Chondromodulin-I expression in the growth plate of young uremic rats

Amil, Benito; Fernández-Fuente, Marta; Molinos, Inés; Rodrı́guez, Julián; Carbajo-Pérez, E; García, Eva; Yamamoto, Tadashi; Santos, Fernando

doi:10.1111/j.1523-1755.2004.00708.x

Cited by 8 publications

(6 citation statements)

References 48 publications

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“…In accordance with this, expression of chondromodulin-I, a potent cartilage-specific anti-angiogenic factor, is confined to the proliferative zone and initial part of the hypertrophic zone of growth cartilage in rats, whereas vascular endothelial growth factor, a strong stimulus for angiogenesis, is highly expressed in the chondrocytes adjacent to the metaphyseal bone. As shown by immunohistochemical and in situ hybridization analysis [23], this pattern of local expression of angiogenesis-controlling factors is not modified in uremic rats. To date, there is no evidence demonstrating that a disturbed process of angiogenesis plays a significant pathogenic role in the depressed longitudinal growth rate of individuals with chronic renal failure.…”

Section: The Uremic Rat Gpmentioning

confidence: 93%

Alterations of the growth plate in chronic renal failure

et al. 2004

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Chronic renal failure modifies the morphology and dynamics of the growth plate (GP) of long bones. In young uremic rats, the height of cartilage columns of GP may vary markedly. The reasons for this variation are unknown, although the severity and duration of renal failure and the type of renal osteodystrophy have been shown to influence the height of GP cartilage. Expansion of GP cartilage is associated with that of the hypertrophic stratum. The interference of uremia with the process of chondrocyte differentiation is suggested by some morphological features. However, analysis by immunohistochemistry and/or in situ hybridization of markers of chondrocyte maturation in the GP of uremic rats has yielded conflicting results. Thus, there have been reported normal and reduced mRNA levels for collagen X, parathyroid hormone/parathyroid hormone-related peptide receptor, and matrix metalloproteinase 9, as well as normal mRNA and protein expression for vascular endothelial growth factor and chondromodulin I, peptides related to the control of angiogenesis. In addition, a decreased immunohistochemical signal for growth hormone receptor and low insulin-like growth factor I mRNA in the proliferative zone of uremic GP are supportive of reduced chondrocyte proliferation. Growth hormone treatment improves chondrocyte maturation and activates bone metabolism in the primary spongiosa.

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Section: The Uremic Rat Gpmentioning

confidence: 93%

Alterations of the growth plate in chronic renal failure

et al. 2004

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“…Although some in situ hybridization studies have shown increased abundance of IGF-I [18], IGF-I receptor [19], type II collagen and type X collagen [20] mRNAs in the growth plate of uremic rats treated with GH, upregulation of these genes has not been consistently found [19]. No modifications in the mRNA levels of matrix metalloproteinase-9, chondromodulin-I, and vascular endothelial growth factor have either been reported [19,21]. In this respect, in situ hybridization and immunohistochemistry are good techniques to disclose modifications in tissue distribution pattern of a given mRNA or protein, respectively, but not to appreciate small -moderate quantitative changes in the level of expression.…”

Section: Discussionmentioning

confidence: 87%

Differential gene expression induced by growth hormone treatment in the uremic rat growth plate

Gil

Lozano

Álvarez-García

et al. 2008

Growth Hormone & IGF Research

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“…Then, both tibiae were dehydrated in graded solutions of ethanol and embedded in methylmethacrylate as described formerly. 25,26 Measurement of longitudinal growth rate Frontal 10-mm thick sections of proximal end of tibiae were obtained using a rotary microtome (HM355S, Microm, Barcelona, Spain) fitted with tungsten carbide blades. Sections were examined under an Olympus incident light fluorescence microscope (Olympus BX41) coupled to a digital camera (Olympus DP11, Olympus Optical España, Barcelona, Spain) to detect calcein label.…”

Section: Samplesmentioning

confidence: 99%

Catch-up growth follows an abnormal pattern in experimental renal insufficiency and growth hormone treatment normalizes it

Molinos

Santos

Carbajo-Pérez

et al. 2006

Kidney International

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The primary goal of this study was to determine if the ability to undergo catch-up growth following a transient injury is preserved in an experimental model of moderate chronic renal failure (CRF) and the effect of growth hormone (GH) administration on such phenomenon. Young rats were subtotally nephrectomized (days 0 and 4) (Nx). From days 11 to 13, food intake was restricted in subgroups of Nx and control (C) rats (NxR and CR). After refeeding, subgroups of NxR and CR rats received GH from days 14 to 20 (NxRGH and CRGH). Rats were killed on days 14 (C, CR, Nx, NxR), 17 and 21 (C, CR, CRGH, Nx, NxR, NxRGH), and 36 (C, CR, Nx, NxR). Longitudinal growth rate was measured by osseous front advance in the proximal tibiae. With refeeding, growth rate of CR, NxR, and NXrGH rats became significantly greater than that of C, indicating catch-up growth. This occurred later and with lower growth rate in NxR than in CR rats, whereas the characteristics of catch-up growth in CR and NxRGH animals were similar. Changes in growth rate were associated with modifications in the morphology and proliferative activity of growth cartilage. We conclude that catch-up growth occurs in renal insufficiency but follows a different pattern from that observed with normal renal function. GH treatment normalizes the pattern of catch-up growth in CRF. Changes in growth velocity are associated to modifications in the structure and dynamics of growth cartilage.

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Chondromodulin-I expression in the growth plate of young uremic rats

Abstract: 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.

Cited by 8 publications

References 48 publications

Alterations of the growth plate in chronic renal failure

Alterations of the growth plate in chronic renal failure

Differential gene expression induced by growth hormone treatment in the uremic rat growth plate

Catch-up growth follows an abnormal pattern in experimental renal insufficiency and growth hormone treatment normalizes it

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