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In Vitro Demonstration of Cell‐to‐Cell Interaction in Growth Plate Cartilage Using Chondrocytes Established From p53 −/− Mice
Author(s) -
Nakamata Takeharu,
Aoyama Tomoki,
Okamoto Takeshi,
Hosaka Taisuke,
Nishijo Koichi,
Nakayama Tomitaka,
Nakamura Takashi,
Toguchida Junya
Publication year - 2003
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2003.18.1.97
Subject(s) - chondrocyte , perichondrium , cartilage , in vitro , chemistry , microbiology and biotechnology , cell culture , parathyroid hormone related protein , calcification , cellular differentiation , cell growth , parathyroid hormone , biology , medicine , anatomy , calcium , biochemistry , gene , genetics , organic chemistry
Three clonal cell lines (MMR14, MMR17, and MMR32) were established from the costal cartilage derived from p53 −/− mice. Expression profiles of cartilage‐related molecules in MMR14 and MMR17 were compatible with those in cells of the hypertrophic zone. Prolonged in vitro culture induced the expression of calcification‐related genes in both cell lines, but calcified nodules were observed only in MMR14. The expression profile of cartilage‐related molecules in MMR32 was compatible with that of cells in the perichondrium, with high expression levels of decorin , bone morphogenetic protein‐3 , and parathyroid hormone‐related peptide ( PTHrP ). When MMR14 was co‐cultured with an equal amount of MMR32 without direct contact, the nodule formation was completely inhibited, whereas no such inhibition was observed when MMR14 was co‐cultured with MMR17, indicating that soluble factors produced by MMR32 were responsible for the inhibition. Blocking the effects of PTHrP by either antagonizing peptide or neutralizing antibody against PTHrP failed to rescue the inhibitory effects of MMR32, and no increase of the cyclic adenosine monophosphate production in MMR14 was observed when co‐cultured with MMR32, suggesting that soluble factors other than PTHrP produced by MMR32 were responsible for the inhibition of terminal differentiation of hypertrophic chondrocytes. This report is the first to show cell‐to‐cell interaction in the growth plate using cell lines, which will be useful material to investigate the regulatory mechanism of chondrocyte differentiation.