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Expression of Deleted in Colorectal Cancer in the Rat Trigeminal Ganglia

  • Lee, Eun-Joo (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Nam-Ryang (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Yoo, Hong-Il (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Yang, So-Young (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kang, Jee-Hae (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Hyun-Jin (Department of Oral Anatomy, College of Dentistry, Wonkwang University) ;
  • Kim, Min-Seok (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Sun-Hun (Dental Science Research Institute, School of Dentistry, Chonnam National University)
  • Received : 2012.08.31
  • Accepted : 2012.12.10
  • Published : 2012.12.31

Abstract

The deleted in colorectal cancer (DCC) protein mediates attractant responses to netrin during axonogenesis. In the rat trigeminal ganglia (TG), axons must extend toward and grow into the trigeminal nerve to innervate target tissues such as dental pulp. Our present study aimed to investigate the expression of DCC in the TG. Four developmental timepoints were assessed in the experiments: postnatal days 0, 7 and 10 and adulthood. RT-PCR and western blotting revealed that the expression of DCC mRNA and protein does not significantly change throughout development. Immunohistochemistry demonstrated that DCC expression in the TG was detectable in the perikarya region of the ganglion cells during development. Nerve injury at 3 and 5 days after the mandibular nerve had been cut did not induce altered expression of DCC mRNA in the TG. Moreover, DCC-positive cell bodies also showed similar immunoreactive patterns after a nerve cut injury. The results of this study suggest that DCC constitutively participates in an axonogenesis attractant in ways other than expression regulation.

Keywords

References

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