ArticleEndocrinology2014
Perfluorooctanesulfonate (PFOS) perturbs male rat Sertoli cell blood-testis barrier function by affecting F-actin organization via p-FAK-Tyr(407): an in vitro study.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 123 citations in OpenAlex.
- Actin Cytoskeleton Dysregulation Links Testicular and Sperm Dysfunction in Type 1 Diabetes.International journal of molecular sciences · 2026Article
- Naproxen and Ibuprofen Exposure Alter the Blood-Testis Barrier in a Novel In Vitro Model.International journal of molecular sciences · 2026Article
- 1α,25(OH)Journal of endocrinological investigation · 2025Article
- In Vitro Investigation of Perfluorooctane Sulphonate and Perfluorooctanoic Acid on Boar Spermatozoa Agglutination.Veterinary medicine and science · 2025Article
- Unveiling the Research Void: Exploring the Reproductive Effects of PFAS Compounds on Male Health.Advances in experimental medicine and biology · 2025Review
- PFAS Exposure is Associated with a Lower Spermatic Quality in an Arctic Seabird.Environmental science & technology · 2024Article
- Blood-testis barrier: a review on regulators in maintaining cell junction integrity between Sertoli cells.Cell and tissue research · 2024Review
- Map-1a regulates Sertoli cell BTB dynamics through the cytoskeletal organization of microtubule and F-actin.Reproductive biology and endocrinology : RB&E · 2024Article
- Assessment of the impact of direct in vitro PFAS treatment on mouse spermatozoa.Reproduction & fertility · 2024Article
- A review of cardiovascular effects and underlying mechanisms of legacy and emerging per- and polyfluoroalkyl substances (PFAS).Archives of toxicology · 2023Review
- PFOS-elicited metabolic perturbation in liver and fatty acid metabolites in testis of adult mice.Frontiers in endocrinology · 2023Article
- Impact of endocrine disrupting chemicals and pharmaceuticals on Sertoli cell development and functions.Frontiers in endocrinology · 2023Review
- Pachypodol attenuates Perfluorooctane sulphonate-induced testicular damage by reducing oxidative stress.Saudi journal of biological sciences · 2022Article
- Review
- Disruption of anchoring junctions in the testes of experimental varicocele rats.Experimental and therapeutic medicine · 2021Article
- Microtubule-associated proteins (MAPs) in microtubule cytoskeletal dynamics and spermatogenesis.Histology and histopathology · 2021Review
- Assessment of the Emerging Threat Posed by Perfluoroalkyl and Polyfluoroalkyl Substances to Male Reproduction in Humans.Frontiers in endocrinology · 2021Review
- Signaling Proteins That Regulate Spermatogenesis Are the Emerging Target of Toxicant-Induced Male Reproductive Dysfunction.Frontiers in endocrinology · 2021Review
- Testis Toxicants: Lesson from Traditional Chinese Medicine (TCM).Advances in experimental medicine and biology · 2021Article
- The Non-hormonal Male Contraceptive Adjudin Exerts its Effects via MAPs and Signaling Proteins mTORC1/rpS6 and FAK-Y407.Endocrinology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Environmental toxicants such as perfluorooctanesulfonate (PFOS) have been implicated in male reproductive dysfunction, including reduced sperm count and semen quality, in humans. However, the underlying mechanism(s) remains unknown. Herein PFOS at 10-20 μM (∼5-10 μg/mL) was found to be more potent than bisphenol A (100 μM) in perturbing the blood-testis barrier (BTB) function by disrupting the Sertoli cell tight junction-permeability barrier without detectable cytotoxicity. We also delineated the underlying molecular mechanism by which PFOS perturbed Sertoli cell BTB function using an in vitro model that mimics the BTB in vivo. First, PFOS perturbed F-actin organization in Sertoli cells, causing truncation of actin filaments at the BTB. Thus, the actin-based cytoskeleton was no longer capable of supporting the distribution and/or localization of actin-regulatory and adhesion proteins at the cell-cell interface necessary to maintain BTB integrity. Second, PFOS was found to perturb inter-Sertoli cell gap junction (GJ) communication based on a dye-transfer assay by down-regulating the expression of connexin-43, a GJ integral membrane protein. Third, phosphorylated focal adhesion kinase (FAK)-Tyr(407) was found to protect the BTB from the destructive effects of PFOS as shown in a study via an overexpression of an FAK Y407E phosphomimetic mutant. Also, transfection of Sertoli cells with an FAK-specific microRNA, miR-135b, to knock down the expression of phosphorylated FAK-Tyr(407) was found to worsen PFOS-mediated Sertoli cell tight junction disruption. In summary, PFOS-induced BTB disruption is mediated by down-regulating phosphorylated FAK-Tyr(407) and connexin-43, which in turn perturbed F-actin organization and GJ-based intercellular communication, leading to mislocalization of actin-regulatory and adhesion proteins at the BTB.
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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.