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At least 937 records · Page 52Linked to original sources
PubMed1999

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats.

Several studies have suggested that testosterone may have a direct, GH-independent effect on growth. In order to assess possible mechanism(s) whereby testosterone exerts its growth-promoting effect, we evaluated its effect on growth mediators of the GH-IGF-I axis, in both the liver and the epiphyseal growth plate (EGP). Testosterone was administered to peripubertal rats and the responses of mRNA of GH receptor, IGF-I, IGF-I receptor and IGF-binding proteins-1 and -3 (IGFBP-1 and IGFBP-3) as well as circulating IGF-I were evaluated in two time-related models: over 12 h after a single injection (short-term study) and 10 days after continuous administration (long-term study). Rats in the short-term study were castrated and were killed 1, 4, 6 and 12 h post injection. Rats in the long-term study were divided into two groups: castrated vs castrated and hypophysectomized, in order to assess the effect of testosterone in the presence and absence of GH. mRNA levels were determined by RNase protection assay, and serum IGF-I by RIA. Testosterone enhanced weight gain in the rats treated for 10 days, a change that was similar in the presence or absence of GH. This effect was relatively small, however, by comparison with the total weight gained without testosterone. Testosterone had no effect on hepatic IGF-I mRNA abundance but induced a reduction in circulating IGF-I levels, in both the short- and long-term study. Testosterone had no effect on hepatic GH receptor and IGFBP-3 mRNA levels but resulted in a transient, short-term elevation in IGFBP-1 mRNA levels that was maximal 4 h post injection. In the EGP, neither testosterone administration nor hypophysectomy had any effect on IGF-I and IGF-I receptor mRNA levels. However, testosterone increased GH receptor mRNA abundance after 10 days of continuous administration in hypophysectomized rats only. These data suggest that the effect of testosterone on growth (as assessed by weight gain) is small and is not mediated by changes in hepatic gene expression of IGF-I, IGF-I receptor, IGFBP-1, IGFBP-3 or circulating IGF-I. At the EGP, the testosterone effect on linear growth is not mediated through changes in mRNA abundance of IGF-I and IGF-I receptor. The small but significant elevation of GH receptor mRNA levels in hypophysectomized rats may suggest a testosterone-mediated augmentation of a GH effect at the target organ.

Animals↗
PubMed1989

Atrial natriuretic peptide and sodium nitroprusside stimulate cyclic GMP accumulation by avian skin fibroblasts and epiphyseal growth-plate chondroprogenitor cells.

Chondroprogenitor cells derived from avian tibia epiphyseal growth plate, and skin fibroblasts were cultured in vitro. In the fibroblasts, human (1-28) and rat (5-28) atrial natriuretic peptide (ANP) stimulated cyclic GMP (cGMP) production in a dose-dependent manner without affecting cAMP. Sodium nitroprusside also stimulated cGMP accumulation by chondroprogenitor cells and fibroblasts, but the maximum cGMP accumulation elicited by sodium nitroprusside was much lower than that obtained with ANP. The effects of ANP and sodium nitroprusside on chondroprogenitor cells and skin fibroblasts were additive. Human ANP increased cGMP production by the particulate fraction prepared either from chondroprogenitor cells or fibroblasts. Sodium nitroprusside, at concentrations of up to 1 mmol/l, did not affect cGMP production by the particulate fraction prepared from either cell type. The present study provides additional evidence that avian growth-plate chondroprogenitor cells and skin fibroblasts are targets for ANP. ANP and nitroprusside activate different guanylate cyclase isoenzymes--the particulate and soluble forms of the enzyme respectively. The data suggest that most of the guanylate cyclase activity in these cells is localized in the particulate fraction.

1-Methyl-3-isobutylxanthine↗
PubMed1993

A double-staining technique for detection of growth hormone and insulin-like growth factor-I binding to rat tibial epiphyseal chondrocytes.

In the present study a double-staining technique was developed to investigate simultaneous GH and insulin-like growth factor-I (IGF-I) binding to chondrocytes in a monolayer cell culture. Rat tibial epiphyseal chondrocytes were isolated by enzymatic digestion and cultured in monolayer. GH and IGF-I were labelled with biotin. The affinity of the biotin-labelled ligands was compared with unlabelled ligands in a radioreceptor assay. To study the distribution of GH and IGF-I binding in the monolayer, chondrocytes were incubated with biotinylated ligands with or without an excess of unlabelled ligands, followed by incubation with Vectastain ABC complex, which was then reacted with diaminobenzidine (DAB). Double staining was accomplished by carrying out the first reaction with DAB in the presence of nickel ammonium sulphate to give a black precipitate, followed by incubation with the second ligand, then ABC complex and finally DAB in the absence of nickel ammonium sulphate to give a brown stain. The presence of type-II collagen was demonstrated by immunohistochemistry and used as a marker for differentiated chondrocytes. Biotin-labelled GH and biotin-labelled IGF-I exhibited dose-dependent displacements of 125I-labelled GH and 125I-labelled IGF-I respectively from the chondrocytes in a radioreceptor assay. The displacement curves were identical to those of unlabelled ligands indicating that the affinity was unaltered. Binding of biotinylated GH to cells was seen throughout the culture in regions where there was little or no type-II collagen staining. IGF-I binding was predominantly localized to cells at high density; areas which also showed a high degree of staining for type-II collagen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

The aromatase inhibitor letrozole increases epiphyseal growth plate height and tibial length in peripubertal male mice.

