Academic literature on the topic '15-PGDH inhibitor'

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Journal articles on the topic "15-PGDH inhibitor"

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Kishore, Annavarapu Hari, Hanquan Liang, Mohammed Kanchwala, et al. "Prostaglandin dehydrogenase is a target for successful induction of cervical ripening." Proceedings of the National Academy of Sciences 114, no. 31 (2017): E6427—E6436. http://dx.doi.org/10.1073/pnas.1704945114.

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The cervix represents a formidable structural barrier for successful induction of labor. Approximately 10% of pregnancies undergo induction of cervical ripening and labor with prostaglandin (PG) E2 or PGE analogs, often requiring many hours of hospitalization and monitoring. On the other hand, preterm cervical ripening in the second trimester predicts preterm birth. The regulatory mechanisms of this paradoxical function of the cervix are unknown. Here, we show that PGE2 uses cell-specific EP2 receptor-mediated increases in Ca2+ to dephosphorylate and translocate histone deacetylase 4 (HDAC4) t
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Patel, Falguni A., Vicki L. Clifton, K. Chwalisz, and John R. G. Challis. "Steroid Regulation of Prostaglandin Dehydrogenase Activity and Expression in Human Term Placenta and Chorio-Decidua in Relation to Labor1." Journal of Clinical Endocrinology & Metabolism 84, no. 1 (1999): 291–99. http://dx.doi.org/10.1210/jcem.84.1.5399.

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NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) is the key catabolic enzyme controlling levels of biologically active PGs. PGDH is localized to syncytiotrophoblast in placenta, and to trophoblast cells in chorion. To examine the regulation of PGDH by steroids and to determine any changes with labor, we obtained placenta and chorion from term elective cesarean section or spontaneous delivery and isolated trophoblast cells using a Percoll density gradient. Cells were treated with varying concentrations of cortisol, progesterone, the synthetic progestins R5020, and medroxyprogesterone
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Yao, Bing, Jie Xu, Raymond C. Harris, and Ming-Zhi Zhang. "Renal localization and regulation of 15-hydroxyprostaglandin dehydrogenase." American Journal of Physiology-Renal Physiology 294, no. 2 (2008): F433—F439. http://dx.doi.org/10.1152/ajprenal.00436.2007.

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Tissue prostaglandin levels are determined by both biosynthesis and catabolism. The current studies report the expression and localization of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme in prostaglandin catabolism in the kidneys. We also investigated potential interactions between 15-PGDH and cyclooxygenase (COX), a key enzyme in prostaglandin biosynthesis. Both 15-PGDH mRNA and protein levels were significantly higher in kidney cortex than in papilla, which is opposite to the expression pattern of COX-2. In situ hybridization indicated that 15-PGDH mRNA was mainly localized
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Liu, Ying, Zhanjun Jia, Ying Sun, et al. "Postnatal regulation of 15-hydroxyprostaglandin dehydrogenase in the rat kidney." American Journal of Physiology-Renal Physiology 307, no. 4 (2014): F388—F395. http://dx.doi.org/10.1152/ajprenal.00512.2013.

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Cyclooxygenase 2 (COX-2) has an established role in postnatal kidney development. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) is recently identified as an endogenous inhibitor of COX-2, limiting the production of COX-2-derived prostanoids in several pathological conditions. The present study was undertaken to examine the regulation of renal 15-PGDH expression during postnatal kidney development in rats compared with COX-2. qRT-PCR and immunoblotting demonstrated that 15-PGDH mRNA and protein in the kidney were present in neonates, peaked in the second postnatal week, and then declined shar
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Hang, L. T. M., and H. Cho. "Synthesis of new thiazolidinedione derivatives as 15-PGDH Inhibitor." Journal of Biotechnology 150 (November 2010): 447. http://dx.doi.org/10.1016/j.jbiotec.2010.09.645.

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Wang, Jiping, Nancy L. Cho, Ann G. Zauber, et al. "Expression of COX-2 and 15-PGDH in adenomas removed during pretreatment colonoscopy to predict chemopreventive efficacy of the selective COX-2 inhibitor, celecoxib." Journal of Clinical Oncology 35, no. 4_suppl (2017): 524. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.524.

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524 Background: The APC trial showed that patients at high risk for colorectal adenoma development experienced a 33-45% reduction in post-polypectomy adenoma detection when treated with the selective cyclooxygenase-2 (cox-2) inhibitor, celecoxib. Unfortunately, this study also found a small increased risk of cardiovascular toxicity among celecoxib users, preventing broad use of this agent for chemoprevention. Celecoxib inhibits expression of prostaglandin E2 (PGE2), an inflammatory mediator produced by fatty acid metabolism via cyclooxygenases, and degraded through the activity of 15-prostagla
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Kim, Hye Jung, Sun-Hee Kim, Minjung Kim, et al. "Inhibition of 15-PGDH prevents ischemic renal injury by the PGE2/EP4 signaling pathway mediating vasodilation, increased renal blood flow, and increased adenosine/A2A receptors." American Journal of Physiology-Renal Physiology 319, no. 6 (2020): F1054—F1066. http://dx.doi.org/10.1152/ajprenal.00103.2020.

