We previously reported that deletion of the Fgf2 gene (Fgf2-/-) resulted in decreased bone mass in adult mice. This study examines the effect of haplo-insuffiency (Fgf2+/-) on bone loss in vertebrae from these mutant mice. Fgf2+/+ mice attained peak bone mass at 8-9 months of age. In contrast BMD was significantly reduced in vertebrae from adult (8-9) Fgf2+/- mice. Exogenous FGF-2 rescued reduced bone nodule formation in Fgf2+/- and Fgf2-/- cultures. Runx2 mRNA was reduced in cultures from Fgf2+/- and Fgf2-/- mice. FGF receptor2 mRNA and protein were markedly reduced in Fgf2+/- and Fgf2-/- mice. Decreased bone formation in Fgf2 mutant mice may correlate with impaired FGFR signaling, decreased Runx2 gene expression.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbrc.2005.10.215 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
NLRP3: a key regulator of skin wound healing and macrophage-fibroblast interactions in mice.
Cell Commun Signal
January 2025
Laboratory of Veterinary Clinical Pharmacology, College of Veterinary Medicine, Inner Mongolia Agricultural University, No. 306, Zhaowuda Road, Hohhot, 010018, China.
Wound healing is a highly coordinated process driven by intricate molecular signaling and dynamic interactions between diverse cell types. Nod-like receptor pyrin domain-containing protein 3 (NLRP3) has been implicated in the regulation of inflammation and tissue repair; however, its specific role in skin wound healing remains unclear. This study highlights the pivotal role of NLRP3 in effective skin wound healing, as demonstrated by delayed wound closure and altered cellular and molecular responses in NLRP3-deficient (NLRP3) mice.
View Article and Find Full Text PDFNEAT1 regulates BMSCs aging through disruption of FGF2 nuclear transport.
Stem Cell Res Ther
January 2025
College & Hospital of Stomatology, Key Laboratory of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei, 230032, China.
Background: The aging of bone marrow mesenchymal stem cells (BMSCs) impairs bone tissue regeneration, contributing to skeletal disorders. LncRNA NEAT1 is considered as a proliferative inhibitory role during cellular senescence, but the relevant mechanisms remain insufficient. This study aims to elucidate how NEAT1 regulates mitotic proteins during BMSCs aging.
View Article and Find Full Text PDF[Development of prognostic clinical and genetic models of the risk of low bone mineral density using neural network training].
Probl Endokrinol (Mosk)
January 2024
Background: Osteoporosis is a common age-related disease with disabling consequences, the early diagnosis of which is difficult due to its long and hidden course, which often leads to diagnosis only after a fracture. In this regard, great expectations are placed on advanced developments in machine learning technologies aimed at predicting osteoporosis at an early stage of development, including the use of large data sets containing information on genetic and clinical predictors of the disease. Nevertheless, the inclusion of DNA markers in prediction models is fraught with a number of difficulties due to the complex polygenic and heterogeneous nature of the disease.
View Article and Find Full Text PDFMelanoma-derived extracellular vesicles transfer proangiogenic factors.
Oncol Res
January 2025
Department of Glycoconjugate Biochemistry, Faculty of Biology, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, 30-387, Poland.
Angiogenesis, the expansion of pre-existing vascular networks, is crucial for normal organ growth and tissue repair, but is also involved in various pathologies, including inflammation, ischemia, diabetes, and cancer. In solid tumors, angiogenesis supports growth, nutrient delivery, waste removal, and metastasis. Tumors can induce angiogenesis through proangiogenic factors including VEGF, FGF-2, PDGF, angiopoietins, HGF, TNF, IL-6, SCF, tryptase, and chymase.
View Article and Find Full Text PDFHypoxia-regulated miR-103-3p/FGF2 axis in adipose-derived stem cells promotes angiogenesis by vascular endothelial cells during ischemic tissue repair.
Int J Cardiol
January 2025
Department of Plastic Surgery, The First Affiliated Hospital of Jinan University, Key Laboratory of Regenerative Medicine, Ministry of Education, Guangzhou, Guangdong Province 510630, China. Electronic address:
Background: Identifying factors mediating adipose-derived stem cells (ADSCs)-induced endothelial cell angiogenesis in hypoxic skin flap tissue is critical for reconstruction. While the paracrine action of VEGF by adipose-derived stem cells (ADSCs) is established in promoting endothelial cell angiogenesis, the role of FGF2 and its regulatory mechanisms in ADSCs paracrine secretion remains unclear.
Methods: We induced hypoxia and examined the expression level of FGF2 in ADSCs using ELISA, qRT-PCR, and western blotting.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!