Anatomy and Embryology

, Volume 196, Issue 2, pp 107–113

Expression of p53 and hsp70 in relation to apoptosis during Meckel’s cartilage development in the mouse

Authors

  • Antigone Trichilis
    • Department of Orthodontics and Pediatric Dentistry, School of Dentistry, Karolinska Institute, Box 4604, S-14104 Huddinge, Sweden
  • J. Wroblewski
    • Department of Basic Oral Sciences, Division of Molecular Biology, School of Dentistry, S-14104 Huddinge, Sweden Tel. 46+8+58587979; Fax 46+8+7745935; e-mail: joanna.wroblewski@ofa.ki.se
ORIGINAL ARTICLE

DOI: 10.1007/s004290050083

Cite this article as:
Trichilis, A. & Wroblewski, J. Anat Embryol (1997) 196: 107. doi:10.1007/s004290050083

Abstract

 The process of Meckel’s cartilage development was examined with regard to expression of p53, a tumor suppressor gene product and hsp70, a stress protein (heat-shock protein), in association with the occurrence of programmed cell death (apoptosis). Balb C mice embryos from embryonic days E13, E14, E15, E16, E17, E18 and 1- and 3-day-old pups were used. P53-positive cells were detected first at E15, and were found in the perichondrium of the distal part of Meckel’s cartilage. During the degeneration process chondrocytes also became p53-positive. In contrast to p53, the expression of hsp70 was high and widespread in the early stages of development (E13–E15); however, it decreased with age, except for Meckel’s cartilage, where hsp70 was found in the cytoplasm or nuclei of the hypertrophic cells. Apoptosis was first detected at E14–E15 in the perichondrium of the distal parts of Meckel’s cartilage. The number of apoptotic bodies increased with age and the ongoing resorption of Meckel’s cartilage. From the present study it can be concluded that expression of p53 and hsp70 varied during the development of Meckel’s cartilage and that both proteins showed nuclear location in hypertrophic cells. No direct spatial or temporal correlation was observed between the expression of p53 and hsp70 and the occurrence of apoptotic bodies.

Key words ChondrocytesApoptosisDegenerationImmunohistochemistry

Copyright information

© Springer-Verlag Berlin Heidelberg 1997