{"id":2516,"date":"2014-04-14T07:00:49","date_gmt":"2014-04-14T11:00:49","guid":{"rendered":"http:\/\/admin.acceleratingscience.com\/?p=2516"},"modified":"2016-04-26T15:25:30","modified_gmt":"2016-04-26T15:25:30","slug":"lipoxin-a-potential-therapeutic-for-endometriosis","status":"publish","type":"post","link":"https:\/\/www.thermofisher.com\/blog\/proteomics\/lipoxin-a-potential-therapeutic-for-endometriosis\/","title":{"rendered":"Lipoxin: A Potential Therapeutic for Endometriosis"},"content":{"rendered":"

Endometriosis is an estrogen-dependent disease affecting approximately 10% of women of reproductive age worldwide and is a leading cause of pelvic pain. The pathophysiology of endometriosis involves inflammatory and angiogenic mediators; diagnosis is confirmed by the presence of endometrial-like tissue outside the uterine cavity.1 <\/sup>The recurrence of endometriosis when treatment ceases is not uncommon, and therefore new drugs inhibiting its progression represent an unmet need.<\/p>\n

A recent study by Kumar et al. sought to investigate mechanisms leading to the establishment and progression of endometriosis.2<\/span><\/sup> Further to this, they recently identified that lipoxins, a form of endogenous eicosanoids that act as lipid mediators, are estrogenic.3<\/sup>\u00a0Because LXA4<\/sub> (lipoxin 4) is the best characterized and exhibits both anti-inflammatory and pro-resolving properties, the team\u00a0also sought the protective role of LXA4<\/span><\/sub> in the development and progression of endometriosis.<\/p>\n

The researchers were able to determine that there are multiple pathways implicated in the pathogenesis of endometriosis in vivo<\/em>. These included pathways for inflammation, angiogenesis, PGE2<\/sub> production and transport, matrix remodeling and estrogen signaling.<\/p>\n

Three groups of mice were established: sham, vehicle-treated with endometriosis (Veh), and LXA4<\/sub>-treated with endometriosis (LXA4<\/sub>). After implantation of endometriosis in two of the groups, the LXA4<\/sub> group was given daily injections of LXA4<\/sub>.<\/p>\n

The researchers\u00a0then extracted the total RNA from individual endometriotic lesions and peritoneal fluid cells (PFCs), checking the RNA concentration and purity\u00a0using a NanoDrop 2000 spectrophotometer (Thermo Scientific). They then used qPCR to analyze the genes involved in the initiation of inflammatory pathways. The researchers observed significantly reduced IL-1b and IL-6 mRNA expression in endometriotic lesions and PFCs from LXA4<\/sub>-treated mice. Overall, they found\u00a0a significant reduction in lesion volume\u00a0in LXA4<\/sub> mice compared to Veh mice.<\/p>\n

LXA4<\/sub> signals via ALX\/FPR2, a G protein-coupled receptor, in many cell types. This receptor was significantly attenuated by LXA4<\/sub> treatment in both the lesions and PFCs. Additionally, LXA4<\/sub> treatment resulted in a significant reduction in COX-2 expression in endometriotic lesions and PFCs; COX is known for its role in inflammation.<\/p>\n

The authors\u00a0also found consistently elevated transcript levels of pro-inflammatory cytokines (IL-1b, IL-6) as well as ALX\/FPR2, HIF-1a, COX-2, VEGF and MRP4 in PFCs of Veh mice as compared to sham mice, confirming the implication of these mediators in the pathogenesis of disease.<\/p>\n

Kumar and colleagues measured VEGF and IL-1b cytokines\u00a0from PFCs at the protein level\u00a0via ELISA. They\u00a0found\u00a0these to be higher in Veh-treated mice, compared to sham mice.\u00a0PGE2<\/sub> was also significantly higher in Veh-treated mice and reduced in the PFCs of LXA4\u00a0<\/sub>(compared to Veh-treated mice). LXA4<\/sub> treatment showed a demonstrable attenuation of the expression of COX-2 protein in endometriotic lesions, in\u00a0comparison to Veh-treated mice.<\/p>\n

Additionally, the LXA4<\/sub> downregulated MMP-2 and MMP-3 but upregulated MMP-9 mRNA expression in endometriotic lesions. The expression of MMP-9 was downregulated in PFCs by LXA4<\/sub> treatment.<\/p>\n

To determine whether these findings could be\u00a0clinically relevant, the team\u00a0investigated the effect of once-daily LXA4<\/sub> treatment on established lesions in the mice. LXA4\u00a0<\/sub> successfully reduced endometriotic lesion volume in established disease. Kumar et al. have not only confirmed a number of potential targets involved in the pathogenesis of endometriosis, but they have also shown that LXA4<\/sub> itself is a potential new therapeutic.<\/p>\n

 <\/p>\n

References<\/strong><\/p>\n

1. Bulun, S.E., et al. (2009) “Endometriosis<\/a>,” New England Journal of Medicine, 360 (pp. 268\u201379).<\/p>\n

2. Kumar, R., et al. (2014) “Lipoxin A4 Prevents the Progression of De Novo and Established Endometriosis in a Mouse Model by Attenuating Prostaglandin E2 Production and Estrogen Signaling<\/a>,” PLOS ONE, 9(2) (p.\u00a0e89742).<\/p>\n

3. Russell, R., et al. (2011) “Lipoxin A4 is a novel estrogen receptor modulator<\/a>,” FASEB Journal, 25(12) (pp. 4326\u201337).<\/p>\n

Post Author: Miriam Pollak. Miriam specialised in neuroscience as an undergraduate but traded in lab work for a post graduate degree in science communication.<\/i><\/p>\n

She has since had a career that has spanned science communication, science education and communications management.<\/p>\n

However, Miriam has found her bliss balancing her love of writing and disseminating medical research with managing a multimillion dollar research budget for a childhood cancer charity in Australia.<\/p>\n","protected":false},"excerpt":{"rendered":"

Endometriosis is an estrogen-dependent disease affecting approximately 10% of women of reproductive age worldwide and is a leading cause of pelvic pain. The pathophysiology of endometriosis involves inflammatory and angiogenic mediators; diagnosis is confirmed by the presence of endometrial-like tissue outside the uterine cavity.1 The recurrence of endometriosis when treatment ceases is not uncommon, and<\/p>\n","protected":false},"author":7,"featured_media":8515,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_monsterinsights_skip_tracking":false,"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[151],"tags":[292,293],"division":[],"class_list":{"0":"post-2516","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-inflammation","8":"tag-endometriosis","9":"tag-lipoxin","10":"entry"},"_selected_authors":"","_selected_reviewers":"","acf":[],"yoast_head":"\nLipoxin: 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