ArticleCell death & disease2017
Glucocorticoid mediates prenatal caffeine exposure-induced endochondral ossification retardation and its molecular mechanism in female fetal rats.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Paternal Nicotine/Ethanol/Caffeine Mixed Exposure Induces Offspring Rat Dysplasia and Its Potential "GC-IGF1" Programming Mechanism.International journal of molecular sciences · 2022Pooled it
- Review
- Tristetraprolin protects against osteoarthritis by restraining chondrocyte mitochondrial DNA release through post-transcriptional regulation.Journal of orthopaedic translation · 2026Article
- Sperm miR-142-3p Reprogramming Mediates Paternal Pre-Pregnancy Caffeine Exposure-Induced Non-Alcoholic Steatohepatitis in Male Offspring Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The effect of coffee consumption on three main bone disorders: a Mendelian randomization trial.Journal of bone and mineral metabolism · 2024Article
- Caffeine regulates both osteoclast and osteoblast differentiation via the AKT, NF-κB, and MAPK pathways.Frontiers in pharmacology · 2024Article
- Effect of caffeine intake on self-reported and genetic prediction of osteoarthritis: an epidemiological study and Mendelian randomization analysis.Frontiers in nutrition · 2024Article
- Causal Association of Coffee Consumption and Total, Knee, Hip and Self-Reported Osteoarthritis: A Mendelian Randomization Study.Frontiers in endocrinology · 2021Article
- The low-expression programming of 11β-HSD2 mediates osteoporosis susceptibility induced by prenatal caffeine exposure in male offspring rats.British journal of pharmacology · 2020Article
- Caffeine, a Risk Factor for Osteoarthritis and Longitudinal Bone Growth Inhibition.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous studies discovered that prenatal caffeine exposure (PCE) could induce intrauterine growth retardation (IUGR) and long-bone dysplasia in offspring rats, accompanied by maternal glucocorticoid over-exposure. This study is to explore whether intrauterine high glucocorticoid level can cause endochondral ossification retardation and clarify its molecular mechanism in PCE fetal rats. Pregnant Wistar rats were intragastrically administered 30 and 120 mg/kg day of caffeine during gestational days (GDs) 9-20, then collected fetal serum and femurs at GD20. In vitro, primary chondrocytes were treated with corticosterone (0-1250 nM), caffeine (0-100 μM), mitogen-inducible gene 6 (Mig-6) siRNA and epidermal growth factor receptor (EGFR) siRNA, respectively, or together. Results showed that the hypertrophic chondrocytes zone (HZ) of PCE fetal femur was widened. Meanwhile, the expression levels of chondrocytes terminal differentiation genes in the HZ were decreased, and the chondrocytes apoptosis rate in the HZ was decreased too. Furthermore, PCE upregulated Mig-6 and suppressed EGFR expression in the HZ. In vitro, a high-concentration corticosterone (1250 nM) upregulated Mig-6 expression, inhibit EGFR/c-Jun N-terminal kinase (JNK) signaling pathway and terminal differentiation genes expression in chondrocytes and reduced cell apoptosis, and these above alterations could be partly reversed step-by-step after Mig-6 and EGFR knockdown. However, caffeine concentration dependently increased chondrocyte apoptosis without significant changes in the expression of terminal differentiation genes. Collectively, PCE caused endochondral ossification retardation in the female fetal rats, and its main mechanism was associated with glucocorticoid (rather than caffeine)-mediated chondrocyte terminal differentiation suppression by the upregulation of Mig-6 and then inhibition of EGFR/JNK pathway-mediated chondrocyte apoptosis.
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