PubMed Health⌕ Search

Biomedical subjects

T Ikebe

Publications and source records attributed to T Ikebe.

At least 55 records · Page 3Linked to original sources
PubMed1998

Involvement of proteasomes in migration and matrix metalloproteinase-9 production of oral squamous cell carcinoma.

We investigated whether proteasomes were involved in the invasiveness of oral squamous cell carcinoma (SCC) cells. The migration of SCC cells through a gelatin-coated membrane was enhanced with tumor necrosis factor alpha (TNF alpha), which was strongly inhibited by a peptide aldehyde, N-acetyl-Leu-Leu-norleucinal (ALLN), but not by its structurally related compound, N-acetyl-Leu-Leu-methioninal (ALLM). Since ALLN is a more potent inhibitor against proteasomal proteolysis than ALLM, cell migration inhibited by ALLN may thus likely depend on proteasomes. The TNF alpha-induced migration through gelatin appeared to be associated with the gelatinolytic activity from the cells, since TNF alpha strongly enhanced the production of matrix metalloproteinase (MMP)-9/gelatinase B in the SCC cells, as detected by gelatin zymography. The production of MMP-9 was also inhibited by pretreatment with ALLN, but not ALLM, in a dose-dependent manner. Moreover, ALLN could block the activation and nuclear translocation of a transcription-activating factor, NF-kappaB, which is known to regulate MMP-9 expression in TNF alpha-stimulated SCC cells. The TNF alpha-induced degradation of IkappaB alpha was also suppressed by ALLN treatment, thus implying that the molecule linking proteasome to MMP-9 production should be IkappaB alpha. We finally reconfirmed the involvement of proteasomes in the invasive behavior of oral SCC using lactacystin, a specific proteasome inhibitor, which could prevent TNF alpha from enhancing MMP-9 production, NF-kappaB activation, induction of MMP-9 mRNA and cell migration.

Carcinoma, Squamous Cell↗
PubMed1998

Activation of NF-kappaB is involved in the survival of osteoclasts promoted by interleukin-1.

We previously reported that interleukin-1 (IL-1) promoted the survival of murine osteoclast-like cells (OCLs) formed in vitro and activated a transcription factor, NF-kappaB, of OCLs. The present study examined whether the activation of NF-kappaB is directly involved in the survival of OCLs promoted by IL-1. The expression of IL-1 type I receptor mRNA in OCLs was detected by the polymerase chain reaction amplification of reverse-transcribed mRNA. An electrophoretic mobility shift assay showed that IL-1 transiently activated NF-kappaB in the nuclei of the OCLs, and the maximal activation occurred at 30 min. The degradation of IkappaBalpha coincided with the activation of NF-kappaB in the OCLs. The immunocytochemical study revealed that p65, a subunit of NF-kappaB, was translocated from the cytoplasm into almost all of the nuclei of the OCLs within 30 min after IL-1 stimulation. The purified OCLs spontaneously died via apoptosis, and IL-1 promoted the survival of OCLs by preventing their apoptosis. The pretreatment of purified OCLs with proteasome inhibitors suppressed the IL-1-induced activation of NF-kappaB and prevented the survival of OCLs supported by IL-1. When OCLs were pretreated with antisense oligodeoxynucleotides to p65 and p50 of NF-kappaB, the expression of respective mRNAs by OCLs was suppressed, and the IL-1-induced survival of OCLs was concomitantly inhibited. These results indicate that IL-1 promotes the survival of osteoclasts through the activation of NF-kappaB.

Animals↗
PubMed1998

Immunohistochemical study of desmosomes in oral squamous cell carcinoma: correlation with cytokeratin and E-cadherin staining, and with tumour behaviour.

