ArticleNature communications2018
A perivascular niche for multipotent progenitors in the fetal testis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 94 citations in OpenAlex.
- Postnatal Cell-Type-Specific Localization of EGFR and Its Ligands (EGF, TGF-α and AREG) in the Rat Testis.Anatomia, histologia, embryologia · 2026Article
- Platelet-derived growth factor receptor alpha regulates fetal testis differentiation via an ERK-CREB axis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Single-cell analysis reveals cellular heterogeneity and molecular features during postnatal pig testis development.BMC genomics · 2025Article
- Mesenchymal-to-epithelial transition of perivascular cells contributes to endometrial re-epithelialization.Nature communications · 2025Article
- Ovarian development is driven by early spatiotemporal priming of the coelomic epithelium.bioRxiv : the preprint server for biology · 2025Article
- The gene regulatory landscape driving mouse gonadal supporting cell differentiation.Science advances · 2025Article
- Circadian disruption impairs Leydig cell maturation and reproductive development in male rats.Reproductive biology and endocrinology : RB&E · 2025Article
- Article
- Single-cell resolution uncovers neighboring cell subtypes that share steroidogenic capacity during fetal testis development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- NR2F2 regulation of interstitial cell fate in the embryonic mouse testis and its impact on differences of sex development.Nature communications · 2025Article
- Transcriptomic dynamics and cell-to-cell communication during the transition of prospermatogonia to spermatogonia revealed at single-cell resolution.BMC genomics · 2025Article
- A new humanHuman reproduction open · 2025Article
- VEGF-dependent testicular vascularisation involves MEK1/2 signalling and the essential angiogenesis factors, SOX7 and SOX17.BMC biology · 2024Article
- Distribution, contribution and regulation of nestinJournal of advanced research · 2024Review
- Loss of PBX1 function in Leydig cells causes testicular dysgenesis and male sterility.Cellular and molecular life sciences : CMLS · 2024Article
- Fetal Leydig cells: What we know and what we don't.Molecular reproduction and development · 2024Review
- Unveiling the roles of Sertoli cells lineage differentiation in reproductive development and disorders: a review.Frontiers in endocrinology · 2024Review
- Analyzing the cellular and molecular atlas of ovarian mesenchymal cells provides a strategy against female reproductive aging.Science China. Life sciences · 2023Article
- Partial male-to-female reprogramming of mouse fetal testis by Sertoli cell ablation.Development (Cambridge, England) · 2023Article
- Revisiting the gonadotropic regulation of mammalian spermatogenesis: evolving lessons during the past decade.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Androgens responsible for male sexual differentiation in utero are produced by Leydig cells in the fetal testicular interstitium. Leydig cells rarely proliferate and, hence, rely on constant differentiation of interstitial progenitors to increase their number during fetal development. The cellular origins of fetal Leydig progenitors and how they are maintained remain largely unknown. Here we show that Notch-active, Nestin-positive perivascular cells in the fetal testis are a multipotent progenitor population, giving rise to Leydig cells, pericytes, and smooth muscle cells. When vasculature is disrupted, perivascular progenitor cells fail to be maintained and excessive Leydig cell differentiation occurs, demonstrating that blood vessels are a critical component of the niche that maintains interstitial progenitor cells. Additionally, our data strongly supports a model in which fetal Leydig cell differentiation occurs by at least two different means, with each having unique progenitor origins and distinct requirements for Notch signaling to maintain the progenitor population.
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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.