ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Exposure to stimulatory CpG oligonucleotides during gestation induces maternal hypertension and excess vasoconstriction in pregnant rats.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Guidelines for assessing maternal cardiovascular physiology during pregnancy and postpartum.American journal of physiology. Heart and circulatory physiology · 2024Guideline
- Acute exposure to cell-free mitochondrial DNA induces pregnancy-specific aortic endothelial dysfunction and organ-selective inflammation in rats.bioRxiv : the preprint server for biology · 2026Article
- Association of Increased Fetal Fraction with Birthweight Discordance and Selective Fetal Growth Restriction: A Retrospective Study.International journal of women's health · 2026Article
- Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy.Comprehensive Physiology · 2024Review
- Deciphering the immunological interactions: targeting preeclampsia with Hydroxychloroquine's biological mechanisms.Frontiers in pharmacology · 2024Review
- Exposure to unmethylated CpG oligonucleotides disrupts blood pressure circadian rhythms and placental clock gene network in pregnant rats.American journal of physiology. Heart and circulatory physiology · 2023Article
- The Clinical Value of Rodent Models in Understanding Preeclampsia Development and Progression.Current hypertension reports · 2023Review
- Mitochondrial might: powering the peripartum for risk and resilience.Frontiers in behavioral neuroscience · 2023Review
- Exosomes facilitate intercellular communication between uterine perivascular adipose tissue and vascular smooth muscle cells in pregnant rats.American journal of physiology. Heart and circulatory physiology · 2022Article
- Animal Models of Preeclampsia: Mechanistic Insights and Promising Therapeutics.Endocrinology · 2022Review
- Circulating Cell-Free Mitochondrial DNA in Pregnancy.Physiology (Bethesda, Md.) · 2022Review
- Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.Current hypertension reports · 2022Review
- Reduced Maternal Circulating Cell-Free Mitochondrial DNA Is Associated With the Development of Preeclampsia.Journal of the American Heart Association · 2022Article
- Cell-free DNA as a potential biomarker for preeclampsia.Expert review of molecular diagnostics · 2021Article
- The Role of Mitochondrial Dysfunction in Preeclampsia: Causative Factor or Collateral Damage?American journal of hypertension · 2021Review
- Toll-Like Receptors Contribute to Sex Differences in Blood Pressure Regulation.Journal of cardiovascular pharmacology · 2020Review
- Inflammation-mediated generation and inflammatory potential of human placental cell-free fetal DNA.Placenta · 2020Article
- Double-stranded RNA and Toll-like receptor activation: a novel mechanism for blood pressure regulation.Clinical science (London, England : 1979) · 2020Review
- Hypertension: a new treatment for an old disease? Targeting the immune system.British journal of pharmacology · 2019Review
- Maternal-fetal cross talk through cell-free fetal DNA, telomere shortening, microchimerism, and inflammation.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Bacterial infections increase risk for pregnancy complications, such as preeclampsia and preterm birth. Unmethylated CpG DNA sequences are present in bacterial DNA and have immunostimulatory effects. Maternal exposure to CpG DNA induces fetal demise and craniofacial malformations; however, the effects of CpG DNA on maternal cardiovascular health have not been examined. We tested the hypothesis that exposure to synthetic CpG oligonucleotides (ODNs) during gestation would increase blood pressure and cause vascular dysfunction in pregnant rats. Pregnant and nonpregnant female rats were treated with CpG ODN (ODN 2395) or saline (Veh) starting on gestational day 14or corresponding day for the nonpregnant groups. Exposure to CpG ODN increased systolic blood pressure in pregnant (Veh: 121 ± 2 mmHg vs. ODN 2395: 134 ± 2 mmHg,P< 0.05) but not in nonpregnant rats (Veh: 111 ± 2 mmHg vs. ODN 2395: 108 ± 5 mmHg,P> 0.05). Mesenteric resistance arteries from pregnant CpG ODN-treated rats had increased contractile responses to U46619 [thromboxane A2(TxA2) mimetic] compared with arteries from vehicle-treated rats [Emax(%KCl), Veh: 87 ± 4 vs. ODN 2395: 104 ± 4,P< 0.05]. Nitric oxide synthase (NOS) inhibition increased contractile responses to U46619, and CpG ODN treatment abolished this effect in arteries from pregnant ODN 2395-treated rats. CpG ODN potentiated the involvement of cyclooxygenase (COX) to U46619-induced contractions. In conclusion, exposure to CpG ODN during gestation induces maternal hypertension, augments resistance artery contraction, increases the involvement of COX-dependent mechanisms and reduces the contribution of NOS-dependent mechanisms to TxA2-induced contractions in mesenteric resistance arteries.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.