Related Experiment Video
Updated: Jan 13, 2026
09:18
Author Spotlight: Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue
Published on: February 24, 2023
10.1K
Spatial Transcriptomics of TMJ Reveals a Remodeling Fibroblast-Immune Microenvironment Driving Arthritis Pain.
Ziying Lin1, Supawadee Jariyasakulroj1,2, Yang Shu1
1Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, California, USA.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 7, 2026
Summary
Spatial transcriptomics reveals how temporomandibular joint (TMJ) arthritis remodels cell neighborhoods. Targeting the Igf1-Il33 axis in fibroblast-immune cells may mitigate TMJ arthritis pain.
Area of Science:
- Molecular Biology
- Immunology
- Anatomy
Background:
- Temporomandibular joint (TMJ) arthritis involves complex cellular and tissue remodeling.
- The precise anatomical organization and microenvironment of TMJ cells in arthritis pathogenesis are not fully understood.
Purpose of the Study:
- To map cell types and their spatial organization in the adult mouse TMJ using spatial transcriptomics.
- To investigate arthritis-induced changes in cell populations and the TMJ microenvironment.
- To elucidate the role of the Igf1-Il33 axis in TMJ arthritis and pain.
Main Methods:
- Sequential Fluorescence In Situ Hybridization (seqFISH) spatial transcriptomics on adult mouse TMJ.
- Analysis of cell type distribution, neighborhoods, and arthritis-induced changes.
- Functional studies involving gene knockout (Igf1, Il33) in specific cell types.
- Validation in human patient synovial tissues.
Main Results:
- Identification of novel cell types and comprehensive mapping of TMJ cell anatomy.
- Discovery of arthritis-associated changes in cell numbers and status.
- Revelation of fibroblast-immune cell microenvironment remodeling via the Igf1-Il33 axis.
- Demonstration that Igf1 knockout in macrophages activates them and upregulates Il33 in fibroblasts, promoting inflammation.
- Confirmation that Il33 deletion in fibroblasts reduces inflammation and pain.
Conclusions:
- Spatial transcriptomics provides a detailed map of TMJ cell types and their organization.
- The Igf1-Il33 signaling axis plays a critical role in the synovial fibroblast-immune cell crosstalk driving TMJ arthritis.
- Targeting this axis offers potential therapeutic strategies for mitigating TMJ arthritis pain.
More Related Videos
12:23Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model
Published on: April 24, 2020
20.8K
06:37Temporomandibular Joint Pain Measurement by Bite Force and Von Frey Filament Assays in Mice
Published on: September 13, 2024
1.8K
Related Concept Videos
01:20The JAK-STAT Signaling Pathway
11.9K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
11.9K
01:24T Cell Types and Functions
2.1K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.1K
01:24Inflammatory Response II: Inflammatory Exudate and Tissue Repair
7.3K
The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
7.3K
01:30Inflammatory Response I: Vascular and Cellular
15.9K
The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
15.9K
01:28Inflammatory Response
15.9K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
15.9K