Sex hormones may influence longitudinal growth, either indirectly, by affecting the growth-hormone-insulin-like growth factor I (IGF-I) axis, or directly, by affecting changes within the epiphyseal growth plate (EGP). The aim of the present study was to investigate the effects of letrozole, an aromatase inhibitor, on longitudinal growth and changes in the EGP in vivo. Eighteen peripubertal male mice were divided into three groups. The first group was killed at baseline, the second was injected with letrozole (Femara) s.c., 2 mg/kg body weight/day, for 10 days, and the third was injected with the vehicle alone. Serum testosterone levels were found to be significantly higher in the treated group than in the controls. Letrozole induced a significant increase in body weight, tail length and serum growth hormone level, but had no significant effect on the level of serum IGF-I. On histomorphometric study, there was a significant increase (12%) in EGP height in the treated animals compared with controls. Immunohistochemistry showed a 3.4-fold letrozole-induced increase in the proliferation of the EGP chondrocytes, as estimated by the number of proliferation cell nuclear antigen-stained cells, and a decrease in the differentiation of the EGP chondrocytes, as estimated by type X collagen staining. Letrozole did not interfere with type II collagen levels. The study group also showed a twofold increase in the number of IGF-I receptor-positive cells compared with controls. In conclusion, the aromatase inhibitor, letrozole, appears to increase the linear growth potential of the EGP in mice.

Animals↗
PubMed1993

Ultrastructure and X-ray microanalysis of epiphyseal growth cartilage of femoral head processed by rapid-freezing and freeze-substitution.

Epiphyseal growth cartilage of the femoral head obtained from Wistar rats was investigated after fixation by a rapid-freezing and freeze-substitution. Liquid helium was used in order to achieve a fast cooling rate without ice-crystal damage during the rapid freezing. Use of the rapid-freezing and freeze-substitution procedure provided better ultrastructural preservation of the chondrocyte than conventional chemical fixation methods. This procedure allowed a more reliable approach to electron probe analysis. X-ray microanalysis of the specimens confirmed that calcium is not detected in the initial matrix vesicles as a result of the freezing process. The results suggest that calcium release from precipitates occurs in the free state without any detectable formation of hydroxyapatite at the initial stage of calcification and that calcium is not tightly bound to the matrix vesicles.

Animals↗
PubMed1982

Localization of sudanophil material at the sites of calcification in dentine, and the compact bone and epiphyseal cartilage plate of tibia in the rat given beryllium carbonate.

The localization of sudanophil material at dentine, the compact bone and epiphyseal cartilage plate of tibia of rat given beryllium carbonate was examined. Sudanophil material was seen at the boundary parts between dentine and widened predentine, and between widened preosseous matrix and calcified bone, but it was not seen at the area corresponding to the zone of provisional calcification. These facts suggest that the localization of sudanophil material in hard tissue of rat with Be rickets was similar to that in vitamin D deficient-induced rickets. This sudanophil material was not disappeared by the enzymes such as papain, pepsin and hyaluronidase as described in vitamin D deficient-induced rickets (Irving, 1960, 1963). Accordingly, it was suggested that the substance was not proteins and mucopolysaccharide.

Animals↗
PubMedDate not supplied

Electron microscopical study in multiple epiphyseal dysplasia type II.

An electron microscopic examination of articular cartilage of two cases with multiple epiphyseal dysplasia type II was performed. The cartilage had a normal cell distribution and no signs of gross degeneration were found. Chondrocytes showed normal ultrastructural characteristics without dilation of the rough endoplasmic reticulum. The matrix contained normal banded collagen fibrils, proteoglycans, and aggregated fibrils.

Adolescent↗
PubMed2006

Chondrocytes embedded in the epiphyseal growth plates of long bones undergo autophagy prior to the induction of osteogenesis.

