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Chondromodulin-I expression in the growth plate of young uremic rats
Benito Amil1, Marta Fernandez-Fuente, Ines Molinos
1Hospital Central de Asturias, Oviedo, Asturias, Spain.
Insights
Growth retardation in chronic kidney disease is not caused by altered expression of chondromodulin I (ChM-I) or vascular endothelial growth factor (VEGF) in the growth plate. Growth hormone treatment did not affect these factors.
Area of Science:
- Endocrinology
- Nephrology
- Skeletal Biology
Background:
- Chronic renal failure causes growth retardation linked to disturbed chondrocyte maturation and vascular invasion in the growth plate.
- Chondromodulin I (ChM-I) is a cartilage-specific angiostatic factor.
- The role of ChM-I and vascular endothelial growth factor (VEGF) in uremic growth plate alterations is unknown.
Purpose of the Study:
- To investigate ChM-I expression patterns in the growth plate of uremic rats.
- To examine the relationship between ChM-I and VEGF expression in experimental uremia.
- To assess the impact of growth hormone (GH) treatment on ChM-I and VEGF expression.
Main Methods:
- Immunohistochemistry, in situ hybridization, and RT-PCR were used to analyze ChM-I expression in growth cartilage.
- VEGF expression was assessed by immunohistochemistry.
- Studies were conducted on young uremic rats, control rats, pair-fed rats, and uremic rats treated with GH.
Main Results:
- ChM-I and its mRNA were localized to the proliferative and early hypertrophic zones.
- The distance of extracellular ChM-I signal from the metaphyseal end was increased in uremic rats, indicating growth plate expansion.
- No significant differences in ChM-I or VEGF expression levels were found between groups, including GH-treated rats.
Conclusions:
- Growth plate expansion in experimental uremia is not due to increased ChM-I or reduced VEGF expression.
- Growth hormone treatment does not alter ChM-I or VEGF expression in the uremic growth plate.
Background:
Growth retardation of chronic renal failure is associated with alterations in the growth plate suggestive of a disturbed chondrocyte maturation process and abnormal vascular invasion at the chondro-osseous interphase. Chondromodulin I (ChM-I) is a potent cartilage-specific angiostatic factor. Its pattern of expression in the uremic rat growth plate is unknown. Persistence of ChM-I synthesis and/or imbalance between ChM-I and vascular endothelial growth factor (VEGF) expressions might play a role in the alterations of uremic growth plate.
Methods:
Growth cartilage ChM-I expression was investigated by immunohistochemistry, in situ hybridization, and reverse transcription-polymerase chain reaction (RT-PCR) in growth-retarded young uremic rats (UREM), control rats, fed ad libitum (SAL) or pair-fed with the UREM group (SPF), and uremic rats treated with growth hormone (UREM-GH). VEGF expression was analyzed by immunohistochemistry.
Results:
ChM-I and ChM-I mRNA were confined to the proliferative and early hypertrophic zones of growth cartilage. A similar number of chondrocytes per column was positive for ChM-I in the 4 groups. In accordance with the elongation of the hypertrophic stratum in uremia, the distance (X+/-SEM, microm) between the extracellular ChM-I signal and the metaphyseal end of growth cartilage was higher (P < 0.003) in UREM (236 +/- 40) and UREM-GH (297 +/- 17) than in SAL (92 +/- 7) and SPF (113 +/- 6). No differences in ChM-I expression were appreciated by RT-PCR. Similar VEGF positivity was observed in the hypertrophic chondrocytes of all groups.
Conclusion:
In experimental uremia, expansion of growth cartilage does not result from increased or persistent expression of ChM-I or from reduced VEGF expression at the cartilage-metaphyseal bone interphase. GH treatment does not modify ChM-I and VEGF expressions.
