ArticlePLoS genetics2020
Inositol 1,4,5-trisphosphate receptors are essential for fetal-maternal connection and embryo viability.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Dll4 assembles the umbilical cord and placental vasculature.JCI insight · 2026Article
- MEOX2: a homeobox transcription factor with multifaceted biological functions and broad disease associations.Frontiers in cell and developmental biology · 2026Review
- From Obscurity to Prominence: IPMK's Expanding Role in Cellular Signaling, Physiology, and Disease.Biomolecules · 2025Review
- Deletion ofJournal of developmental biology · 2025Article
- Feto-placental blood vessel development.Development (Cambridge, England) · 2025Review
- Conditional deletion of IPJournal of gastroenterology · 2025Article
- Loss-of-function mutation of NSD2 is associated with abnormal placentation accompanied by fetal growth retardation in mice.PloS one · 2025Article
- Inositol 1,4,5-Trisphosphate Receptors Regulate Vascular Smooth Muscle Cell Proliferation and Neointima Formation in Mice.Journal of the American Heart Association · 2024Article
- Uterus proliferative period ceRNA network of Yunshang black goat reveals candidate genes on different kidding number trait.Frontiers in endocrinology · 2023Article
- Article
- Dynamic regulation of the transcriptome and proteome of the equine embryo during maternal recognition of pregnancy.FASEB bioAdvances · 2022Article
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- KRAP is required for diffuse and punctate IPCell calcium · 2022Article
- Melatonin and Myo-Inositol: Supporting Reproduction from the Oocyte to Birth.International journal of molecular sciences · 2021Review
- Genes and pathways associated with pregnancy loss in dairy cattle.Scientific reports · 2021Article
- The discovery and development of IP3 receptor modulators: an update.Expert opinion on drug discovery · 2021Article
- Atypical protein kinase C is essential for embryonic vascular development in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- Histone Lysine Methyltransferase SETD2 Regulates Coronary Vascular Development in Embryonic Mouse Hearts.Frontiers in cell and developmental biology · 2021Article
- Minimal contribution of IPActa pharmacologica Sinica · 2020Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are a family of intracellular Ca2+ release channels located on the ER membrane, which in mammals consist of 3 different subtypes (IP3R1, IP3R2, and IP3R3) encoded by 3 genes, Itpr1, Itpr2, and Itpr3, respectively. Studies utilizing genetic knockout mouse models have demonstrated that IP3Rs are essential for embryonic survival in a redundant manner. Deletion of both IP3R1 and IP3R2 has been shown to cause cardiovascular defects and embryonic lethality. However, it remains unknown which cell types account for the cardiovascular defects in IP3R1 and IP3R2 double knockout (DKO) mice. In this study, we generated conditional IP3R1 and IP3R2 knockout mouse models with both genes deleted in specific cardiovascular cell lineages. Our results revealed that deletion of IP3R1 and IP3R2 in cardiomyocytes by TnT-Cre, in endothelial / hematopoietic cells by Tie2-Cre and Flk1-Cre, or in early precursors of the cardiovascular lineages by Mesp1-Cre, resulted in no phenotypes. This demonstrated that deletion of both IP3R genes in cardiovascular cell lineages cannot account for the cardiovascular defects and embryonic lethality observed in DKO mice. We then revisited and performed more detailed phenotypic analysis in DKO embryos, and found that DKO embryos developed cardiovascular defects including reduced size of aortas, enlarged cardiac chambers, as well as growth retardation at embryonic day (E) 9.5, but in varied degrees of severity. Interestingly, we also observed allantoic-placental defects including reduced sizes of umbilical vessels and reduced depth of placental labyrinth in DKO embryos, which could occur independently from other phenotypes in DKO embryos even without obvious growth retardation. Furthermore, deletion of both IP3R1 and IP3R2 by the epiblast-specific Meox2-Cre, which targets all the fetal tissues and extraembryonic mesoderm but not extraembryonic trophoblast cells, also resulted in embryonic lethality and similar allantoic-placental defects. Taken together, our results demonstrated that IP3R1 and IP3R2 play an essential and redundant role in maintaining the integrity of fetal-maternal connection and embryonic viability.
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