- Title
- Lipopolysaccharide stimulation of trophoblasts induces corticotropin-releasing hormone expression through MyD88
- Creator
- Uh, Andy; Nicholson, Richard C.; Gonzalez, Gustavo V.; Simmons, Charles F.; Gombart, Adrian; Smith, Roger; Equils, Ozlem
- Relation
- American Journal of Obstetrics and Gynecology Vol. 199, Issue 3
- Publisher Link
- http://dx.doi.org/10.1016/j.ajog.2008.06.091
- Publisher
- Mosby
- Resource Type
- journal article
- Date
- 2008
- Description
- Objective: We hypothesized that intrauterine infection may lead to placental corticotrophin-releasing hormone (CRH) expression via Toll-like receptor signaling. Study Design: To test this hypothesis JEG3 cells were stimulated with lipopolysaccharide (LPS), chlamydial heat shock protein 60, and interleukin (IL)-1. CRH expression was assessed by reverse transcription polymerase chain reaction (RT-PCR). The signaling mechanisms that were involved were examined in transient transfection experiments with β-galactosidase, CRH-luciferase, cyclic adenosine monophosphate (AMP) response element-luciferase, dominant-negative (DN)-myeloid differentiation primary response gene (MyD88) and DN-toll-IL-1-receptor domain containing adapter inducing interferon (TRIF) vectors. Luciferase activity was determined by luciferase assay. β-galactosidase assay was performed to determine transfection efficiency. Results: LPS, chlamydial heat shock protein 60, and IL-1 stimulation led to CRH expression in the JEG3 cells. LPS-induced CRH expression was not due to the autocrine effect of LPS-induced IL-1 because the supernatant from LPS-conditioned JEG3 cells did not induce CRH expression in the naïve cells. DN-MyD88, but not DN-TRIF, blocked the LPS-induced CRH expression. The cAMP response element did not play a role in LPS-induced CRH expression. Conclusion: Toll-like receptor signaling 4 may induce placental CRH expression through MyD88.
- Subject
- LPS; MyD88; placenta; pregnancy; preterm delivery; signaling; Toll-like receptors; TRIF; trophoblast
- Identifier
- http://hdl.handle.net/1959.13/43110
- Identifier
- uon:5238
- Identifier
- ISSN:0002-9378
- Language
- eng
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