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In the present study, we demonstrated the marked activity of SW033291, an inhibitor of 15-hydoxyprostaglandin dehydrogenase (15-PGDH), in preventing acute kidney injury (AKI) in a murine model of ischemia-reperfusion injury. AKI due to ischemic injury represents a significant clinical problem. PGE2 is vasodilatory in the kidney, but it is rapidly degraded in vivo due to catabolism by 15-PGDH. We investigated the potential of SW033291, a potent and specific 15-PGDH inhibitor, as prophylactic treatment for ischemic AKI. Prophylactic administration of SW033291 significantly increased renal tissue
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Frenkian, Mélinée, Nadine Segond, Elisabeth Pidoux, Régis Cohen, and Annick Jullienne. "Indomethacin, a COX inhibitor, enhances 15-PGDH and decreases human tumoral C cells proliferation." Prostaglandins & Other Lipid Mediators 65, no. 1 (2001): 11–20. http://dx.doi.org/10.1016/s0090-6980(01)00116-2.

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Pang, Qianqian, Yuping Xu, Xuan Qi, et al. "The first case of primary hypertrophic osteoarthropathy with soft tissue giant tumors caused by HPGD loss-of-function mutation." Endocrine Connections 8, no. 6 (2019): 736–44. http://dx.doi.org/10.1530/ec-19-0149.

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Background Primary hypertrophic osteoarthropathy (PHO) is a rare genetic multi-organic disease characterized by digital clubbing, periostosis and pachydermia. Two genes, HPGD and SLCO2A1, which encodes 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and prostaglandin transporter (PGT), respectively, have been reported to be related to PHO. Deficiency of aforementioned two genes leads to failure of prostaglandin E2 (PGE2) degradation and thereby elevated levels of PGE2. PGE2 plays an important role in tumorigenesis. Studies revealed a tumor suppressor activity of 15-PGDH in tumors, such as lung
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Wang, Jiping, Nancy L. Cho, Ann G. Zauber, et al. "Chemopreventive Efficacy of the Cyclooxygenase-2 (Cox-2) Inhibitor, Celecoxib, Is Predicted by Adenoma Expression of Cox-2 and 15-PGDH." Cancer Epidemiology Biomarkers & Prevention 27, no. 7 (2018): 728–36. http://dx.doi.org/10.1158/1055-9965.epi-17-0573.

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Dissertations / Theses on the topic "15-PGDH inhibitor"

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Rastogi, Shruti. "The Role of Prostaglandin E2 in causing susceptibility towards Anaphylaxis." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/21632.

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Die Ausbildung und der Schweregrad einer Anaphylaxie kann durch verschiedene Co-Faktoren beeinflusst werden. Zu diesen zählen die nichtsteroidalen Antiphlogistika (NSAIDs), die ihre Wirkung über die Inhibition der COX entfalten. Wie NSAIDs den Schweregrad der Anaphylaxie beeinflussen, ist bisher nicht genau bekannt. Interessanterweise zeigen Anaphylaxie-Patienten mit einer NSAID-Hypersensibilität niedrige Konzentrationen des regulatorischen Prostaglandins E2 (PGE2). Zudem zeigen ASA-tolerante und –intolerante Asthma-Patienten variable anaphylaktische Sensitivitäten. Anhand der vorliegenden A
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Ivester, Clifford. "15-PGDH Inhibition in Reducing Chemotherapy Induced Intestinal Mucositis and Increasing Hematopoietic Stem Cell Transplant Efficiency." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1468405171.

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Conference papers on the topic "15-PGDH inhibitor"

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Lu, Dongdong, Chang Han, and Tong Wu. "Abstract 1179: 15-PGDH inhibits cholangiocarcinogenesis through the induction of TAp63." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1179.

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Ishimoto, Takatsugu, Kota Arima, Tomoyuki Uchihara, et al. "Abstract 4677: Inhibition of 15-PGDH causes Kras-driven tumor expansion through prostaglandin E2-ALDH1 signaling in the pancreas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4677.

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Ishimoto, Takatsugu, Kota Arima, Tomoyuki Uchihara, et al. "Abstract 4677: Inhibition of 15-PGDH causes Kras-driven tumor expansion through prostaglandin E2-ALDH1 signaling in the pancreas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4677.

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