ArticleThe Journal of clinical investigation2013
Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Covert Clue for Potential Therapy.Inflammation · 2021Pooled it
- A randomized, double-blind study on the efficacy of oral domperidone versus placebo for reducing SARS-CoV-2 viral load in mild-to-moderate COVID-19 patients in primary health care.Annals of medicine · 2023Trial
- Metoclopramide-induced hyperprolactinemia during pregnancy and lactating alters chondrocyte proliferation and apoptosis in the murine femoral and tibial epiphyseal growth plate.Clinics (Sao Paulo, Brazil) · 2026Article
- Growth Without GH: A Case Series and Literature Review.Journal of clinical medicine · 2025Review
- Article
- Gossypol Acetic Acid Alleviates the Ferroptosis of Chondrocytes in Osteoarthritis by Inhibiting GPX4 Methylation.Current medicinal chemistry · 2025Article
- Prolactin: A Key Immunoregulator in Viral Infections and Autoimmune Diseases.International journal of endocrinology · 2025Review
- Prolactin Role in COVID-19 and Its Association with the Underlying Inflammatory Response.International journal of molecular sciences · 2024Article
- Exploring the association of serum prolactin with serum glucose levels and clinical findings in a cohort of patients with early rheumatoid arthritis.Advances in rheumatology (London, England) · 2024Observational
- Deciphering the Involvement of Chronic Inflammation in Osteoarthritis: Evaluation of Complement 3 and Cathepsin D in Osteoarthritic Patients-A Retrospective Case Study.Journal of pharmacy & bioallied sciences · 2024Article
- Effect of Hyperprolactinemia on Bone Metabolism: Focusing on Osteopenia/Osteoporosis.International journal of molecular sciences · 2024Review
- Engineering approaches to investigate the roles of lymphatics vessels in rheumatoid arthritis.Microcirculation (New York, N.Y. : 1994) · 2023Review
- Enhancer selection dictates gene expression responses in remote organs during tissue regeneration.Nature cell biology · 2022Article
- Vasoinhibin is Generated and Promotes Inflammation in Mild Antigen-induced Arthritis.Endocrinology · 2022Article
- Sex-dependent pain trajectories induced by prolactin require an inflammatory response for pain resolution.Brain, behavior, and immunity · 2022Article
- Exosomes derived from platelet-rich plasma administration in site mediate cartilage protection in subtalar osteoarthritis.Journal of nanobiotechnology · 2022Article
- Dual Roles of Prolactin and Vasoinhibin in Inflammatory Arthritis.Frontiers in endocrinology · 2022Review
- A link between migraine and prolactin: the way forward.Future science OA · 2021Review
- Chondrocytes from Osteoarthritis Patients Adopt Distinct Phenotypes in Response to Central TInternational journal of molecular sciences · 2021Article
- Perspectives on long pentraxin 3 and rheumatoid arthritis: several potential breakthrough points relying on study foundation of the past.International journal of medical sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrocytes are the only cells in cartilage, and their death by apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA). A putative therapeutic intervention for RA is the inhibition of apoptosis-mediated cartilage degradation. The hormone prolactin (PRL) frequently increases in the circulation of patients with RA, but the role of hyperprolactinemia in disease activity is unclear. Here, we demonstrate that PRL inhibits the apoptosis of cultured chondrocytes in response to a mixture of proinflammatory cytokines (TNF-α, IL-1β, and IFN-γ) by preventing the induction of p53 and decreasing the BAX/BCL-2 ratio through a NO-independent, JAK2/STAT3-dependent pathway. Local treatment with PRL or increasing PRL circulating levels also prevented chondrocyte apoptosis evoked by injecting cytokines into the knee joints of rats, whereas the proapoptotic effect of cytokines was enhanced in PRL receptor-null (Prlr(-/-)) mice. Moreover, eliciting hyperprolactinemia in rats before or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, proinflammatory cytokine expression, pannus formation, bone erosion, joint swelling, and pain. These results reveal the protective effect of PRL against inflammation-induced chondrocyte apoptosis and the therapeutic potential of hyperprolactinemia to reduce permanent joint damage and inflammation in RA.
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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.