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Wednesday, 18 December 2013

The Effects of Hormone Prostaglandins(3)

Prostaglandins
Prostaglandins, are a group of lipid mediators, found and isolated from human semen in the 1930s by Ulf von Euler of Sweden, responsible for inflammation features, such as swelling, pain, stiffness, redness and warmth. The hormones are produced by almost all nucleated cells and synthesized in the cell from the essential fatty acids (EFAs), include prostacyclin I2 (PGI2), prostaglandin E2 (PGE2), and prostaglandin F (PGF).
21. Prostaglandin E2 (PGE2) and orthodontic tooth movement and bone metabolism
In the study to to investigate and compare the in vivo effects of prostaglandin E2 (PGE2) administered by different methods on orthodontic tooth movement and bone metabolism macroscopically, histopatologically, and biochemically, showed that Tooth movement was observed in the experimental and positive control groups, but the intraligamentous PGE2 group had the highest values of all analyzed parameters, including serum calcium and phosphorus levels and osteoclastic and osteoblastic populations (p < 0.001)(21).

22. Prostaglandin E2 and voltage-dependent calcium channels
According to the study by the University of Occupational and Environmental Health, in the study of The effects of PGE2 on voltage-dependent Ca2+ channel currents in dissociated rat melanotrophs by the whole-cell configuration of the patch-clamp technique, indicated that PGE2 inhibits P/Q- and L-type Ca2+ channels of rat melanotrophs via EP1 and EP3 receptors, which are coupled to pertussis toxin-sensitive G proteins, and produces both voltage-sensitive and -insensitive inhibition of Ca2+ channels(22).

23. Prostaglandins in pregnancy and parturition
Prostaglandin (PG) production by intrauterine tissues plays a key part in the control of pregnancy and parturition. In the study to to investigate the role of placenta-derived CRH and CRH-related peptides in the regulation of PG synthesis and metabolism, showed that CRH and CRH-related peptides act on CRH-R1 and CRH-R2 to exert different effects on PG biosynthetic enzymes cPLA2 and COX-2 and thereby modulate output of PGs from placenta, which would be important for controlling pregnancy and parturition(23).

24. Prostaglandins in regulation of PPARγ function in adipocytes
Adipocytes and fat cells play critical roles in the regulation of energy homeostasis. Adipogenesis (adipocyte differentiation) is regulated via a complex process including coordinated changes in hormone sensitivity and gene expression. According to the study by the Osaka University of Pharmaceutical Sciences,  Prostaglandins (PGs), which are lipid mediators, are associated with the regulation of PPARγ function in adipocytes. Prostacyclin promotes the differentiation of adipocyte-precursor cells to adipose cells via activation of the expression of C/EBPβ and δ. These proteins are important transcription factors in the activation of the early phase of adipogenesis, and they activate the expression of PPARγ, which event precedes the maturation of adipocytes. PGE(2) and PGF(2α) strongly suppress the early phase of adipocyte differentiation by enhancing their own production via receptor-mediated elevation of the expression of cycloxygenase-2, and they also suppress the function of PPARγ(24).

25. Prostaglandins in prevulatory phase
In the study to to evaluate the effect of luteinizing hormone (LH), steroids, prostaglandins (PGs) and peptides on the oviductal contraction and secretion of PGs and endothelin (ET-1) in cows, showed that the preovulatory LH surge, together with increasing E(2) levels from the Graafian follicle and a basal P(4) from regressing corpora lutea (CL), stimulates maximum oviductal production of PG and ET-1, resulting in oviductal contraction for a rapid transport of gametes. OT released from the newly-formed CL may block these mechanisms, and slow contractions for transport of the embryo to the uterus(25).

26. Prostaglandins hormone regulation
The optimal oviductal environment, including contractile activity for gamete transport, fertilization and early embryonic development, is mediated by physiological and anatomical changes in the oviduct during the estrous cycle. In the study by the University of Peradeniya, indicated that the preovulatory LH surge, together with locally re-circulated high levels of E2 from the Graafian follicle and basal P4 from regressing corpus luteum (CL), induces the maximum stimulatory effect on oviductal PGE2, PGF2 alpha and ET-1 production during the periovulatory period. Consequently, the elevated local ET-1 concentration during periovulatory period may induce the high contractile activity of the oviduct and, at the same time, the stimulation of PG production. Thus, ET-1 may act as a local amplifier for oviductal PG production stimulated by LH and ovarian steroids(26).

