Tibial dyschondroplasia is a disease of rapid growth rate that occurs in many avian species. It is characterized by an avascular lesion in which the life span of the growth plate chondrocyte is essentially doubled. A characteristic pattern of gene expression and gene product localization has emerged that mimics the pattern observed with endoplasmic reticulum (ER) stress in growth plate chondrocytes. This activates a cell-survival mechanism called autophagy. The initial phases of this mechanism appear to originate in the avascular transition zone of the growth plate. Because specific genes and gene products are associated with autophagy and ER stress, it should now be possible to identify the mechanisms involved in the development of this cartilage abnormality. The potential biochemical pathways responsible for initiating ER stress are discussed.
Bibliographical noteFunding Information:
The authors were supported by BARD Research Grant Award IS-3403-03R. We also wish to acknowledge the assistance of Patti Burns and Linda Houtz for manuscript preparation and Donna Sosnoski for preparation of the figure.
- Endoplasmic reticulum stress
- Gene expression
- Tibial dyschondroplasia