ArticleThe Journal of biological chemistry2011
Nuclear factor-kappaB (NF-kappaB) p65 interacts with Stat5b in growth plate chondrocytes and mediates the effects of growth hormone on chondrogenesis and on the expression of insulin-like growth factor-1 and bone morphogenetic protein-2.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
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- Intra-Articular Delivery of Nanoemulsified Curcumin Ameliorates Joint Degeneration in a Chemically Induced Model of Osteoarthritis.International journal of molecular sciences · 2025Article
- The Ex Vivo Organ Culture of Bone and Cartilage.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Role of the NF-kB signalling pathway in heterotopic ossification: biological and therapeutic significance.Cell communication and signaling : CCS · 2024Review
- Thrombospondin-2 Couples Pressure-Promoted Chondrogenesis through NF-κB Signaling.Tissue engineering and regenerative medicine · 2023Article
- Peptide Regulation of Chondrogenic Stem Cell Differentiation.International journal of molecular sciences · 2023Review
- The protective activity of natural flavonoids against osteoarthritis by targeting NF-κB signaling pathway.Frontiers in endocrinology · 2023Review
- Growing Pains: The Need for Engineered Platforms to Study Growth Plate Biology.Advanced healthcare materials · 2022Review
- Bioengineering Approaches for Delivering Growth Factors: A Focus on Bone and Cartilage Regeneration.Bioengineering (Basel, Switzerland) · 2022Review
- The Active Compound Thymoquinone Alters Chondrogenic Differentiation of Human Mesenchymal Stem Cells via Modulation of Intracellular Signaling.Medeniyet medical journal · 2022Article
- Effects of GH/IGF axis on bone and cartilage.Molecular and cellular endocrinology · 2021Review
- Article
- Innovative Three-Dimensional Microscopic Analysis of Uremic Growth Plate Discloses Alterations in the Process of Chondrocyte Hypertrophy: Effects of Growth Hormone Treatment.International journal of molecular sciences · 2020Article
- Regulation of gene expression by growth hormone.Molecular and cellular endocrinology · 2020Review
- NF-κB Signaling Regulates Physiological and Pathological Chondrogenesis.International journal of molecular sciences · 2019Review
- A 42-Year-Old Woman with Untreated Growth Hormone Insensitivity, Diabetic Retinopathy, and Gene Sequencing Identifies a Variant of Laron Syndrome.The American journal of case reports · 2019Article
- Transcriptional control of chondrocyte specification and differentiation.Seminars in cell & developmental biology · 2017Review
- Autophagic dysfunction is improved by intermittent administration of osteocalcin in obese mice.International journal of obesity (2005) · 2016Article
- Hydroxylation of methylated DNA by TET1 in chondrocyte differentiation of C3H10T1/2 cells.Biochemistry and biophysics reports · 2016Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth with its stimulatory effects primarily mediated by insulin-like growth factor-1 (IGF-1) both systemically and locally in the growth plate. It has been shown that the transcription factor Stat5b mediates the GH promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signaling molecules are activated by GH in growth plate chondrocytes. We have previously demonstrated that nuclear factor-κB p65 is a transcription factor expressed in growth plate chondrocytes where it facilitates chondrogenesis. We have also shown that fibroblasts isolated from a patient with growth failure and a heterozygous mutation of inhibitor-κBα (IκB; component of the nuclear factor-κB (NF-κB) signaling pathway) exhibit GH insensitivity. In this study, we cultured rat metatarsal bones in the presence of GH and/or pyrrolidine dithiocarbamate (PDTC), a known NF-κB inhibitor. The GH-mediated stimulation of metatarsal longitudinal growth and growth plate chondrogenesis was neutralized by PDTC. In cultured chondrocytes isolated from rat metatarsal growth plates, GH induced NF-κB-DNA binding and chondrocyte proliferation and differentiation and prevented chondrocyte apoptosis. The inhibition of NF-κB p65 expression and activity (by NF-κB p65 siRNA and PDTC, respectively) in chondrocytes reversed the GH-mediated effects on chondrocyte proliferation, differentiation, and apoptosis. Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-κB-DNA binding, whereas the inhibition of NF-κB p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression.
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