Age, but not short-term intensive swimming, affects chondrocyte turnover in zebrafish vertebral cartilage

Abstract

Both age and intensive exercise are generally considered critical risk factors for osteoarthritis. In this work, we intend to establish zebrafish models to assess the role of these two factors on cartilage homeostasis. We designed a swimming device for zebrafish intensive exercise. The body measurements, bone mineral density (BMD) and the histology of spinal cartilages of 4- and 12-month-old zebrafish, as well the 12-month-old zebrafish before and after a 2-week exercise were compared. Our results indicate that both age and exercise affect the body length and body weight, and the micro-computed tomography reveals that both age and exercise affect the spinal BMD. However, quantitative analysis of immunohistochemistry and histochemistry indicate that short-term intensive exercise does not affect the extracellular matrix (ECM) of spinal cartilage. On the other hand, the cartilage ECM significantly grew from 4 to 12 months of age with an increase in total chondrocytes. dUTP nick end labeling staining shows that the percentages of apoptotic cells significantly increase as the zebrafish grows, whereas the BrdU labeling shows that proliferative cells dramatically decrease from 4 to 12 months of age. A 30-day chase of BrdU labeling shows some retention of labeling in cells in 4-month-old spinal cartilage but not in cartilage from 12-month-old zebrafish. Taken together, our results suggest that zebrafish chondrocytes are actively turned over, and indicate that aging is a critical factor that alters cartilage homeostasis. Zebrafish vertebral cartilage may serve as a good model to study the maturation and homeostasis of articular cartilage.

SEM Analyses of Fossilized Chondrocytes in the Extinct Birds Yanornis and Confuciusornis: Insights on Taphonomy and Modes of Preservation in the Jehol Biota

“…The only logical explanation is that the intralacunar material represents original chondrocytes, but because they do not resemble healthy chondrocytes, they may have been partially autolyzed prior to permineralization and secondarily obtained this curious filamentous morphology (Figure 4K). Additionally, it is also possible that some of the filamentous material may be extracellular coatings that the cells secreted in vivo, as is sometimes seen within chondrocyte lacunae in extant cartilage under the SEM (e.g., see Figure 3D in Jian et al, 2018;also Clarke, 1974). However, the hypothesis of partially autolyzed cells makes the most sense based on the presence of extensively decayed soft tissues and the clear absence of well-preserved (originally) unmineralized cartilage attached to the calcified cartilage, altogether suggesting that IVPP V11521 underwent extensive decay before or during burial, and that its permineralization was especially delayed.…”

Mutantdlx3bdisturbs normal tooth mineralization and bone formation in zebrafish

“…S1). The spine curvatures were seen in dlx3b −/− fish at both the juvenile and adult stages, ahead of the age at which senescent bending of the spine might occur in aged zebrafish (around 52 months) (Gerhard et al, 2002;Jian et al, 2018). The bone density changes found in individuals with TDO were not detected in the pharyngeal bone or spine of our zebrafish model, possibly due to the differences in function of the mutated protein or the evolutionary differences existing between different vertebrate skeletal systems.…”

CHD7 regulates craniofacial cartilage development via controlling HTR2B expression

“…Col2a1 is required in the ECM of various cell types including osteoblasts, chondrocytes, external ligament connective tissue cells, as well as notochord basal cells and expressed in the corresponding tissues. 58 , 59 Additionally, col2a1a expression is observed throughout ossification of the notochord in zebrafish. 60 Reduction in this collagen matrix in the notochord can affect proper calcification and is known to cause spondyloepiphyseal dysplasia congenita, which affects skeletal and spine development.…”