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Biomedical subjects

S Jingushi

Publications and source records attributed to S Jingushi.

33 records · Page 2Linked to original sources
PubMed1996

Basic fibroblast growth factor inhibits osteoclast-like cell formation.

Basic fibroblast growth factor (bFGF) inhibited osteoclast-like cell formation in co-cultures of mouse bone marrow cells either with the mouse stromal cell line, ST2, or with primary osteoblastic cells. Basic FGF significantly inhibited the osteoclast-like cell formation, induced by 1 alpha,25-dihydroxyvitamin D3[1 alpha, 25(OH)2D3] when the cytokine was added to the culture, at an intermediate stage, suggesting that bFGF inhibits the differentiation of the osteoclast progenitors. With regard to target cells, bFGF directly affected ST2; it increased [3H] thymidine uptake and decreased the number of alkaline phosphatase-positive cells. In contrast, bFGF had no inhibitory effect on the colony formation of bone marrow cells induced by macrophage colony stimulating factor in methylcellulose culture. In addition, ST2 cells treated with bFGF produced similar amounts of colony forming activity to those without the cytokine. These findings indicated that the bFGF is not involved in the proliferation of progenitor cells even in the presence of ST2 cells. Furthermore, bFGF inhibited osteoclast-like cell formation induced not only by 1 alpha,25(OH)2D3, but also by prostaglandin E2 and by interleukin-11. These results suggest that bFGF inhibits the common site of osteoclast-like cell formation, as induced by different mechanisms. Our data also indicated that the target cells for bFGF in inhibiting osteoclast formation are not osteoclast progenitors but stromal cells such as ST2 and osteoblastic cells, which support osteoclast development.

Acid Phosphatase↗
PubMed1996

Basic fibroblast growth factor stimulates articular cartilage enlargement in young rats in vivo.

Basic fibroblast growth factor is a potent mitogen for chondrocytes and influences the protein synthesis of their extracellular matrix in vitro. To investigate its effect on normal developing articular cartilage in vivo, we injected basic fibroblast growth factor once into the knee joints of 4-week-old rats. Phosphate buffered saline was similarly injected into the contralateral knee joints as controls. A histological analysis showed that an injection of basic fibroblast growth factor induced enlargement of the articular cartilage area, especially in the condylar ridge region on day 7 after the injection. The extent of the enlargement was dose-dependent. The localization and amount of proliferating cells in the articular cartilage were analyzed immunohistochemically by the detection of proliferating cell nuclear antigen. On day 1 after the injection, the number of cells positive for proliferating cell nuclear antigen increased significantly in the joints that were injected compared with the controls, and Northern blot analysis showed that the level of messenger RNA for alpha 1(II) procollagen was lower in these joints than in the controls. The message in the joints that had been injected increased on day 7, and it was greater than that in the controls. This suggests that proliferating chondrocytes in developing articular cartilage respond to basic fibroblast growth factor with a resulting proliferation of chondrocytes followed by enlargement of cartilage.

Animals↗
PubMed1995

Transforming growth factor-beta 1 and fibroblast growth factors in rat growth plate.

Chondrocytes in the growth plate progress in an orderly fashion from resting through proliferating to hypertrophic cells. In the region of hypertrophic chondrocytes, the cartilage is invaded by capillary loops and endochondral ossification is initiated. It is currently believed that growth factors may regulate the proliferation and maturation of chondrocytes and the synthesis of extracellular matrix in the growth plate. The ordered sequence of proliferation and differentiation observed in the growth plate provides a unique opportunity to study the role of acidic fibroblast growth factor, basic fibroblast growth factor, and transforming growth factor-beta 1 in the regulation of these processes. In this study, expression of the mRNA of these growth factors was examined using total RNA extracted from the physis and epiphysis of rat tibias. Transforming growth factor-beta 1 mRNA was detected by Northern hybridization. Expression of the genes encoding acidic and basic fibroblast growth factors was demonstrated by polymerase chain reaction amplification. In addition, using polyclonal antibodies against these growth factors, we localized them by immunohistochemical analysis. Strong intracellular staining with a predominantly nuclear pattern was observed in chondrocytes from the proliferating and upper hypertrophic zones. In contrast, chondrocytes in the resting zone stained only faintly for the presence of these growth factors. Some chondrocytes in the resting zone adjacent to the proliferating zone stained with these antibodies, and the antibodies also stained cells in the zone of Ranvier, which regulates latitudinal bone growth. Lastly, the location of transforming growth factor-beta 1 was examined further with use of a polyclonal antipeptide antibody specific for its extracellular epitope.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Administration of growth hormone modulates the gene expression of basic fibroblast growth factor in rat costal cartilage, both in vivo and in vitro.

