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- Haeggstrom, A, et al.
(författare)
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Nasal mucosal swelling and reactivity during a menstrual cycle
- 2000
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Ingår i: ORL. - : S. Karger AG. - 0301-1569 .- 1423-0275. ; 62:1, s. 39-42
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Tidskriftsartikel (refereegranskat)abstract
- <i>Introduction:</i> Nasal stuffness is a great problem for many women in the later part of pregnancy. <i>Objective:</i> This study was performed to evaluate whether oestrogen causes nasal congestion and/or a hyperreactive reaction of the nasal mucosa. <i>Material and Methods:</i> Ten healthy fertile women were examined during menstruation. Nasal mucosal congestion was studied with rhinostereometry and acoustic rhinometry. The nasal mucosa was challenged with 3 doses of histamine solution to study nasal reactivity. Measurements were made 3 times during menstruation. To find the exact time of ovulation, when oestrogen reaches its peak value, intravaginal ultrasound tests were done and blood samples taken, to determine the oestrogen and progesterone levels. <i>Results:</i> The nasal mucosa became hyperreactive to histamine in connection with ovulation, when the blood level of oestrogen reached its peak. This does not occur during the menstrual or the luteal phase. No significant alteration was found in the baseline position during the menstruation. <i>Conclusion:</i> There is a connection between high oestrogen level and nasal mucosal reactivity.
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- Kintscher, Ulrich, et al.
(författare)
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PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4
- 2002
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Ingår i: Circulation Research. - 0009-7330 .- 1524-4571. ; 91:11, s. e35-e44
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Tidskriftsartikel (refereegranskat)abstract
- Integrins play an important role in vascular smooth muscle cell (VSMC) migration, a crucial event in the development of restenosis and atherosclerosis. Transforming growth factor-beta (TGF-beta) is highly expressed in restenotic and atherosclerotic lesions, and known to induce integrin expression. Peroxisome proliferator-activated receptor alpha (PPARalpha), a member of the nuclear receptor superfamily, regulates gene expression in a variety of vascular cells. We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors.
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