ArticleJournal of bone and mineral metabolism2017
4-Phenyl butyric acid prevents glucocorticoid-induced osteoblast apoptosis by attenuating endoplasmic reticulum stress.
Article in Journal of bone and mineral metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Endoplasmic reticulum stress in steroid-induced osteonecrosis: translational bottlenecks and targeted therapeutic strategies.Frontiers in pharmacology · 2026Review
- Stage-dependent endoplasmic reticulum homeostasis in osteogenic differentiation.Frontiers in cell and developmental biology · 2026Review
- Sodium Phenylbutyrate Ameliorates Ovariectomy-Induced Bone Loss in Rats.Medicina (Kaunas, Lithuania) · 2025Article
- Pharmacological inhibition of endoplasmic reticulum stress mitigates osteoporosis in a mouse model of hindlimb suspension.Scientific reports · 2024Article
- Bone and the Unfolded Protein Response: In Sickness and in Health.Calcified tissue international · 2023Review
- A Review on the Molecular Mechanisms of Action of Natural Products in Preventing Bone Diseases.International journal of molecular sciences · 2022Review
- Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism.Frontiers in veterinary science · 2022Review
- Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress.Molecular medicine reports · 2021Article
- Preliminary results of PBA-loaded nanoparticles development and the effect on oxidative stress and neuroinflammation in rats submitted to a chemically induced chronic model of MSUD.Metabolic brain disease · 2021Article
- Inhibition of PERK Signaling Prevents Against Glucocorticoid-induced Endotheliocyte Apoptosis and Osteonecrosis of the Femoral Head.International journal of biological sciences · 2020Article
- Haem oxygenase-1 induction prevents glucocorticoid-induced osteoblast apoptosis through activation of extracellular signal-regulated kinase1/2 signalling pathway.Journal of orthopaedic translation · 2019Article
- Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells.International journal of molecular medicine · 2018Article
- Gastrodin alleviates glucocorticoid induced osteoporosis in rats via activating the Nrf2 signaling pathways.Oncotarget · 2018Article
- Zebrafish models for glucocorticoid-induced osteoporosis.Tzu chi medical journalReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of osteoblasts triggered by high-dose glucocorticoids (GCs) has been identified as a major cause of osteoporosis. However, the molecular mechanisms underlying GC-induced osteoporosis remain elusive. This study was conducted to make clear the mechanism of GC-induced osteoblast apoptosis and to examine whether reduction of ER stress by 4-PBA inhibited osteoblast apoptosis. After treatment with dexamethasone (Dex) or hydrocortisone, cell viability was assessed using an MTT assay. Flow cytometry was performed to assess the apoptosis of MC3T3-E1 cells. The expression levels of ER stress-related proteins (CHOP, GRP78, eIF2α, and phospho-eIF2α) and apoptosis-related proteins (cleaved Caspase-3, Bcl-2, and Bax) in MC3T3-E1 cells were measured by Western blot analysis. We found that both Dex and hydrocortisone reduced cell proliferation and promoted apoptosis in MC3T3-E1 cells. In addition, the protein expression levels of cleaved Caspase-3 and Bax increased and the protein expression level of Bcl-2 decreased in MC3T3-E1 cells exposed to Dex. In addition, the Dex exposure also resulted in a release of cytochrome c (Cyt C) from mitochondria. The cellular ATP content was decreased following prolonged treatment with Dex. 4-PBA attenuated ER stress and mitochondrial dysfunction induced by Dex in MC3T3-E1 cells. Dex-mediated apoptosis of MC3T3-E1 cells is aggravated by ER stress. Moreover, Dex-induced apoptosis in MC3T3-E1 cells was inhibited by 4-PBA, suggesting that ER stress involved in Dex-induced apoptosis. In conclusion, inhibition of ER stress by 4-PBA could reduce GC-induced apoptosis in MC3T3-E1 cells.
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