Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Fractures: Bone Repair01:27

Fractures: Bone Repair

3.2K
Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
Minor fractures with no bone displacement are treated by immobilizing the fractured bone using a cast or splint. However, in the case of fractures with displaced bones, the broken bones are repositioned before immobilization to ensure successful healing without deformation and loss of function. The realignment of fractured bone ends is performed through a process called reduction. If the...
3.2K
Bone Remodeling01:40

Bone Remodeling

38.3K
Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
38.3K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

2.9K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
2.9K
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

784
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
784
Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

3.3K
Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
3.3K
Phases of Wound Repair01:28

Phases of Wound Repair

6.0K
Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...
6.0K
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Osteochondroprogenitor Cells And Neutrophils Expressing P21 And Senescence Markers Modulate Fracture Repair

Osteochondroprogenitor cells and neutrophils expressing p21 and senescence markers modulate fracture repair

Dominik Saul, Madison L Doolittle, Jennifer L Rowsey

    Biorxiv : the Preprint Server for Biology
    |February 19, 2024

    Related Experiment Videos

    Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice
    06:10

    Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice

    Published on: September 16, 2020

    2.3K
    Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
    10:30

    Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair

    Published on: May 23, 2014

    10.5K
    Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
    05:10

    Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model

    Published on: February 7, 2025

    351

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Senescent-like cells expressing p21 rapidly appear after skeletal injury, aiding repair. Clearing these cells accelerated fracture healing, highlighting their role in tissue regeneration.

    Area of Science:

    • Cellular senescence
    • Tissue repair and regeneration
    • Skeletal biology

    Background:

    • Senescent cells, marked by p21 and p16, transiently appear after injury, but their specific roles and differences from age-related senescence are unclear.
    • Understanding these injury-induced senescent cells is crucial for developing targeted therapies for tissue repair.

    Approach:

    • Skeletal injury was modeled to study the rapid appearance of p21+ cells, primarily osteochondroprogenitors (OCHs) and neutrophils.
    • Genetic clearance of p21+ cells was used to assess their impact on fracture healing and senescence markers.
    • p21+ and p16+ cell clearance effects were compared in both injury and aging models.

    Key Points:

    • p21+ cells, including OCHs and neutrophils, rapidly emerged post-fracture.
    • Targeted clearance of p21+ cells accelerated fracture healing and reduced senescence signatures.

    Related Experiment Videos

    Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice
    06:10

    Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice

    Published on: September 16, 2020

    2.3K
    Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
    10:30

    Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair

    Published on: May 23, 2014

    10.5K
    Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
    05:10

    Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model

    Published on: February 7, 2025

    351
  • p21+ neutrophils signaled for stromal senescence, while p21+ OCHs secreted factors impairing bone formation.
  • p16+ cell clearance did not impact fracture healing, distinguishing roles from aging.

    • Conclusions:

    • Interacting senescent-like neutrophils and mesenchymal progenitor cells are key regulators of bone repair.
    • Context-specific roles of p21+ versus p16+ senescent cells offer therapeutic potential for tissue regeneration.
    • Injury-induced p21+ OCHs exhibit inflammatory, stem cell-like properties relevant to tissue repair.