ArticlePLoS genetics2019
Risk of spontaneous preterm birth and fetal growth associates with fetal SLIT2.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- A systematic review of genetic association studies on the susceptibility of preterm birth in Asia.Molecular genetics and genomics : MGG · 2025Pooled it
- Integrated analysis of transcriptomic datasets to identify placental biomarkers of spontaneous preterm birth.Placenta · 2022Pooled it
- AAT/SERPINA1 Pi*Z variant linked to gestational length and preterm birth prevention via AAT in mice.Nature communications · 2026Article
- Genomic Differences between Spontaneous versus Indicated Extreme Preterm Birth.American journal of perinatology · 2025Article
- Recent Advances in Genomic Studies of Gestational Duration and Preterm Birth.Clinics in perinatology · 2024Review
- Genomic Insights into Gestational Weight Gain: Uncovering Tissue-Specific Mechanisms and Pathways.Research square · 2024Article
- Maternal serum alpha-1 antitrypsin levels in spontaneous preterm and term pregnancies.Scientific reports · 2024Article
- Review
- Genomic insights into gestational weight gain uncover tissue-specific mechanisms and pathways.npj women's health · 2024Article
- Modulation of local immunity by the vaginal microbiome is associated with triggering spontaneous preterm birth.Frontiers in immunology · 2024Article
- Identifying selection signatures for immune response and resilience to Aleutian disease in mink using genotype data.Frontiers in genetics · 2024Article
- Genetic architecture of body weight, carcass, and internal organs traits of Ghanaian local chickens.Frontiers in genetics · 2024Article
- Unravelling the genetic landscape of cervical insufficiency: Insights into connective tissue dysfunction and hormonal pathways.PloS one · 2024Article
- Genome-wide identification of transcriptional enhancers during human placental development and association with function, differentiation, and disease†.Biology of reproduction · 2023Article
- The Role of Genetics in Preterm Birth.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Genetic association study of Preterm birth and Gestational age in a population-based case-control study in Peru: Genetics of PTB and GA in pregnant women in Peru.medRxiv : the preprint server for health sciences · 2023Article
- Molecular and Cellular Insights: A Focus on Glycans and the HNK1 Epitope in Autism Spectrum Disorder.International journal of molecular sciences · 2023Article
- Microdiversity of the vaginal microbiome is associated with preterm birth.Nature communications · 2023Article
- Elevated human placental heat shock protein 5 is associated with spontaneous preterm birth.Pediatric research · 2023Article
- Time-varying effects are common in genetic control of gestational duration.Human molecular genetics · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Spontaneous preterm birth (SPTB) is the leading cause of neonatal death and morbidity worldwide. Both maternal and fetal genetic factors likely contribute to SPTB. We performed a genome-wide association study (GWAS) on a population of Finnish origin that included 247 infants with SPTB (gestational age [GA] < 36 weeks) and 419 term controls (GA 38-41 weeks). The strongest signal came within the gene encoding slit guidance ligand 2 (SLIT2; rs116461311, minor allele frequency 0.05, p = 1.6×10-6). Pathway analysis revealed the top-ranking pathway was axon guidance, which includes SLIT2. In 172 very preterm-born infants (GA <32 weeks), rs116461311 was clearly overrepresented (odds ratio 4.06, p = 1.55×10-7). SLIT2 variants were associated with SPTB in another European population that comprised 260 very preterm infants and 9,630 controls. To gain functional insight, we used immunohistochemistry to visualize SLIT2 and its receptor ROBO1 in placentas from spontaneous preterm and term births. Both SLIT2 and ROBO1 were located in villous and decidual trophoblasts of embryonic origin. Based on qRT-PCR, the mRNA levels of SLIT2 and ROBO1 were higher in the basal plate of SPTB placentas compared to those from term or elective preterm deliveries. In addition, in spontaneous term and preterm births, placental SLIT2 expression was correlated with variations in fetal growth. Knockdown of ROBO1 in trophoblast-derived HTR8/SVneo cells by siRNA indicated that it regulate expression of several pregnancy-specific beta-1-glycoprotein (PSG) genes and genes involved in inflammation. Our results show that the fetal SLIT2 variant and both SLIT2 and ROBO1 expression in placenta and trophoblast cells may be correlated with susceptibility to SPTB. SLIT2-ROBO1 signaling was linked with regulation of genes involved in inflammation, PSG genes, decidualization and fetal growth. We propose that this receptor-ligand couple is a component of the signaling network that promotes SPTB.
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