We examined the effect of growth hormone on local growth factor mRNA expression in male Sprague-Dawley rats. Repetitive systemic administration of growth hormone (0.4 IU every 4 h) increased the expression of IGF-I mRNA up to 2.8-fold in costal cartilage tissue compared with controls. Basic FGF (bFGF) mRNA expression gradually increased up to 15.5-fold compared with pre-injection samples, where the mRNA expression was 5.3-times greater than vehicle-injected controls. TGF-beta mRNA showed little changes. Moreover, one microgram/ml of growth hormone enhanced the expression of bFGF mRNA in costal chondrocytes in culture. We conclude that growth hormone increased the local expression of bFGF, as well as that of IGF-I, in cartilage, and suggest that bFGF is directly regulated by growth hormone within a local area.

Animals↗
PubMed1992

Genetic expression of extracellular matrix proteins correlates with histologic changes during fracture repair.

We characterized gene expression in the reparative callus that formed after fracture of the rat femur. The callus was divided into regions of bone formation (hard callus) and cartilage formation (soft callus), and gene expression was examined separately in each region. Expression of extracellular matrix protein genes varied with the progression of repair and differed between hard and soft calluses. Messenger ribonucleic acids (mRNAs) for osteonectin, alkaline phosphatase, and type I procollagen were detected in the hard callus at maximal levels during endochondral ossification and bone remodeling (day 15) and at 50% maximal levels during intramembranous bone formation (day 7). Messenger RNAs for these proteins in the soft callus were detected at low levels during chondrogenesis (day 9) but increased to 80% of maximal levels with chondrocyte hypertrophy and mineralization of the cartilage matrix (day 13). Messenger RNAs for type II procollagen and proteoglycan core protein were detected at maximal levels in the soft callus during chondrogenesis (day 9). Osteocalcin gene expression was detected in the hard callus during endochondral ossification and remodeling but not during intramembranous bone formation or at any time in the soft callus. Osteonectin mRNA was detected in both the hard and soft callus throughout the entire course of fracture repair. Expression of cartilage and bone-related genes correlated with the temporal sequence of histologic changes, suggesting transcriptional regulation of gene expression during repair. Differences in gene expression between hard and soft callus and in each of these regions as repair progressed suggest local regulation of gene expression during cell differentiation and matrix synthesis.

Alkaline Phosphatase↗
PubMed1990

Acidic fibroblast growth factor (aFGF) injection stimulates cartilage enlargement and inhibits cartilage gene expression in rat fracture healing.

The effect of the administration of acidic fibroblast growth factor (aFGF) on normal fracture healing was examined in a rat fracture model. One microgram of aFGF was injected into the fracture site between the first and the ninth day after fracture either every other day or every day. aFGF-injected calluses were significantly larger than control calluses, although this does not imply an increased mechanical strength of the callus. Histology showed a marked increase in the size of the cartilaginous soft callus. Total DNA and collagen content in the cartilaginous portion of the aFGF-injected calluses were greater than those of controls, although the collagen content/DNA content ratio was not different between the aFGF-injected and control calluses. Fracture calluses injected with aFGF remained larger than controls until 4 weeks after fracture. The enlarged cartilaginous portion of the aFGF-injected calluses seen at 10 days after fracture was replaced by trabecular bone at 3 and 4 weeks. Northern blot analysis of total cellular RNA extracted separately from the cartilaginous soft callus and the bony hard callus showed decreased expression of type II procollagen and proteoglycan core protein mRNA in the aFGF-injected calluses when compared with controls. A slight decrease in types I and III procollagen mRNA expression was also observed. We concluded that aFGF injections induced cartilage enlargement and decreased mRNA expression for type II procollagen and proteoglycan core protein.

