ArticleMolecular and cellular biochemistry2011
Prolactin alters the mRNA expression of osteoblast-derived osteoclastogenic factors in osteoblast-like UMR106 cells.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- From depression to bone health: examining the skeletal effects of classical and rapid-acting antidepressants.The international journal of neuropsychopharmacology · 2026Review
- Osteometabolic complications in patients with secreting pituitary adenomas: Is there an impact of gender?Pituitary · 2026Review
- The influence of hormonal changes during pregnancy on bone metabolism - a mini review.Frontiers in endocrinology · 2026Review
- The Interplay of Prolactin with Inflammatory Nutritional Markers and NT-proBNP in Chronic Kidney Disease.International journal of molecular sciences · 2025Observational
- Modern approach to bone comorbidity in prolactinoma.Pituitary · 2024Review
- Consideration of hormonal changes for orthodontic treatment during pregnancy and lactation - a review.Reproductive biology and endocrinology : RB&E · 2024Review
- Diagnosis and therapeutic approach to bone health in patients with hypopituitarism.Reviews in endocrine & metabolic disorders · 2024Review
- Effect of Hyperprolactinemia on Bone Metabolism: Focusing on Osteopenia/Osteoporosis.International journal of molecular sciences · 2024Review
- Editorial: Crosstalk between bone and other cells.Frontiers in physiology · 2023Article
- Article
- The Relationship Between Bone and Reproductive Hormones Beyond Estrogens and Androgens.Endocrine reviews · 2021Review
- Excessive salt consumption causes systemic calcium mishandling and worsens microarchitecture and strength of long bones in rats.Scientific reports · 2021Article
- Potential mechanisms linking psychological stress to bone health.International journal of medical sciences · 2021Review
- Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment.Frontiers in cell and developmental biology · 2021Review
- Hyperprolactinemia and bone.Pituitary · 2020Review
- Bone loss caused by dopaminergic degeneration and levodopa treatment in Parkinson's disease model mice.Scientific reports · 2019Article
- Impairment of bone microstructure and upregulation of osteoclastogenic markers in spontaneously hypertensive rats.Scientific reports · 2019Article
- The osteoprogenitor-specific loss of ephrinB1 results in an osteoporotic phenotype affecting the balance between bone formation and resorption.Scientific reports · 2018Article
- What Is Breast in the Bone?International journal of molecular sciences · 2016Review
- Bayesian modeling suggests that IL-12 (p40), IL-13 and MCP-1 drive murine cytokine networks in vivo.BMC systems biology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolactin (PRL) is known to participate in the lactation-induced maternal bone loss, presumably by inducing the release of receptor activator of nuclear factor-κB ligand (RANKL), a potent osteoclastogenic factor from osteoblasts. Since maternal bone resorption was too massive to be solely explained by RANKL and osteoclasts did not express PRL receptors (PRLR), the involvement of some other osteoblast-derived osteoclastogenic modulators was anticipated. Herein, the authors used quantitative real-time PCR to investigate the mRNA expressions of various osteoclastogenic factors in osteoblast-like UMR106 cells directly exposed to PRL for 48 h. These cells were found to express PRLR and respond to 300 ng/ml PRL by increasing RANKL mRNA expression. This PRL concentration (comparable to plasma PRL levels in lactation) also induced the upregulation of monocyte chemoattractant protein (MCP)-1, cyclooxygenase (Cox)-2, and ephrin-B1, whereas a higher concentration (500 ng/ml) was required to upregulate tumor necrosis factor (TNF)-α and interleukin (IL)-1. However, 100-500 ng/ml PRL affected neither the cell proliferation, the cell viability nor the mRNA expressions of macrophage colony-stimulating factor, IL-6, ephrin type-B receptor 4 and ephrin-B2. In conclusion, besides RANKL overexpression, PRL upregulated the expressions of other osteoclastogenic modulators, i.e., MCP-1, Cox-2, TNF-α, IL-1, and ephrin-B1, thus, further explaining how PRL induced bone loss in lactating mothers.
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