Mandibular Condylar Chondrocytes Research Articles

Fos- and Jun-related transcription factors are involved in the signal transduction pathway of mechanical loading in condylar chondrocytes

The chondrocytes of the articular condylar cartilage proliferate, hypertrophy and ultimately undergo apoptosis (programmed cell death), being replaced by osteoblasts. Converging results consolidate activator protein-1 (AP-1) transcription factor as the pivotal downstream effector in the early response of stress-sensitive cells to mechanical loading, and the Fra-1, Fra-2, JunB and JunD members of the AP-1 transcription factor family, as mediators in bone remodelling and apoptotic phenomena. The aim of the present study was to examine the involvement of the Fra-1, Fra-2, JunB and JunD proteins in the biochemical response of functionally loaded mandibular condylar cartilage, and the subsequent initiation of cartilage maturation and apoptotic phenomena. Thirty, female, 14-day-old Wistar rats were assigned to two groups: one group was fed a soft diet and the other a hard diet. At day 21 after weaning, experimental animals from both groups were killed at 6, 12 and 48 hours and their condyles harvested. The condylar cartilage of both groups was immunostained using specific antibodies against Fra-1, Fra-2, JunB and JunD. Statistical analysis of the data revealed over-expression of Fra-1, Fra-2, JunB and JunD proteins in all stages of differentiation of chondrocytes derived from the mandibular condylar cartilage of animals fed on a hard diet. Moreover, the involvement of these proteins significantly increased with time in both groups. Since the aforementioned proteins play key roles in remodelling phenomena of bone and cartilage tissue, influencing pivotal cellular functions such as maturation, differentiation and apoptosis, the results of the present study suggest that mandibular condylar chondrocytes sense functional loading changes and respond by induction of proteins associated with biological phenomena that ultimately influence the growth of the condylar cartilage.

Effects of mechanical pressure on intracellular calcium release channel and cytoskeletal structure in rabbit mandibular condylar chondrocytes

Many signal molecules are involved in mechanotransduction process, among which intracellular calcium and cytoskeleton are two of the most important ones. This study investigated the changes of intracellular calcium and cytoskeleton under pressure and the effects of intracellular calcium variation on cytoskeleton responses to the pressure in rabbit mandibular condylar chondrocytes (MCCs). In vitro cultured MCCs from 2-week-old New Zealand rabbits were incubated for observation of intracellular calcium variation under laser scanning microscope. Coomassie BB staining was used to observe the characteristics of cytoskeleton. We found that intracellular calcium increased following the irritation by 1,25(OH) 2D 3, whereas it remained unchanged when inositol triphosphate receptor (IP 3R) channel was blocked by heparin. Pretreatment with pressure of 90 kPa for 60 min enhanced the sensitivity of IP 3R channel and caused higher intracellular calcium concentration. The cytoskeletons of MCCs were revealed correspondingly uniform and reticular in the control, most of which showed higher expression in tighter arrangement under continuous pressure of 90 kPa for 60 min but lower expression when the pressure time was prolonged to 360 min. When MCCs were pretreated with heparin, the cytoskeleton of them displayed sparsely and discontinuously under 90 kPa for 60 min. To sum up, both cytoskeleton and intracellular calcium participate in the transition process of mechanical signal to biological effects of MCC. However, the decrease of intracellular calcium resulted from IP 3R channel blocking obviously interferes the recomposition of cytoskeleton under mechanical pressure, which suggests that calcium message is indispensable to the cytoskeleton response of MCC under pressure.

Effects of Mechanical Pressure on the Ultrastructure and Integrin-cytoskeleton System of Mandibular Condylar Chondrocytes(Cellular & Tissue Engineering)

Effects of Mechanical Pressure on the Ultrastructure and Integrin-cytoskeleton System of Mandibular Condylar Chondrocytes(Cellular & Tissue Engineering)

Ultrastructural demonstration of soybean agglutinin binding sites in mandibular condylar chondrocytes from normal, hypophysectomized, and growth hormone-treated hypophysectomized rats.

Ultrastructural demonstration of soybean agglutinin binding sites in mandibular condylar chondrocytes from normal, hypophysectomized, and growth hormone-treated hypophysectomized rats.

Mechanical loading triggers specific biochemical responses in mandibular condylar chondrocytes

The effect of mechanical loading on the phosphorylation state of condylar cartilage proteins was investigated by high resolution electrophoretic analysis of 32P-labelled proteins from mechanically stimulated rat mandibular condylar chondrocytes. Specific dephosphorylation (and/or loss) of an acidic, 35–36 kDa protein(s) and of proteins overlapping with members of the ras superfamily of small GTP-binding proteins was observed. These responses may constitute part of a mechanically induced transduction system which establishes the differentiated phenotype.

In vivo effects of tunicamycin on chondrocytes of rat mandibular condyles as revealed by lectin cytochemistry.

The in vivo effects of tunicamycin on the glycosylation of proteoglycans and link protein in rat mandibular condylar chondrocytes were studied by ultrastructural lectin histochemistry. The binding of wheat-germ agglutinin was shown by using anti-lectin antibody followed by protein A-gold complex. In normal rats, wheat-germ agglutinin labeling was restricted to trans cisternae and vacuoles of the Golgi complex, whereas it was observed in neither the cis region of the Golgi complex nor in the rough endoplasmic reticulum. By 3 h after the drug administration, wheat-germ agglutinin binding sites on the disorganized Golgi vacuoles were dramatically reduced in number. At 6 h after the drug administration, the lectin binding sites on the Golgi vacuoles were restored. These results demonstrate that the in vivo use of tunicamycin in combination with histochemical analysis using lectin probes is of significant value for the study of protein glycosylation in chondrocytes of the rat mandibular condyle.