The prostaglandin E2 (PGE2) receptors are G protein-coupled receptors that bind and are activated by prostaglandin E2. They are members of the prostaglandin receptors class of receptors and include the following Protein isoforms:

Studies

An antagonist of a prostaglandin E2 receptor has been shown to serve as an affective contraceptive for female macaques while unaffecting their menstrual cyclicity as well as hormonal patterns. The exact reason behind the reduced amount of successful pregnancies of primates during the study is unclear due a number of possibilities that may affect such result.[1] Inhibition of the prostaglandin E2 EP4 receptor has been shown to inhibit tumor growth, angiogenesis, lymphangiogenesis, and metastasis. [2][3]

Prostaglandin E2 and its effect on inflammation

Prostaglandins are derived from the parent molecule arachidonic acid. The synthesis of prostaglandins can be blocked by anti-inflammatory drugs such as ibuprofen. Anti-inflammatory drugs block the synthesis of cyclooxygenases which in turn produce prostaglandins.[4] Prostaglandins (PG) are the result of an enzyme cascade pathway that includes two enzymes cyclooxygenase and PG synthase. Prostaglandin E2 is produced by PGE synthase via the activation of EP1-4 receptors. Prostaglandin E2s (PGEs) are associated with the development of vascular diseases that lead to inflammation in the body. In the human body, PGEs are involved in the control of the vascular smooth muscle, cell migration and the division of a cell into two daughter cells.[5] The process of producing two daughter cells via cell division is called cell proliferation.

See also

References

  1. ↑ Peluffo, M.C.; Stanley, J.; Braeuer, N.; Rotgeri, A.; Fritzemeier, K.-H.; Fuhrmann, U.; Buchmann, B.; Adevai, T.; Murphy, M.J.; Zelinski, M.B.; Lindenthal, B.; Hennebold, J.D.; Stouffer, R.L. (July 2014). "A prostaglandin E2 receptor antagonist prevents pregnancies during a preclinical contraceptive trial with female macaques". Human Reproduction. 29 (7): 1400–1412. doi:10.1093/humrep/deu083. PMC 4059334. PMID 24781425.
  2. ↑ Majumder, Mousumi; Xin, Xiping; Liu, Ling; Girish, Gannareddy V.; Lala, Peeyush K. (September 2014). "Prostaglandin E2 receptor EP4 as the common target on cancer cells and macrophages to abolish angiogenesis, lymphangiogenesis, metastasis, and stem-like cell functions". Cancer Science. 105 (9): 1142–1151. doi:10.1111/cas.12475. PMC 4462388. PMID 24981602.
  3. ↑ Han, ShouWei; Roman, Jesse (February 2004). "Suppression of prostaglandin E2 receptor subtype EP2 by PPARγ ligands inhibits human lung carcinoma cell growth". Biochemical and Biophysical Research Communications. 314 (4): 1093–1099. doi:10.1016/j.bbrc.2004.01.007. PMID 14751245.
  4. ↑ Ricciotti, Emanuela; Fitzgerald, Garret A. (May 2011). "Prostaglandins and Inflammation". Arteriosclerosis, Thrombosis, and Vascular Biology. 31 (5): 986–1000. doi:10.1161/ATVBAHA.110.207449. PMC 3081099. PMID 21508345.
  5. ↑ Gomez, I.; Foudi, N.; Longrois, D.; Norel, X. (22 November 2012). "The role of prostaglandin E2 in human vascular inflammation". Prostaglandins, Leukotrienes and Essential Fatty Acids. 89 (2–3): 55–63. doi:10.1016/j.plefa.2013.04.004. PMID 23756023.


This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.