Animals↗
PubMed1990

Transforming growth factor-beta in the regulation of fracture repair.

The complexity of the fracture repair process has been apparent to both clinicians and scientists since its first histologic description. How fracture repair is regulated, however, remains unclear. Transforming growth factor-beta (TGF-beta), one member of a class of proteins known as growth factors, may be involved in the formation of bone and cartilage. Our experimental findings implicate TGF-beta as an important regulator of cell proliferation, differentiation, and synthesis of extracellular matrix. Further elucidation of how TGF-beta regulates bone physiology is necessary to improve therapy in pathologic conditions.

Animals↗
PubMed1989

Defects of early fracture-healing in experimental diabetes.

Diabetes has been implicated as a cause of impaired fracture-healing. To test this hypothesis, we tested the tensile strength of femora from normal rats and from untreated and insulin-treated diabetic rats two weeks after the production of a closed fracture. One week before the fracture, diabetes was induced by administration of streptozotocin (sixty-five milligrams per kilogram of body weight). The concentration of serum glucose increased from 6.1 +/- 0.3 millimoles per liter (110 +/- 5 milligrams per deciliter) in the control animals to 31.1 +/- 0.8 millimoles per liter (560 +/- 15 milligrams per deciliter) in the untreated diabetic animals. After two weeks of healing, fracture callus from the untreated diabetic animals had a 29 per cent decrease in tensile strength and a 50 per cent decrease in stiffness compared with the controls. Treatment of the diabetic animals with insulin resulted in a mean concentration of serum glucose of 14.4 +/- 0.6 millimoles per liter (260 +/- 10 milligrams per deciliter) and restored the tensile strength and stiffness of the callus to a value that was not statistically different from that of the controls. Between the fourth and eleventh days of healing, there was a 50 to 55 per cent decrease in the collagen content of the callus of the untreated diabetic animals compared with the controls. In addition, on the fourth day of healing, DNA content, an indicator of cellularity of the callus, was decreased 40 per cent in the untreated diabetic group. Between the fourth and eleventh days of healing, the collagen-to-DNA ratio, which was determined as an indicator of net collagen synthesis per cell, was decreased 15 to 50 per cent in callus from the untreated diabetic animals.

Animals↗
PubMed1987

Suppression of collagen arthritis in rats by heterologous anti-idiotypic antisera against anticollagen antibodies.

Affinity-purified rat anti-type II collagen antibodies were used to prepare anti-idiotypic antibodies in rabbits. It has been demonstrated that such anti-idiotypic antibodies are capable of binding to anti-type II collagen antibodies in vitro. Intravenous administration of heterologous anti-idiotypic antisera at the time of immunization with type II collagen resulted in a significant suppression of anti-type II collagen antibody formation and the development of arthritis, although delayed-type hypersensitivity skin test response to type II collagen was not affected. However, treatment of rats with heterologous anti-idiotypic antisera at Day 7 after immunization was ineffective in altering disease expression. On the other hand, treatment with heterologous anti-idiotypic antisera had no significant suppressive effect on the incidence or severity of adjuvant arthritis. These results indicate that the effect of heterologous anti-idiotypic antisera directed toward anti-type II collagen antibodies is disease specific and is restricted to collagen arthritis.

Animals↗
PubMed1987

Antigenic determinants on fimbriae of Serratia marcescens US5 analyzed using monoclonal antibodies.

The antigenic sites on small thin fimbriae of Serratia marcescens strain US5 were investigated using immunoelectron microscopy and monoclonal antibodies (MAbs). Negative staining of the fimbriae after treatment with MAbs showed a regularly spaced arrangement of the antibody molecules. When the subunit peptide was subjected to immunoblotting using the MAbs, a single band with a molecular weight of approximately 19kD was evident. This binding of the MAbs to the subunit peptide was completely abrogated after treatment with 2-mercaptoethanol, thereby suggesting the important role of disulfide linkage in the maintenance of the conformation of the antigenic site reacted with MAbs. Amino acid analysis of the subunit peptide revealed two cysteine residues, and cysteine residues were absent in the N-terminal portion.

