ArticlePloS one2009
Proteomic-based detection of a protein cluster dysregulated during cardiovascular development identifies biomarkers of congenital heart defects.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Host-derived protein profiles of human neonatal meconium across gestational ages.Nature communications · 2024Article
- Nogo-A reduces ceramide de novo biosynthesis to protect from heart failure.Cardiovascular research · 2023Article
- Clinical implications of plasma Nogo-A levels in patients with coronary heart disease.Archives of medical science : AMS · 2017Article
- Endothelial Nogo-B regulates sphingolipid biosynthesis to promote pathological cardiac hypertrophy during chronic pressure overload.JCI insight · 2016Article
- Role of the Wnt-Frizzled system in cardiac pathophysiology: a rapidly developing, poorly understood area with enormous potential.The Journal of physiology · 2013Review
- The heart-placenta axis in the first month of pregnancy: induction and prevention of cardiovascular birth defects.Journal of pregnancy · 2013Article
- Karyotypic and molecular genetic changes associated with fetal cardiovascular abnormalities: results of a retrospective 4-year ultrasonic diagnosis study.International journal of biological sciences · 2013Article
- Deletion of a single-copy DAAM1 gene in congenital heart defect: a case report.BMC medical genetics · 2012Article
- Notch signaling and cardiac repair.Journal of molecular and cellular cardiology · 2012Review
- RNT4 3'-UTR insertion/deletion polymorphisms are not associated with atrial septal defect in Chinese Han population: a brief communication.DNA and cell biology · 2012Article
- GVI phospholipase A2 role in the stimulatory effect of sphingosine-1-phosphate on TRPC5 cationic channels.Cell calcium · 2011Article
- Rapid and contrasting effects of rosiglitazone on transient receptor potential TRPM3 and TRPC5 channels.Molecular pharmacology · 2011Article
- Nogo-A knockdown inhibits hypoxia/reoxygenation-induced activation of mitochondrial-dependent apoptosis in cardiomyocytes.Journal of molecular and cellular cardiology · 2011Article
- Properties and therapeutic potential of transient receptor potential channels with putative roles in adversity: focus on TRPC5, TRPM2 and TRPA1.Current drug targets · 2011Review
- TRPC5 channel sensitivities to antioxidants and hydroxylated stilbenes.The Journal of biological chemistry · 2011Article
- Stimulation of TRPC5 cationic channels by low micromolar concentrations of lead ions (Pb2+).Biochemical and biophysical research communications · 2010Article
- Hierarchical approaches for systems modeling in cardiac development.Wiley interdisciplinary reviews. Systems biology and medicineReview
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCardiovascular development is vital for embryonic survival and growth. Early gestation embryo loss or malformation has been linked to yolk sac vasculopathy and congenital heart defects (CHDs). However, the molecular pathways that underlie these structural defects in humans remain largely unknown hindering the development of molecular-based diagnostic tools and novel therapies. METHODOLOGY/PRINCIPAL
findingsMurine embryos were exposed to high glucose, a condition known to induce cardiovascular defects in both animal models and humans. We further employed a mass spectrometry-based proteomics approach to identify proteins differentially expressed in embryos with defects from those with normal cardiovascular development. The proteins detected by mass spectrometry (WNT16, ST14, Pcsk1, Jumonji, Morca2a, TRPC5, and others) were validated by Western blotting and immunoflorescent staining of the yolk sac and heart. The proteins within the proteomic dataset clustered to adhesion/migration, differentiation, transport, and insulin signaling pathways. A functional role for several proteins (WNT16, ADAM15 and NOGO-A/B) was demonstrated in an ex vivo model of heart development. Additionally, a successful application of a cluster of protein biomarkers (WNT16, ST14 and Pcsk1) as a prenatal screen for CHDs was confirmed in a study of human amniotic fluid (AF) samples from women carrying normal fetuses and those with CHDs. CONCLUSIONS/SIGNIFICANCE: The novel finding that WNT16, ST14 and Pcsk1 protein levels increase in fetuses with CHDs suggests that these proteins may play a role in the etiology of human CHDs. The information gained through this bed-side to bench translational approach contributes to a more complete understanding of the protein pathways dysregulated during cardiovascular development and provides novel avenues for diagnostic and therapeutic interventions, beneficial to fetuses at risk for CHDs.
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