol upregulates L-type calcium channel activity in human and rat bladder." American Journal of Physiology-Cell Physiology 294, no. 5 (May 2008): C1206—C1214. http://dx.doi.org/10.1152/ajpcell.90634.2007.

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Human bladder contraction mainly depends on Ca2+ influx via L-type voltage-gated Ca2+ channels and on RhoA/Rho kinase contractile signaling, which is upregulated in overactive bladder (OAB). Elocalcitol is a vitamin D receptor agonist inhibiting RhoA/Rho kinase signaling in rat and human bladder. Since in the normal bladder from Sprague-Dawley rats elocalcitol treatment delayed the carbachol-induced contraction without changing maximal responsiveness and increased sensitivity to the L-type Ca2+ channel antagonist isradipine, we investigated whether elocalcitol upregulated L-type Ca2+ channels in human bladder smooth muscle cells (hBCs). In hBCs, elocalcitol induced a rapid increase in intracellular [Ca2+], which was abrogated by the L-type Ca2+ channel antagonist verapamil. Moreover, hBCs exhibited L-type voltage-activated Ca2+ currents ( ICa), which were selectively blocked by isradipine and verapamil and enhanced by the selective L-type agonist BAY K 8644. Addition of elocalcitol (10−7 M) increased L-type ICa size and specific conductance by inducing faster activation and inactivation kinetics than control and BAY K 8644, while determining a significant negative shift of the activation and inactivation curves, comparable to BAY K 8644. These effects were strengthened in long-term treated hBCs with elocalcitol (10−8 M, 48 h), which also showed increased mRNA and protein expression of pore-forming L-type α1C-subunit. In the bladder from Sprague-Dawley rats, BAY K 8644 induced a dose-dependent increase in tension, which was significantly enhanced by elocalcitol treatment (30 μg·kg−1·day−1, 2 wk). In conclusion, elocalcitol upregulated Ca2+ entry through L-type Ca2+ channels in hBCs, thus balancing its inhibitory effect on RhoA/Rho kinase signaling and suggesting its possible efficacy for the modulation of bladder contractile mechanisms.
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Borgogni, E., E. Sarchielli, M. Sottili, V. Santarlasci, L. Cosmi, S. Gelmini, A. Lombardi, et al. "Elocalcitol Inhibits Inflammatory Responses in Human Thyroid Cells and T Cells." Endocrinology 149, no. 7 (March 27, 2008): 3626–34. http://dx.doi.org/10.1210/en.2008-0078.

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T-helper 1 (Th1) cell-mediated inflammatory responses predominate in the early pathogenesis of Graves’ disease (GD), whereas Th2 cell-mediated immunity may play a role in later stages. The chemokine CXCL10 and its receptor CXCR3 are expressed in most thyroid glands of early GD patients. Circulating CXCL10 levels inversely correlate with disease duration; CXCL10 maximal expression also correlates with interferon (IFN)γ levels in recent GD onset. Methimazole (MMI) reduces CXCL10 secretion by isolated thyrocytes, decreases serum CXCL10 levels, and promotes a transition from Th1 to Th2 dominance in patients in GD active phase. Vitamin D receptor agonists exhibit antiinflammatory properties and promote tolerance induction. We investigated the effects and the mechanism of action of a nonhypercalcemic vitamin D receptor agonist, elocalcitol (BXL-628), compared with MMI on CXCL10 secretion induced by proinflammatory cytokines. Furthermore, we studied the effects of both drugs on Th1, Th17, and Th2 cytokine secretion in CD4+ T cells. ELISA, cytometry, immunocytochemistry, Western blot, and quantitative real-time PCR were used for protein and gene analysis. In human thyrocytes, elocalcitol inhibited IFNγ and TNFα-induced CXCL10 protein secretion more potently than MMI. Elocalcitol impaired both cytokine intracellular pathways, whereas MMI was effective only on the IFNγ pathway. In CD4+ T cells, elocalcitol decreased Th1- and Th17-type cytokines, and promoted Th2-type cytokine secretion. Elocalcitol and MMI inhibited Th1 cytokine-mediated responses in thyrocytes and CD4+ T cells. In addition, elocalcitol promoted a shift toward a Th2 response. In conclusion, elocalcitol could represent a novel pharmacological tool in the treatment of autoimmune thyroid diseases.
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Revill, P., N. Serradell, and J. Bolós. "Elocalcitol." Drugs of the Future 31, no. 12 (2006): 1042. http://dx.doi.org/10.1358/dof.2006.031.12.1060203.

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&NA;. "Elocalcitol beneficial for benign prostatic hyperplasia." Inpharma Weekly &NA;, no. 1610 (October 2007): 8. http://dx.doi.org/10.2165/00128413-200716100-00015.

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&NA;. "BXL 628* [Elocalcitol] is effective in the treatment of overactive bladder,." Inpharma Weekly &NA;, no. 1538 (May 2006): 6. http://dx.doi.org/10.2165/00128413-200615380-00015.

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Streng, T., K. E. Andersson, P. Hedlund, C. Gratzke, E. Baroni, D. D'Ambrosio, and F. Benigni. "548 ELOCALCITOL IMPROVES EFFECTS BY TOLTERODINE IN RATS WITH PARTIAL URETHRAL OBSTRUCTION." European Urology Supplements 10, no. 2 (March 2011): 181–82. http://dx.doi.org/10.1016/s1569-9056(11)60539-3.

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Streng, Tomi, Karl-Erik Andersson, Petter Hedlund, Christian Gratzke, Enrico Baroni, Daniele D'Ambrosio, and Fabio Benigni. "Effects on bladder function of combining elocalcitol and tolterodine in rats with outflow obstruction." BJU International 110, no. 2b (January 30, 2012): E125—E131. http://dx.doi.org/10.1111/j.1464-410x.2011.10838.x.

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Tiwari, Atul. "Elocalcitol (BXL-628): a novel, investigational therapy for the therapeutic management of benign prostatic hyperplasia." Expert Opinion on Investigational Drugs 17, no. 5 (April 30, 2008): 819–24. http://dx.doi.org/10.1517/13543784.17.5.819.

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Adorini, Luciano, Giuseppe Penna, Susana Amuchastegui, Chiara Cossetti, Francesca Aquilano, Roberto Mariani, Benedetta Fibbi, et al. "Inhibition of prostate growth and inflammation by the vitamin D receptor agonist BXL-628 (elocalcitol)." Journal of Steroid Biochemistry and Molecular Biology 103, no. 3-5 (March 2007): 689–93. http://dx.doi.org/10.1016/j.jsbmb.2006.12.065.

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Montorsi, Francesco, and Enrico Colli. "ELOCALCITOL IN THE TREATMENT OF BPH: A MULTICENTER, RANDOMIZED, PLACEBO-CONTROLLED PHASE IIB CLINICAL TRIAL." Journal of Urology 179, no. 4S (April 2008): 700–701. http://dx.doi.org/10.1016/s0022-5347(08)62043-1.

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Dissertations / Theses on the topic "Elocalcitolo"

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FIBBI, BENEDETTA. "Studi sugli effetti di elocalcitolo sulle tre componentipatogenetiche dell’ipertrofia prostatica benigna: la statica, ladinamica e l’infiammatoria." Doctoral thesis, 2008. http://hdl.handle.net/2158/599078.

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