ArticleCell cycle (Georgetown, Tex.)2015
Prostaglandin E2 promotes proliferation of skeletal muscle myoblasts via EP4 receptor activation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 117 citations in OpenAlex.
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- Prostaglandin E2 receptor EP2 is indispensable for maintenance of skeletal muscle stem cells.Stem cells (Dayton, Ohio) · 2026Article
- The Inflammation-Energy Metabolism Axis: A Central Driver of Sarcopenia-Osteoporosis: A Narrative Review.Calcified tissue international · 2026Review
- Exploring osteosarcopenia from the gut microbiota perspective: mechanistic insights and therapeutic potentials based on the gut-muscle-bone Axis.Frontiers in microbiology · 2026Review
- Celecoxib disrupts temporal coordination of TGF-β/α-SMA signaling in skeletal muscle repair: a time-dependent study of fibrosis and inflammation.European journal of medical research · 2025Article
- Parathyroid Hormone as a Modulator of Skeletal Muscle: Insights into Bone-Muscle and Nerve-Muscle Interactions.International journal of molecular sciences · 2025Review
- Bone mechanical loading reduces heart rate and increases heart rate variability in mice.Bone reports · 2025Article
- Bone and muscle crosstalk in ageing and disease.Nature reviews. Endocrinology · 2025Review
- Aging: A struggle for beneficial to overcome negative factors made by muscle and bone.Mechanisms of ageing and development · 2025Review
- Spatiotemporal characterization of cyclooxygenase pathway enzymes during vertebrate embryonic development.Developmental biology · 2025Article
- Effect of Common Medications on Longitudinal Pectoralis Muscle Area in Smokers.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2025Article
- Osteocytes function as biomechanical signaling hubs bridging mechanical stress sensing and systemic adaptation.Frontiers in physiology · 2025Review
- Molecular communication from bone to skeletal muscle: an overview.Frontiers in cell and developmental biology · 2025Review
- The role of bone-derived factors in bone and muscle communication.Frontiers in endocrinology · 2025Review
- Association between bone mineral density T-score and respiratory sarcopenia in older adults.Frontiers in medicine · 2025Article
- Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024Review
- Both enantiomers of β-aminoisobutyric acid BAIBA regulate Fgf23 via MRGPRD receptor by activating distinct signaling pathways in osteocytes.Cell reports · 2024Article
- Bone-organ axes: bidirectional crosstalk.Military Medical Research · 2024Review
- Article
- Deletion of FNDC5/Irisin modifies murine osteocyte function in a sex-specific manner.bioRxiv : the preprint server for biology · 2024Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We recently demonstrated that conditioned media (CM) from osteocytes enhances myogenic differentiation of myoblasts, suggesting that signaling from bone may be important for skeletal muscle myogenesis. The effect of CM was closely mimicked by prostaglandin E2 (PGE2), a bioactive lipid mediator in various physiological or pathological conditions. PGE2 is secreted at high levels by osteocytes and such secretion is further enhanced under loading conditions. Although four types of receptors, EP1 to EP4, mediate PGE2 signaling, it is unknown whether these receptors play a role in myogenesis. Therefore, in this study, the expression of EPs in mouse primary myoblasts was characterized, followed by examination of their roles in myoblast proliferation by treating myoblasts with PGE2 or specific agonists. All four PGE2 receptor mRNAs were detectable by quantitative real-time PCR (qPCR), but only PGE2 and EP4 agonist CAY 10598 significantly enhance myoblast proliferation. EP1/EP3 agonist 17-phenyl trinor PGE2 (17-PT PGE2) and EP2 agonist butaprost did not have any significant effects. Moreover, treatment with EP4 antagonist L161,982 dose-dependently inhibited myoblast proliferation. These results were confirmed by cell cycle analysis and the gene expression of cell cycle regulators. Concomitant with the inhibition of myoblast proliferation, treatment with L161,982 significantly increased intracellular reactive oxygen species (ROS) levels. Cotreatment with antioxidant N-acetyl cysteine (NAC) or sodium ascorbate (SA) successfully reversed the inhibition of myoblast proliferation and ROS overproduction caused by L161,982. Therefore, PGE2 signaling via the EP4 receptor regulates myogenesis by promoting myoblast proliferation and blocking this receptor results in increased ROS production in myoblasts.
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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.