title: Chondromodulin-I expression in the growth plate of young uremic rats.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Hospital Central de Asturias, Oviedo, Asturias, Spain.
authors.forename: Benito
authors.initials: B
authors.lastname: Amil
authors.forename: Marta
authors.initials: M
authors.lastname: Fernandez-Fuente
authors.forename: Ines
authors.initials: I
authors.lastname: Molinos
authors.forename: Julian
authors.initials: J
authors.lastname: Rodriguez
authors.forename: Eduardo
authors.initials: E
authors.lastname: Carbajo-Pérez
authors.forename: Enrique
authors.initials: E
authors.lastname: Garcia
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Fernando
authors.initials: F
authors.lastname: Santos
mesh_terms: D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D002455:Cell Division; D019902:Chondrocytes / Q000378:metabolism; D005260:Female; D006128:Growth; D006132:Growth Plate / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D007668:Kidney / Q000503:physiopathology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014511:Uremia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: C489407:Cnmd protein, rat; D036341:Intercellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A