ArticleThe Journal of clinical investigation2019
Sialic acid is a critical fetal defense against maternal complement attack.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 93 citations in OpenAlex.
- Platelets link coagulation and complement in regulating murine placental vascular development.The Journal of clinical investigation · 2026Article
- Biosynthetic and genetic pathways related to sialic acid metabolism.The Journal of biological chemistry · 2026Review
- Defective HLA-G1 glycosylation disrupts Siglec-7-mediated NK cell tolerance at the maternal-fetal interface in recurrent pregnancy loss.Cell communication and signaling : CCS · 2026Article
- Deficient extravillous trophoblast invasion caused by impaired sialylation-Siglec-7 interaction contributes to recurrent pregnancy loss.Cell death & disease · 2026Article
- TidyMass2: advancing LC-MS untargeted metabolomics through metabolite origin inference and metabolic feature-based functional module analysis.Nature communications · 2026Article
- Integrative Multi-Omics Analysis Unveils Biomarkers Linking the Gut Microbiota, Blood Metabolites, and Recurrent Pregnancy Loss.International journal of women's health · 2026Article
- Shared glycosylation-related molecular mechanism and immune infiltration patterns of fetal growth restriction and preeclampsia.Frontiers in immunology · 2026Article
- B Cell Responses to the Placenta and Fetus.Annual review of pathology · 2025Review
- Multi-Layered Mechanisms of Immunological Tolerance at the Maternal-Fetal Interface.Immune network · 2024Review
- Evolutionarily conserved ovarian fluid proteins are responsible for extending egg viability in salmonid fish.Scientific reports · 2024Article
- Bluetongue Virus Infection in Farm Dogs Exposed to an Infected Sheep Flock in South Africa.Transboundary and emerging diseases · 2024Article
- Unveiling sialoglycans' immune mastery in pregnancy and their intersection with tumor biology.Frontiers in immunology · 2024Review
- Sialic acids on T cells are crucial for their maintenance and survival.Frontiers in immunology · 2024Article
- Complement, Coagulation, and Fibrinolysis: The Role of the Endothelium and Its Glycocalyx Layer in Xenotransplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- Edible bird's nest improves hemorheology and immune function in mice with transplanted uterine leiomyomas.American journal of translational research · 2024Article
- Insights into the Structure, Metabolism, Biological Functions and Molecular Mechanisms of Sialic Acid: A Review.Foods (Basel, Switzerland) · 2023Review
- Neurodevelopmental defects in human cortical organoids withScience advances · 2023Article
- The monosialoganglioside GM1a protects against complement attack.Cell death discovery · 2023Article
- The vertebrate sialylation machinery: structure-function and molecular evolution of GT-29 sialyltransferases.Glycoconjugate journal · 2023Review
- Control of lupus activity during pregnancy via the engagement of IgG sialylation: novel crosstalk between IgG sialylation and pDC functions.Frontiers of medicine · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The negatively charged sugar sialic acid (Sia) occupies the outermost position in the bulk of cell surface glycans. Lack of sialylated glycans due to genetic ablation of the Sia-activating enzyme CMP-sialic acid synthase (CMAS) resulted in embryonic lethality around day 9.5 post coitum (E9.5) in mice. Developmental failure was caused by complement activation on trophoblasts in Cmas-/- implants and was accompanied by infiltration of maternal neutrophils at the fetal-maternal interface, intrauterine growth restriction, impaired placental development, and a thickened Reichert's membrane. This phenotype, which shared features with complement receptor 1-related protein Y (Crry) depletion, was rescued in E8.5 Cmas-/- mice upon injection of cobra venom factor, resulting in exhaustion of the maternal complement component C3. Here we show that Sia is dispensable for early development of the embryo proper but pivotal for fetal-maternal immune homeostasis during pregnancy, i.e., for protecting the allograft implant against attack by the maternal innate immune system. Finally, embryos devoid of cell surface sialylation suffered from malnutrition due to inadequate placentation as a secondary effect.
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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.