Amino Acid Sequence↗
PubMed1987

Antigenic analysis of Serratia marcescens fimbriae with monoclonal antibodies.

Monoclonal antibodies (MAbs) were raised against the purified fimbriae of Serratia marcescens US46, a strain expressing three morphologically distinct fimbriae. The widths of these fimbriae were 7, 4.5, and 3 nm, respectively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the purified fimbriae showed three bands with molecular weights of 21,000, 20,000, and 19,000, respectively. This strain had mannose-resistant (MR) hemagglutinating activity and was agglutinated by yeast cells. Therefore, strain US46 appeared to have both MR and mannose-sensitive fimbriae. In the immunoblot analysis, all MAbs reacted with the 20,000-molecular-weight subunit when given a choice of three differently sized subunits. Immunoelectron microscopy showed these MAbs attached to the MR fimbriae with the largest width (7 nm). The antigenic cross-reactivity of fimbriae was examined by an MAb-mediated agglutination test. All MR strains of S. marcescens and some mannose-sensitive strains were agglutinated by the MAbs. The serological homogeneity of MR fimbriae was confirmed by a spot test, using the crude purified fimbriae from several MR strains of S. marcescens. In other gram-negative rods, clinical isolates of Klebsiella spp. with hemagglutinating activity were agglutinated, but clinical isolates of Escherichia coli and Enterobacter spp. were not.

Antibodies, Bacterial↗
PubMed1984

Pathogenetic difference between collagen arthritis and adjuvant arthritis.

Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d gave complete suppression of the development of collagen arthritis and adjuvant arthritis in Sprague-Dawley rats during an observation period of 45 d. To study whether the immunologic unresponsiveness produced by cyclosporin is antigen specific, we rechallenged the cyclosporin-protected rats with either type II collagen or complete Freund's adjuvant (CFA) after discontinuation of cyclosporin treatment. Type II collagen-immunized, cyclosporin-protected rats did not develop arthritis in response to reimmunization with type II collagen, but, they did develop arthritis in response to a subsequent injection of CFA. Similarly, CFA-injected, cyclosporin-protected rats showed a suppressed arthritogenic reaction in response to reinjection of CFA, whereas their response to a subsequent immunization with type II collagen was unaffected. On the other hand, the rats that were treated with cyclosporin without any prior antigenic challenge could develop arthritis in response to a subsequent injection of CFA or type II collagen after cessation of cyclosporin treatment. These results indicate that specific immunologic unresponsiveness can be induced by cyclosporin in the two experimental models of polyarthritis, collagen arthritis and adjuvant arthritis, and that there is no cross-reactivity between type II collagen and the mycobacterial cell wall components. The results further indicate that immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but that its pathogenetic role in adjuvant arthritis is insignificant.

Animals↗
PubMedDate not supplied

Deficiency of a parathyroid hormone fragment containing the midportion and 1,25-dihydroxyvitamin D in serum of patients with slipped capital femoral epiphysis.

The endocrine abnormality that causes slipped capital femoral epiphysis (SCFE) has not been revealed. Recent studies have shown that parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] are involved in growth-plate chondrogenesis and matrix mineralization. Thus we examined in 13 patients with SCFE the serum levels of three immunoreactive forms of PTH (iPTH): the whole peptide [(1-84)PTH], the fragment containing the COOH-terminal portion (C-PTH), and the midportion (M-PTH). Additionally, serum levels of 25-hydroxyvitamin D [25-(OH)D] and 1,25-(OH)2D were measured. We found that the levels of M-PTH were significantly lower than those of controls, whereas levels of C-PTH and (1-84)PTH were not significantly different from those of controls. Similarly, levels of 1,25-(OH)2D were also significantly lower than control levels. In patients with initially low levels of M-PTH and 1,25-(OH)2D in whom the levels were monitored over a period, all levels returned to normal within a year after the onset of disease. The deficiency of M-PTH or 1,25-(OH)2D during the growth spurt could result in SCFE, although in this study, we cannot deny the possibility that the slippage may cause the deficiency.

Adolescent↗