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.
Papachristou
Dionisios
D
Department of Pathology, School of Medicine, University of Ioannina, Greece.
Pirttiniemi
Pertti
P
Kantomaa
Tuomo
T
Agnantis
Niki
N
Basdra
Efthimia K
EK
D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002358:Cartilage, Articular / Q000166:cytology / Q000378:metabolism; D002454:Cell Differentiation / Q000235:genetics; D019902:Chondrocytes / Q000378:metabolism*; D020219:Chondrogenesis / Q000235:genetics*; D003799:Dental Stress Analysis; D005260:Female; D005502:Food; D051921:Fos-Related Antigen-2 / Q000032:analysis / Q000096:biosynthesis; D007124:Immunoenzyme Techniques; D008335:Mandibular Condyle / Q000378:metabolism*; D008409:Mastication; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000096:biosynthesis; D016755:Proto-Oncogene Proteins c-jun / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000502:physiology*; D000099169:Fos-Related Antigen 1
D051921:Fos-Related Antigen-2; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1; D000099169:Fos-Related Antigen 1; C497874:Fosl2 protein, rat