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Parathyroid hormone/parathyroid hormone‐related peptide modulates growth of avian sternal cartilage via chondrocytic proliferation
Author(s) -
Harrington Erik Kern,
Roddy Gavin W.,
West Randy,
Svoboda Kathy K.H.
Publication year - 2007
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.20416
Subject(s) - parathyroid hormone , extracellular matrix , medicine , endocrinology , cyclin d1 , chemistry , cartilage , type ii collagen , chondrogenesis , cell growth , proliferation marker , type i collagen , chondrocyte , biology , cell cycle , cell , calcium , anatomy , biochemistry
Parathyroid hormone (PTH; 10 −7 to 10 −15 M) decreased terminal chondrogenesis in the avian sterna. During the first half of an 8‐day culture, 100 nM PTH (1–34) significantly increased sternal length and downregulated the deposition of type X collagen and its mRNA expression. However, it remains unclear how PTH increased cartilaginous growth. In this study, we examined growth by both cell proliferation and analysis of cyclin d1 and collagen mRNA. Types II, IX, and X collagens and cyclin d1 mRNA were quantified through real‐time RT‐PCR, while Ki‐67 was used as an immunohistochemical proliferation marker. Extracellular matrix content was measured through mRNA quantification of types II, IX, and X collagen and observing deposition of the same collagens. PTH significantly increased the proliferation marker Ki‐67 in the sternal cephalic region. There was less type II and X collagen in PTH‐treated sterna with concomitant decreases in mRNA production, suggesting that proliferation was the major contributor to cartilage growth in the presence of PTH/PTH‐related peptide receptor activation. In conclusion, these experiments demonstrated that PTH increased cartilage growth by upregulating cell proliferation or other extracellular matrix components. Anat Rec, 290:155–167, 2007. © 2007 Wiley‐Liss, Inc.