Abstract:
:Preterm birth (PTB) is the single largest cause of death in infants and young children. The rate of PTB is significantly higher in male infants, particularly those that are born very preterm. Here we present evidence to suggest that the decidual renin-angiotensin system may play a role in inhibiting inflammation and maintaining the integrity of the fetal membranes during pregnancy, and that sex-specific alterations in the intrauterine RAS could contribute to the increased risk of PTB in male babies. Women carrying female fetuses have high levels of expression of decidual prorenin at term. Decidua from 'female' pregnancies also have greater expression of the anti-inflammatory angiotensin (Ang)-(1-7) pathway, than decidua from 'male' pregnancies, and have lower levels of the pro-inflammatory Ang II pathway. We propose that in 'female' pregnancies, the very high levels of decidual prorenin drive the anti-inflammatory Ang-(1-7) pathway, thus reducing the likelihood of PTB. In addition, the high levels of prorenin produced by the decidua in 'female' pregnancies are able to diffuse into the amnion and bind to the PRR. We postulate that PRR/prorenin interactions, possibly through both angiotensin dependent and independent pathways, stimulate the production of ECM proteins, inhibit ECM degradation and prevent apoptosis, thus strengthening the amnion. Thus control of the inflammatory signature and the integrity of the fetal membranes prior to parturition may partly depend on the sexually determined activity of the decidual and amniotic renin-angiotensin system pathways.
journal_name
Clin Exp Pharmacol Physioljournal_title
Clinical and experimental pharmacology & physiologyauthors
Pringle KG,Zakar T,Lumbers ERdoi
10.1111/1440-1681.12734subject
Has Abstractpub_date
2017-05-01 00:00:00pages
605-610issue
5eissn
0305-1870issn
1440-1681journal_volume
44pub_type
杂志文章,评审abstract::1. Levodopa markedly reduces parkinsonism during the first years of treatment. However, with continued therapy the response to levodopa becomes erratic and is complicated by involuntary movements. To improve the therapy of parkinsonism, the challenge is to understand why fluctuations in response develop and, once deve...
journal_title:Clinical and experimental pharmacology & physiology
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doi:10.1111/j.1440-1681.1995.tb01946.x
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pub_type: 信件
doi:10.1111/1440-1681.12941
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pub_type: 杂志文章
doi:10.1111/j.1440-1681.1998.t01-19-.x
更新日期:1998-03-01 00:00:00
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pub_type: 杂志文章,评审
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pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:2004-07-01 00:00:00
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pub_type: 临床试验,杂志文章,随机对照试验
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pub_type: 杂志文章,评审
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