ArticlePLoS genetics2016
TGFβ and BMP Dependent Cell Fate Changes Due to Loss of Filamin B Produces Disc Degeneration and Progressive Vertebral Fusions.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 52 citations in OpenAlex.
- FLNB and TTC26 regulate ciliary Hedgehog signaling to maintain intervertebral disc matrix homeostasis in adolescent idiopathic scoliosis.Genome biology · 2026Article
- GREM1 acts in leptin receptor-expressing skeletal cells to mediate peri-implant fibrosis.Nature communications · 2026Article
- Metabolic reprogramming in intervertebral disc degeneration: mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Effects ofAnimals : an open access journal from MDPI · 2025Article
- An overview of mechanical microenvironment and mechanotransduction in intervertebral disc degeneration.Experimental & molecular medicine · 2025Review
- Trophoblast fusion in fetal growth restriction is inhibited by CTGF in a cell-cycle-dependent manner.Journal of molecular histology · 2024Article
- Unraveling the Link of Altered TGFβ Signaling with Scoliotic Vertebral Malformations in Osteogenesis Imperfecta: A Comprehensive Review.Journal of clinical medicine · 2024Review
- Progress in regulating inflammatory biomaterials for intervertebral disc regeneration.Bioactive materials · 2024Review
- Effect of Tuina along "bladder meridian" alleviating intervertebral disc degeneration by regulating the transforming growth factor-β1/Smad signaling pathway in a rabbit model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Musculoskeletal defects associated with myosin heavy chain-embryonic loss of function are mediated by the YAP signaling pathway.EMBO molecular medicine · 2023Article
- Loss of function mutation in Ank causes aberrant mineralization and acquisition of osteoblast-like-phenotype by the cells of the intervertebral disc.Cell death & disease · 2023Article
- Preclinical in vivo animal models of intervertebral disc degeneration. Part 1: A systematic review.JOR spine · 2023Review
- Review
- Roles of focal adhesion proteins in skeleton and diseases.Acta pharmaceutica Sinica. B · 2023Review
- Cytokine Imbalance as a Biomarker of Intervertebral Disk Degeneration.International journal of molecular sciences · 2023Review
- Identification of a novel, MSC-induced macrophage subtype via single-cell sequencing: implications for intervertebral disc degeneration therapy.Frontiers in cell and developmental biology · 2023Article
- Regulated cell death: Implications for intervertebral disc degeneration and therapy.Journal of orthopaedic translation · 2022Review
- Intervertebral disc degeneration is rescued by TGFβ/BMP signaling modulation in an ex vivo filamin B mouse model.Bone research · 2022Article
- gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes.Communications biology · 2022Article
- Identification of SMIM1 and SEZ6L2 as Potential Biomarkers for Genes Associated with Intervertebral Disc Degeneration in Pyroptosis.Disease markers · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Spondylocarpotarsal synostosis (SCT) is an autosomal recessive disorder characterized by progressive vertebral fusions and caused by loss of function mutations in Filamin B (FLNB). FLNB acts as a signaling scaffold by linking the actin cytoskleteon to signal transduction systems, yet the disease mechanisms for SCT remain unclear. Employing a Flnb knockout mouse, we found morphologic and molecular evidence that the intervertebral discs (IVDs) of Flnb-/-mice undergo rapid and progressive degeneration during postnatal development as a result of abnormal cell fate changes in the IVD, particularly the annulus fibrosus (AF). In Flnb-/-mice, the AF cells lose their typical fibroblast-like characteristics and acquire the molecular and phenotypic signature of hypertrophic chondrocytes. This change is characterized by hallmarks of endochondral-like ossification including alterations in collagen matrix, expression of Collagen X, increased apoptosis, and inappropriate ossification of the disc tissue. We show that conversion of the AF cells into chondrocytes is coincident with upregulated TGFβ signaling via Smad2/3 and BMP induced p38 signaling as well as sustained activation of canonical and noncanonical target genes p21 and Ctgf. These findings indicate that FLNB is involved in attenuation of TGFβ/BMP signaling and influences AF cell fate. Furthermore, we demonstrate that the IVD disruptions in Flnb-/-mice resemble aging degenerative discs and reveal new insights into the molecular causes of vertebral fusions and disc degeneration.
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