27. Prostaglandin D2 and Oral cancer
Prostaglandins are secreted by oral carcinomas and may be involved in eosinophil infiltration. In the study to determine the factors contributing to eosinophil migration and potential anti-neoplastic effects on oral squamous carcinoma (OSC), eosinophil degranulation was evaluated by measuring release of eosinophil peroxidase (EPO), showed that growth inhibition of the OSC cell line, SCC-9, during co-culture with human eosinophils, in vitro, which correlated with EPO activity that possesses growth inhibitory activity. The PGD2 synthase inhibitor, HQL-79, abrogated migration towards SCC-9. Our data suggest that OSC-derived PGD2 may play an important role via CRTH2 (the PGD2 receptor on eosinophils) in eosinophil recruitment and subsequent anti-tumor activity through the action of eosinophil cationic proteins(27).

28. Prostaglandins in T cells activation
In the study to investigate the role of PGE(2), which binds to the E-prostanoid family of G protein-coupled receptors through four subtypes of receptors called EP 1-4, in the regulation of CD46 expression and function, showed that addition of PGE(2) strongly downregulates CD46 expression in activated T cells. Moreover, PGE(2) differentially affects T cell activation, cytokine production, and phenotype depending on the activation signals received by the T cells. This was correlated with a distinct pattern of the PGE(2) receptors expressed, with EP4 being preferentially induced by CD46 activation. Indeed, addition of an EP4 antagonist could reverse the effects observed on cytokine production after CD46 costimulation. These data demonstrate a novel role of the PGE(2)-EP4 axis in CD46 functions, which might at least partly explain the diverse roles of PGE(2) in T cell functions(28).

29. Prostaglandins and lymphangiogenesis
One of the hallmarks of inflammation is lymphangiogesis that drains the interstitial fluids. During chronic inflammation, angiogenesis is induced by a variety of inflammatory mediators, such as prostaglandins (PGs). According to the study by the Kitasato University School of Medicine, suggested that COX-2 and prostaglandin E2-EP3/EP4 signaling contributes to lymphangiogenesis in proliferative inflammation, possibly via induction of VEGF-C and VEGF-D, and may become a therapeutic target for controlling lymphangiogenesis(29).

30. Prostaglandin E2 and colorectal carcinoma cells
Chronic use of nonsteroidal anti-inflammatory drugs results in a significant reduction of risk and mortality from colorectal cancer in humans. They are known to inhibit cyclooxygenase activity. The cyclooxygenase enzymes catalyze a key reaction in the conversion of arachidonic acid to prostaglandins, such as prostaglandin E(2) (PGE(2)). In the study to demonstrate that PGE(2) treatment of LS-174 human colorectal carcinoma cells leads to increased motility and changes in cell shape by Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, indicated that
PGE(2) treatment results in an activation of phosphatidylinositol 3-kinase/protein kinase B pathway that is required for the PGE(2)-induced changes in carcinoma cell motility and colony morphology. PGE(2) might enhance the invasive potential of colorectal carcinoma cells via activation of major intracellular signal transduction pathways not previously reported to be regulated by prostaglandins(30).
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Sources

21) http://www.ncbi.nlm.nih.gov/pubmed/23112942
(22) http://www.ncbi.nlm.nih.gov/pubmed/9832416
(23) http://www.ncbi.nlm.nih.gov/pubmed/18325997
(24) http://www.ncbi.nlm.nih.gov/pubmed/23319937
(25) http://www.ncbi.nlm.nih.gov/pubmed/11139776
(26) http://www.ncbi.nlm.nih.gov/pubmed/10735120
(27) http://www.ncbi.nlm.nih.gov/pubmed/23369060
(28) http://www.ncbi.nlm.nih.gov/pubmed/22544928
(29) http://www.ncbi.nlm.nih.gov/pubmed/21311040
(30) http://www.ncbi.nlm.nih.gov/pubmed/11278548