ArticlePloS one2020
Complement inhibitor Crry expression in mouse placenta is essential for maintaining normal blood pressure and fetal growth.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Complement Activation in Maternal and Placental Pathology of Preeclampsia.Hypertension (Dallas, Tex. : 1979) · 2026Article
- The Role of Complement and CD4 T Cells in Preeclampsia and Offspring Neurodevelopment.Current opinion in physiology · 2026Article
- Complement as a driver of immune-vascular heterogeneity across preeclampsia subtypes: toward a precision medicine framework.Frontiers in immunology · 2026Review
- Therapeutic strategies targeting complement in myasthenia gravis patients.Journal of neurology · 2025Review
- The role of complement in normal pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Function of immune cells and effector molecules of the innate immune system in the establishment and maintenance of pregnancy in mammals - A review.Animal bioscience · 2024Article
- Inhibition of complement C3 signaling ameliorates locomotor and visual dysfunction in autoimmune inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Many circumstantial evidences from human and animal studies suggest that complement cascade dysregulation may play an important role in pregnancy associated complications including preeclampsia. Deletion of rodent specific complement inhibitor gene, Complement Receptor 1-related Gene/Protein y (Crry) produces embryonic lethal phenotype due to complement activation. It is not clear if decreased expression of Crry during pregnancy produces hypertensive phenotype. We downregulated Crry in placenta by injecting inducible lentivialshRNA vectors into uterine horn of pregnant C57BL/6 mice at the time of blastocyst hatching. Placenta specific downregulation of Crry without significant loss of embryos was achieved upon induction of shRNA using an optimal doxycycline dose at mid gestation. Crry downregulation resulted in placental complement deposition. Late-gestation measurements showed that fetal weights were reduced and blood pressure increased in pregnant mice upon downregulation of Crry suggesting a critical role for Crry in fetal growth and blood pressure regulation.
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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.