Growth retardation induced by dexamethasone is associated with increased apoptosis of the growth plate chondrocytes
| Autor: | Dionisios Chrysis, E M Ritzén, Lars Sävendahl |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Male
medicine.medical_specialty Peptide Hormones Endocrinology Diabetes and Metabolism bcl-X Protein Apoptosis Caspase 3 Biology Dexamethasone Rats Sprague-Dawley Chondrocytes Endocrinology Internal medicine medicine Animals Growth Plate Glucocorticoids TUNEL assay Tibia Parathyroid hormone-related protein Parathyroid Hormone-Related Protein Genes bcl-2 Rats Hypertropic Proto-Oncogene Proteins c-bcl-2 Caspases Glucocorticoid Homeostasis medicine.drug |
| Zdroj: | Karolinska Institutet |
| ISSN: | 1479-6805 0022-0795 |
| Popis: | Glucocorticoids cause significant growth retardation in mammals and humans and decreased proliferation of chondrocytes has been considered as the main local mechanism. Death by apoptosis is an important regulator of homeostasis in multicellular organisms. Here we chose to study the role of apoptosis in growth retardation caused by glucocorticoid treatment. We treated 7-week-old male rats with dexamethasone (5 mg/kg/day) for 7 days. Apoptosis was studied in tibiae growth plates by the TUNEL method. Immunoreactivity for parathyroid hormone-related peptide (PTHrP), caspase-3, and the anti-apoptotic proteins Bcl-2 and Bcl-x was also studied. Apoptosis was mainly localized in terminal hypertropic chondrocytes (THCs) in both control and dexamethasone-treated animals. Dexamethasone caused an increase in apoptosis which was fourfold in THCs (2.45+/-0.12 vs 0.62+/-0.09 apoptotic cells/mm growth plate, P |
| Databáze: | OpenAIRE |
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