https://scholars.lib.ntu.edu.tw/handle/123456789/458225
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | LING-HUNG WEI | en_US |
dc.contributor.author | Chou C.-H | en_US |
dc.contributor.author | Chen M.-W | en_US |
dc.contributor.author | Rose-John S | en_US |
dc.contributor.author | Kuo M.-L | en_US |
dc.contributor.author | SHEE-UAN CHEN | en_US |
dc.contributor.author | YU-SHIH YANG | en_US |
dc.creator | Yang Y.-S.;Chen S.-U;Kuo M.-L;Rose-John S;Chen M.-W;Chou C.-H;LING-HUNG WEI | - |
dc.date.accessioned | 2020-02-12T05:48:26Z | - |
dc.date.available | 2020-02-12T05:48:26Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 0021-972X | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/458225 | - |
dc.description.abstract | Context: The inflammatory cytokine IL-6 is related to ovarian hyperstimulation syndrome (OHSS), although the functional role of IL-6 in OHSS remains largely unknown. Objective: A key feature of the IL-6 response is that its regulation is dependent on IL-6 trans-signaling via soluble IL-6 receptor-α (sIL-6Rα). The objective of the study was to elucidate the mechanistic role of IL-6 trans-signaling in the vascular leakage that underlies the pathophysiology of OHSS. Design: Ovarian endothelial cells (ECs) and granulosa-lutein cells were obtained from women undergoing in vitro fertilization. OHSS was induced in mice by administering gonadotropins for 2 days followed by human chorionic gonadotropin. The functional role of IL-6 trans-signaling in OHSS was verified using the designer cytokines Hyper IL-6 and sgp130-Fc. Results: The follicular fluid levels of sIL-6Rα were elevated in women at high risk for OHSS. In the murine OHSS model, stimulation with gonadotropins significantly induces ovarian IL-6 and sIL-6Rα expression. In vitro, FSH induces de novo sIL-6Rα synthesis in granulosa-lutein cells through a protein kinase C-dependent pathway. In addition, sIL-6Rα was released by leukocytes in the presence of conditioned medium from human chorionic gonadotropin-treated granulosa-lutein cells. Ovarian ECs responded to the IL-6Rα-IL-6 complex (Hyper IL-6) but not to IL-6 alone. With activation of signal transducer and activator of transcription 3 (STAT3) and ERK, Hyper IL-6 increased vascular endothelial growth factor expression and the vascular permeability of ECs. Selective blockade of IL-6 trans-signaling by sgp130-Fc significantly inhibited vascular endothelial growth factor expression and prevented OHSS in mice. Conclusions: IL-6 trans-signaling is activated during the ovarian stimulation process. Our findings provide insight into the biologic effects of IL-6 trans-signaling in OHSS and highlight that IL-6 trans-signaling can induce vascular leakage in this disease. Copyright ? 2013 by The Endocrine Society. | en_US |
dc.relation.ispartof | Journal of Clinical Endocrinology and Metabolism | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | interleukin 6; interleukin 6 receptor alpha; mitogen activated protein kinase; protein kinase C; soluble interleukin 6 receptor alpha; STAT3 protein; unclassified drug; vasculotropin; adult; animal experiment; animal model; animal tissue; article; blood vessel permeability; controlled study; endothelium cell; female; granulosa cell; human; human cell; in vitro study; luteal cell; major clinical study; nonhuman; ovary hyperstimulation; pathophysiology; priority journal; protein expression; protein synthesis; signal transduction; vascular disease; vascular leakage; Animals; Capillary Permeability; Chorionic Gonadotropin; Cytokine Receptor gp130; Disease Models, Animal; Endothelial Cells; Female; Follicle Stimulating Hormone; Follicular Fluid; Granulosa Cells; Hormones; Humans; Interleukin-6; Mice; Mice, Inbred ICR; Ovarian Hyperstimulation Syndrome; Ovulation Induction; Protein Kinase C; Receptors, Interleukin-6; Reproductive Control Agents; Risk Factors; Signal Transduction; Vascular Endothelial Growth Factor A | - |
dc.title | The role of IL-6 trans-signaling in vascular leakage: Implications for ovarian hyperstimulation syndrome in a murine model | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1210/jc.2012-3462 | - |
dc.identifier.pmid | 23348396 | - |
dc.identifier.scopus | 2-s2.0-84874830783 | - |
dc.relation.pages | E472-E484 | en_US |
dc.relation.journalvolume | 98 | en_US |
dc.relation.journalissue | 3 | en_US |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.orcid | 0000-0001-8789-0859 | - |
crisitem.author.orcid | 0000-0001-7592-3238 | - |
crisitem.author.orcid | 0000-0002-8633-0873 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 醫學系 |
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