Related Experiment Video

Updated: Jun 30, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
08:42

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Increased bone mass, altered trabecular architecture and modified growth plate organization in the growing skeleton

V E Macrae1, S Horvat, S C Pells

  • 1Bone Biology Group, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin Biocentre, Roslin, UK. vicky.macrae@roslin.ed.ac.uk

Journal of Cellular Physiology
|September 23, 2008
PubMed

Insights

Suppressor of cytokine signalling-2 (SOCS2) negatively regulates bone formation and growth. Pro-inflammatory cytokines inhibit bone growth independently of SOCS2, suggesting new therapeutic targets for bone disorders.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Molecular Regulation

Background:

  • Suppressor of cytokine signalling-2 (SOCS2) is a negative regulator of cytokine signal transduction.
  • Socs2 knockout mice exhibit enhanced skeletal growth, indicating a role in bone regulation.

Purpose of the Study:

  • To investigate the role of SOCS2 in endochondral ossification and bone formation.
  • To determine if pro-inflammatory cytokines, relevant to chronic inflammatory disorders, exert effects via SOCS2.

Main Methods:

  • Comparative analysis of skeletal growth and bone parameters in Socs2(-/-) and wild-type mice.
  • In vitro studies involving TNF-alpha exposure to growth plate chondrocytes and metatarsal explants.

Main Results:

  • Socs2(-/-) mice displayed significantly increased body length, tibial length and width, and growth plate dimensions.
  • Bone analysis revealed increased cross-sectional area, bone volume, trabecular number, and thickness in Socs2(-/-) mice.
  • TNF-alpha increased SOCS2 expression but inhibited metatarsal growth independently of genotype, indicating SOCS2-independent cytokine effects.

Conclusions:

  • Physiological levels of SOCS2 negatively regulate bone formation and endochondral growth.
  • Pro-inflammatory cytokines inhibit longitudinal bone growth through a SOCS2-independent mechanism.

More Related Videos

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification07:23

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Published on: December 3, 2016

Trabecular Bone Microarchitecture Evaluation in an Osteoporosis Mouse Model06:59

Trabecular Bone Microarchitecture Evaluation in an Osteoporosis Mouse Model

Published on: September 8, 2023

Related Concept Videos

Spongy Bone01:09

Spongy Bone

All bones comprise an outer layer of compact bone, and an interior made up of spongy bone tissue, also called cancellous or trabecular bone. In long bones, spongy bone tissue is mainly found in the interior of the epiphyses (broad ends of the bone).
Spongy bone is more porous, and less dense compared to compact bone. It is composed of concentric lamellae that are arranged irregularly to form the trabecular network. In some bones, the spaces between trabeculae contain red marrow, where...
Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

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...
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Changes in the Appendicular Skeleton with Age01:09

Changes in the Appendicular Skeleton with Age

The upper and lower limb initially develops as a small bulge called a limb bud, which appears on the lateral side of the early embryo. The upper limb bud appears near the end of the fourth week of development, with the lower limb bud appearing shortly after.
Initially, the limb buds consist of a core of mesenchyme covered by a layer of ectoderm. The ectoderm at the end of the limb bud thickens to form a narrow crest called the apical ectodermal ridge. This ridge stimulates the underlying...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...