A5016251061- Bone Metabolism and Diseases
- Bone health and treatments
- Osteoarthritis Treatment and Mechanisms
- Histone Deacetylase Inhibitors Research
- Epigenetics and DNA Methylation
- TGF-β signaling in diseases
- Cancer-related gene regulation
- NF-κB Signaling Pathways
- Cancer-related molecular mechanisms research
- Connective tissue disorders research
- Peptidase Inhibition and Analysis
- Bone health and osteoporosis research
- Ubiquitin and proteasome pathways
- Genetics and Neurodevelopmental Disorders
- GDF15 and Related Biomarkers
- Spine and Intervertebral Disc Pathology
- Mesenchymal stem cell research
- RNA modifications and cancer
- Fibroblast Growth Factor Research
- Bone and Joint Diseases
- MicroRNA in disease regulation
- Knee injuries and reconstruction techniques
- Cytokine Signaling Pathways and Interactions
- RNA Research and Splicing
- Biochemical and Molecular Research
University of Minnesota
2004-2025
University of Minnesota System
2025
University of Minnesota Medical Center
2024
Science Museum of Minnesota
2024
Mayo Clinic in Florida
2022
Mayo Clinic in Arizona
2008-2021
Albany College of Pharmacy and Health Sciences
2021
Mayo Clinic
2010-2019
WinnMed
2008-2016
Augusta University
2015
Osteoarthritis (OA) is the leading form of arthritis in elderly, causing pain, disability, and immobility. OA has been associated with accumulation senescent cells or near joints. However, evidence for a causal link between cellular senescence lacking. Here, we present novel cell transplantation model involving injection small numbers nonsenescent from ear cartilage luciferase-expressing mice into knee joint area wild-type mice. By using bioluminescence 18FDG PET imaging, could track...
A cancer-promoting histone protein Mutations in the chromatin H3 are found a number of pediatric cancers. The lysine-36–to–methionine (K36M) “oncohistone” mutation is seen almost all chondroblastomas. Fang et al. show that K36M mutant histones inhibit normal methylation this same residue wild-type histones. They do so by interfering with enzymes normally methylate residue. altered patterns alter expression known cancer-related genes and impart characteristics to chondrocyte cells. Science ,...
Abstract We have examined highly purified osteoclasts that were generated in vitro from murine co‐culture of marrow precursors with stromal support cells and found evidence activation the MEK/ERK AKT/NFκB survival pathways. Many mature marrow‐derived survived for at least 48 h culture whether or not they are maintained cells. Moreover, supplementing RANKL and/or M‐CSF had no impact on their pattern. In addition, spleen‐derived treatment exhibited a similar Blocking MEK, AKT, NFκB activity...
Abstract Although genetic evidence demonstrated a requirement for Wnt5a during cartilage development, little is known about the mechanisms underlying Wnt5a-regulated chondrocyte growth and differentiation. We therefore investigated signaling pathways by which influences chondrogenesis differentiation to hypertrophy. treatment of chondroprogenitor cells increased hypertrophy was associated with an increase in nuclear factor activated T (NFAT) decrease factor-κB (NF-κB) activation. In...
Histone deacetylase 3 prevents chondrocytes from producing inflammatory mediators that prevent bone development.
Abstract Although genetic evidence has demonstrated a role for Wnt5b during cartilage and limb development, little is known about the mechanisms underlying Wnt5b‐regulated chondrocyte differentiation. We observed that inhibited hypertrophy expression of type X collagen. In addition, regulated overall size chondrogenic cultures, suggesting regulates other processes involved in development. therefore investigated signaling pathways by which influences activated calcium‐dependent JNK, component...
Histone deacetylases (Hdacs) regulate endochondral ossification by suppressing gene transcription and modulating cellular responses to growth factors cytokines. We previously showed that Hdac7 suppresses Runx2 activity osteoblast differentiation. In this study, we examined the role of in postnatal chondrocytes. was highly expressed proliferating cells within plate. Postnatal tissue-specific ablation with a tamoxifen-inducible collagen type 2a1-driven Cre recombinase increased proliferation...
Abstract While M‐CSF‐mediated MEK/ERK activation promotes osteoclast survival, the signaling pathway by which M‐CSF activates is unresolved. Functions for PI3K, Ras, and Raf have been implicated in support of although interaction between these components has not examined. Therefore, interplay Ras M‐CSF‐promoted survival was investigated. to coordinate PI3K Raf/MEK/ERK, since inhibition decreased did block activation. As further Ras‐mediated signaling, constitutively active (ca) promoted...
Background/Objectives: In contrast to endochondral bone healing, the process of intramembranous regeneration is poorly understood. This limits our ability repair and regenerate craniofacial skeleton either correct deformity or optimally heal tissues following injury. While there are several preclinical models within skeleton, some not load bearing others technically challenging. The goal this pilot study therefore describe a simple method for induction cortical defects mandible that does...
Determining the underlying mechanisms of macrophage colony-stimulating factor (M-CSF)-mediated osteoclast survival may be important in identifying novel approaches for treating excessive bone loss. This study investigates M-CSF-mediated MEK/ERK activation and identifies a downstream effector this pathway. M-CSF activates induces MEK-dependent expression immediate early gene Egr2. Inhibition either MEK1/2 or inhibition Egr2 increases apoptosis. In contrast, wild-type an point mutant unable to...