Bone growth takes place through the activities of chondrocytes embedded in the epiphyseal growth plate. Stress conditions in the plate can promote the autophagic response through the modulation of genes controlling metabolite utilization. mTOR plays a critical role in autophagy serving as the sensor that integrates metabolic and growth factor signals. Ongoing studies indicate that terminal chondrocytes exhibit autophagic characteristics. Morphologically, the arrested cells contain double membrane vacuoles; there is a loss of membrane structure, limited staining and organelle destruction. Since the life history of the growth plate chondrocyte is very short, even minor disturbances in the metabolic state can result in gross impairment of growth. We contend that the induction of the autophagic response, permits the terminally differentiated cells to survive the brief rigors of the harsh local microenvironment. Whether chondrocytes can recover from this state, and possibly participate in osteogenesis, is not known at this time.

Animals↗
PubMed1976

[Decrease in the excretion of antigonadotropic factor in patients with cancer of the uterine cervix and prostate gland. Experimental antitumor effect of an epiphyseal extract].

Kaolin-acetone extracts from the urine of patients with cancer of the prostatic gland and uterine neck were found to contain much less quantity of antigonadotropic factor than corresponding substances from the urine of control groups of males and females. This evidences a decreased function of the epiphysis in these groups of tumor patients. Acetic acid extract from cattle epiphyses inhibits the growth of transplantable tumor of mice strain RSM.

Animals↗
PubMed1976

Multiple epiphyseal dysplasia. A family case report.

Six cases of multiple epiphyseal dysplasia were found in a 30-member kindred. The kindred showed an increased incidence of other joint abnormalities. A dominant pattern of inheritance was not confirmed.

Abnormalities, Multiple↗
PubMed1999

Cellular and subcellular distribution of galectin-3 in the epiphyseal cartilage and bone of fetal and neonatal mice.

Galectin-3 is a 30 kDa beta-galactoside binding protein that belongs to the galectin family of animal lectins. By immunocytochemistry we show the presence of galectin-3 protein in the differentiated chondrocytes of the epiphyseal plate cartilage of long bones of both fetal and neonatal mice. The highest concentrations of galectin-3 are found in the cytoplasm of mature and early hypertrophic chondrocytes. Very little protein is detected in the late hypertrophic chondrocytes undergoing terminal maturation and cell death. Galectin-3 has also been found in osteoblasts and osteocytes of the woven bone of the metaphysis and the cortical bone of the diaphysis, as well as in osteoclasts and mononuclear cells within bone marrow cavities. Galectin-3 is never detected extracellularly, the protein seems restricted to the cytoplasm of chondrocytes and bone cells, although it is occasionally detected in the nuclei of dense non-hypertrophic chondrocytes in the zone of calcification and in young osteoblasts. The results indicate that galectin-3 is a marker of both chondrogenic and osteogenic cell lineages. They also suggest that galectin-3 could be involved in the process of endochondral bone formation, possibly as a regulator of chondrocyte survival.

Animals↗
PubMed2000

Splicing mutations in the COL3 domain of collagen IX cause multiple epiphyseal dysplasia.

We report on a three-generation family with multiple epiphyseal dysplasia (MED). The propositus had typical MED findings of knees, ankles, elbows, and hands in childhood. The 2 other affected relatives were adults. The main clinical findings consisted of osteochondritis dissecans and osteoarthritis of the knees. DNA of the propositus was screened for mutations by conformation sensitive gel electrophoresis in all known candidate genes for MED, cartilage oligomeric matrix protein, and the COL9A1, COL9A2, and COL9A3 genes coding for the alpha1, alpha2, and alpha3 chains of collagen IX. The screening identified a unique change in PCR products of exon 3 of the COL9A3 gene. Sequencing indicated a G to A mutation in the acceptor splice site (G(-1)IVS2-->A) of intron 2 in all affected relatives, but not in unaffected relatives. Analysis of RNA from the propositus indicated a skipping of exon 3, and thus, a deletion of 12 amino acid residues as a consequence of the mutation. All four other collagen IX mutations previously described in MED have consequences identical to that characterized here, thus it seems likely that this type of mutation in collagen IX plays an important role in the pathogenesis of MED.

Adult↗
PubMed2002

Alternative splicing of type II procollagen gene in the dedifferentiation of rat epiphyseal chondrocytes serially cultured in monolayer.

Type II procollagen is synthesized in two forms (IIA and IIB), generated by the alternative splicing of its precursor mRNA. The purpose of this study was to determine whether alternative splicing of type II procollagen pre-mRNA occurs during the dedifferentiation of chondrocytes in monolayer culture. We serially cultured rat epiphyseal chondrocytes for eight weeks in monolayer, and investigated the expression patterns of the two forms of type II procollagen transcripts according to the duration of the culture period. Reverse transcription-polymerase chain reaction and northern analysis revealed that both transcripts peaked on the day of cell isolation, but the expression level of IIB form was much higher than that of IIA form. The expression of IIA form decreased gradually, whereas the expression of IIB form decreased so rapidly that the ratio of type IIB and type IIA transcripts was reversed in the second week. In situ hybridization showed that all cells expressed type IIA mRNA throughout the culture period. The signal intensity for type IIA transcript decreased gradually in accordance with the results of RT-PCR and northern analysis. In situ hybridization of type IIB mRNA showed different results from in situ hybridization of type IIA mRNA. Like type IIA transcript, the freshly isolated chondrocytes and the cells in the first week showed positive signals for type IIB transcript. However, in the second week, positive signal was detected neither in polygonal cells nor large fibroblastic cells. Only a few cells of small size were weakly positive. From the third to the eighth week, no positive signal was detected. These findings indicate that alternative splicing of type II procollagen gene does occur and is regulated during the dedifferentiation of chondrocytes in monolayer culture.

