ArticleMolecular and cellular endocrinology2018
Deletion of fetoplacental Fshr inhibits fetal vessel angiogenesis in the mouse placenta.
Article in Molecular and cellular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Placental Steroid Hormones in Preeclampsia: Multilayered Regulation of Endocrine Pathogenesis.Endocrine reviews · 2026Review
- Article
- FSH, bone, belly and brain.The Journal of endocrinology · 2024Review
- Targeting the FSH/FSHR axis in ovarian cancer: advanced treatment using nanotechnology and immunotherapy.Frontiers in endocrinology · 2024Review
- Association of Polymorphisms inBiomedicines · 2023Article
- Abnormal angiogenesis of placenta in progranulin‑deficient mice.Molecular medicine reports · 2020Article
- Extragonadal FSHR Expression and Function-Is It Real?Frontiers in endocrinology · 2019Review
- FSH Actions and Pregnancy: Looking Beyond Ovarian FSH Receptors.Endocrinology · 2018Review
- Molecular and functional insights into gonadotropin hormone receptor dimerization and oligomerization.Minerva ginecologica · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It has been shown in both human and mouse placentas that follicle stimulating hormone receptor (FSHR) is expressed in fetal vascular endothelium. There are conflicting reports, however, on the role of FSH to stimulate angiogenesis in vitro in cultured endothelial cells from umbilical veins. Therefore, in this study we undertook an in vivo approach utilizing Fshr null mice to definitively address this question. In the context where all pregnant dams have identical Fshr genotypes, we generated fetuses and associated fetal portions of placenta that were Fshr wt or Fshr null and analyzed angiogenesis within the placental labyrinths. Quantitative morphometric analyses of placentas obtained at mid-gestation revealed that the percentage of the placenta composed of labyrinth is significantly decreased in Fshr null placentas relative to wt placentas. Furthermore, data presented demonstrate that within the Fshr null labyrinths, fetal vessel angiogenesis was significantly reduced relative to wt labyrinths. The results obtained with this combination of in vivo and genetic approaches conclusively demonstrate that signaling through endothelial FSHR does indeed stimulate angiogenesis and that placental Fshr is essential for normal angiogenesis of the fetal placental vasculature.
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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.