ArticleAmerican journal of physiology. Renal physiology2023
B2 cells contribute to hypertension and natural killer cell activation possibly via AT1-AA in response to placental ischemia.
Article in American journal of physiology. Renal physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Reduced uterine perfusion pressure as a model for preeclampsia and fetal growth restriction in murine: a systematic review and meta-analysis.American journal of physiology. Heart and circulatory physiology · 2024Pooled it
- Analysis of the evolution of placental oxidative stress research from a bibliometric perspective.Frontiers in pharmacology · 2024Pooled it
- Sex differences in the developmental programming of cardiovascular and renal risk across the lifespan.American journal of physiology. Renal physiology · 2026Review
- The Immunopathology of Preeclampsia.Biomedicines · 2026Review
- Immune Cells in Preeclampsia.International journal of molecular sciences · 2025Review
- Higher Levels of Cardiovascular Biomarkers Following Hypertensive Compared to Normotensive Pregnancy.Pregnancy (Hoboken, N.J.) · 2025Article
- Angiotensin II type-1 receptor autoantibodies and effects in neonates of women with preeclampsia.BMC pregnancy and childbirth · 2025Article
- Multiple analytical perspectives of mitochondrial genes in the context of preeclampsia: potential diagnostic markers.Frontiers in immunology · 2025Article
- The role of complement in normal pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy.Comprehensive Physiology · 2024Review
- IL-33 supplementation improves uterine artery resistance and maternal hypertension in response to placental ischemia.American journal of physiology. Heart and circulatory physiology · 2024Article
- AT1-AA Is Produced in Offspring in Response to Placental Ischemia and Is Lowered by B-Cell Depletion Without Compromising Overall Offspring Health.Journal of the American Heart Association · 2024Article
- Setting a stage: Inflammation during preeclampsia and postpartum.Frontiers in physiology · 2023Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Preeclampsia, new onset hypertension during pregnancy, is associated with activated T helper cells (Th) and B cells secreting agonistic autoantibodies against the angiotensin II type 1 receptor (AT1-AA). The reduced uterine perfusion pressure (RUPP) model of placental ischemia recapitulates these characteristics. We have shown that Th-B cell communication contributes to AT1-AA and symptoms of preeclampsia in the RUPP rat. B2 cells are classical B cells that communicate with Th cells and are then transformed into memory B cells. We hypothesize that B2 cells cause hypertension, natural killer (NK) cell activation, and complement activation during pregnancy through the production of AT1-AA. To test this hypothesis, total splenic B cells and B2 cells were isolated from normal pregnant (NP) or RUPP rats on gestational day (GD)19 and adoptively transferred into GD12 NP rats. A group of recipient rats was treated with a specific inhibitor peptide of AT1-AA. On GD19, mean arterial pressure was measured, tissues were collected, activated NK cells were measured by flow cytometry, and AT1-AA was measured by cardiomyocyte assay. NP recipients of RUPP B cells or RUPP B2 cells had increased mean arterial pressure, AT1-AA, and circulating activated NK cells compared with recipients of NP B cells. Hypertension in NP recipients of RUPP B cells or RUPP B2 was attenuated with AT1-AA blockade. This study demonstrates that B cells and B2 cells from RUPP rats cause hypertension and increased AT1-AA and NK cell activation in response to placental ischemia during pregnancy.
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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.