Alternative Splicing↗
PubMed1976

The fate of hypertrophic chondrocytes of the epiphyseal plate. An electron microscopic study.

An ultrastructural study of the distal femoral epiphyseal-metaphyseal junction of C3H mice revealed that the hypertrophic chondrocytes undergo degenerative changes leading to their death. While most chondrocytes will die before their lacunae are opened to the marrow, others survive for a time in lacunae which communicate with the primary spongiosa, but they also ultimately die. There was no evidence to indicate that hypertrophic chondrocytes survive or are transformed into other cells.

Animals↗
PubMed2002

[When does a pediatric fracture become a fracture of the adult? Age and significance of epiphyseal closures].

Surgical treatment of fractures of adolescents is often difficult as the epiphyses are still open or not yet completely closed. The osteosynthesis chosen has to consider the remaining prospective growth of the affected bone and biomechanical needs. Due to high physical maturity with small remaining growth capacity in adolescents, a number of different techniques known from osteosynthesis in adults with minor modifications can be used to treat these fractures.

Adolescent↗
PubMed1992

Immunohistochemical investigation on the presence of chondroitin sulfate in calcification nodules of epiphyseal cartilage.

Chondroitin sulfate localization in mouse epiphyseal cartilage was studied using CS-56 monoclonal antibody immunospecific for the glycosaminoglycan portion of the molecule. For light and fluorescence microscopy, decalcified specimens were embedded in paraffin, Lowicryl, or were frozen and cryostat-sectioned, and the antigen-antibody reaction was demonstrated by treating sections with IgM-peroxidase, IgM-alkaline phosphatase, or IgM-fluorescein conjugates. For electron microscopy, decalcified and undecalcified specimens were embedded in Lowicryl; ultrathin sections from undecalcified specimens were decalcified by flotation on EDTA; sections from both types of specimens were treated with IgM-immunogold conjugate for demonstration of CS-56 reaction. Before immunoreaction, part of all decalcified sections were digested with Streptomyces or testicular hyaluronidase. Control sections were treated with either mouse and goat non-immune serum, or mouse monoclonal antiserum to human dendritic reticulum cells. Both light and electron microscopy show CS-56 reaction with cytoplasmic components of maturing and hypertrophic chondrocytes. Under the light microscope, immunoreaction was not visible in calcified matrix, and was visible in uncalcified matrix only after hyaluronidase digestion. Under the electron microscope, it was evident both in uncalcified and calcified matrix, although the latter showed few immunogold particles, usually placed on areas which appeared incompletely calcified. Gold particles were chiefly distributed at the periphery of calcification nodules and fully calcified matrix. These results show that CS-56, besides reacting with cytoplasm of maturing and hypertrophic chondrocytes, binds to crystal ghosts and other components of cartilage matrix, immunoreactivity decreasing as calcification increases. This suggests that chondroitin sulfate molecules are either degraded during calcification, or segregated into macromolecular complexes, or both degraded and segregated. The second possibility is supported by the increase of immunosensitivity induced by hyaluronidase digestion.

Animals↗
PubMed1992

Identification of endogenous 5S,12S-dihydroxy-6,8,10,14-(E,Z,E,Z)-eicosatetraenoic acid (5S,12S-diHETE) in chick osteoblasts and epiphyseal cartilage.

Cell homogenates were obtained from chick osteoblast-like cells and epiphyseal growth plates. The lipid fraction was extracted with ethyl acetate and separated by RP-phase HPLC. Reverse-phase HPLC analysis of this fraction showed a major peak displayed a conjugated tetraene structure and this endogenous synthetic compound could be partially blocked by heat treatment at 100 degrees C for 5 min. After methylation, this peak was further purified by SP-HPLC and a major peak was identified by an U.V. absorption at lambda max of 271 nm and shoulders at 261 and 281 nm. The compound was hypothetically proposed by gas chromatography and mass spectrometry (GC/MS) as the cyclohexadiene derivative of 5S,12S-dihydroxy-6,8,10,14-(E,Z,E,Z)-eicosatetraenoic acid (5S,12S-diHETE) with a ring closure at C6 and C11. These results demonstrated that the 5S,12S-diHETE is an endogenous eicosanoid in both intramembranous and endochondral skeletal tissues.

Animals↗