Reduction or loss of the intercellular junctions known as desmosomes may contribute to the invasive and metastatic behaviour of various carcinomas. Previous studies have shown that metastasis of oral squamous cell carcinomas of the head and neck correlates with a reduction in immunohistochemical staining for desmoplakin and desmoglein at the invasion front. The primary aim of the present study was to extend these observations to include a third component of desmosomes, the glycoprotein desmocollin. An additional aim was to determine whether the differentiation status of tumours is reflected in their staining for cytokeratins 1, 13, and 19, and, if so, whether these parameters correlate with desmosomal staining and/or metastasis. The study included 54 primary tumours of which 28 showed lymph node metastases. The results of this investigation show that tumours can be divided into three groups according to whether they have lost staining for no, one or more than one desmosomal component. A statistically significant correlation was found between the number of desmosomal components lost and metastasis. Tumours could also be divided into five groups according to their staining for different combinations of cytokeratins. Furthermore, differentiation status as indicated both histologically and by cytokeratin staining correlated with reduced desmosomal staining and metastasis. Tumours were also examined for intensity of staining for the adhesion molecule E-cadherin. Reduction in E-cadherin staining was correlated with mode of invasion and with reduction in desmosomal staining, but not with poor differentiation as indicated by cytokeratin staining. The results of this extensive study reinforce the view that adhesive junctions and adhesion molecules contribute to the suppression of tumour invasion and metastasis.

Adult↗
PubMed1998

Hepatocellular carcinoma with chondrosarcomatous variation: case report with immunohistochemical findings, and review of the literature.

Hepatocellular carcinoma with chondrosarcomatous variation is very rare. We report a case with the results of pathology examination, and review the literature. The patient, a 72-year-old may had a very large tumor in the liver revealed during follow-up for diabetes mellitus. The liver mass, which was 14 cm in diameter, was diagnosed as hepatocellular carcinoma by abdominal ultrasonography. Anterior segmentectomy and partial liver resection were performed. Histopathology examination revealed that the tumor consisted of two different components: the major one was hepatocellular carcinoma (HCC), which occupied most of the tumor; and a sarcomatous component, which occupied a smaller area, and included spindle-shaped cells with chondroscarcomatous variation. Intrahepatic metastases and tumor thrombi of HCC were also found in portal and hepatic veins. Investigations of the immunohistochemical localization of keratin (KRT), vimentin (VMT), and S-100 protein (S 100) were performed by the avidin-biotin complex method. Some of the spindle cells were immunohistochemically positive for both KRT and VMT, and the chondrosarcomatous cells were positive for S 100. These results strongly suggested that the sarcomatous lesion resulted from a sarcomatous change of HCC.

Aged↗
PubMed1998

Changes and results of surgical strategies for hepatocellular carcinoma: results of a 15-year study on 452 consecutive patients.

In an attempt to define better surgical strategies for patients with hepatocellular carcinoma (HCC), we conducted a retrospective analysis of 452 patients who underwent hepatic resection at our institute during a period of 15 years. The patients were divided into two groups: group A, comprising 188 patients who underwent hepatic resection before 1988, and group B, comprising 264 patients after 1989. These groups were compared clinicopathologically. The percentage of patients with Child's A disease but without cirrhosis, in group A was lower. The diameter of the resected tumor was larger in group A, and major hepatic resections and curative operations were more frequently performed in group A. In group B, there was less blood loss, the specimen weighed less, and the hospital mortality was lower. Although the tumor-free survival rates were similar between the two groups, the survival rate in group B was significantly better. While even minor hepatic resection accompanied by a lower rate of surgical margin-free surgery has contributed to making hepatic resection safer, it has not improved the tumor-free survival rate. Conversely, recent advances in imaging modalities used during follow-up for the early detection of recurrence and for planning multimodality treatment have contributed to increasing the survival rate.

Carcinoma, Hepatocellular↗
PubMed1998

Synovial chondromatosis of the temporomandibular joint: the effect of interleukin-1 on loose-body-derived cells.

OBJECTIVE: The purpose of this study was to investigate the effect of interleukin-1 on cells from loose bodies of synovial chondromatosis of the temporomandibular joint. STUDY DESIGN: The cells were isolated from uncalcified loose bodies in a case of synovial chondromatosis of the temporomandibular joint and cultured in alpha-MEM medium containing 10% fetal bovine serum. The cells were treated with or without interleukin-1alpha and then stained with toluidine blue. Their conditioned media were analyzed with gelatin zymography to detect matrix-degrading proteinase(s). RESULTS: The cells from loose bodies produced toluidine-blue-stained matrix. When the cells were treated with 100 ng/ml of interleukin-1alpha for 3 days, toluidine-blue-stained matrix was strikingly reduced. Gelatin zymography revealed that interleukin-1alpha-treated cells released 62-kDa gelatinase. CONCLUSIONS: Interleukin-1alpha may lead loose-body-derived cells to degrade the cartilaginous matrix of loose bodies in synovial chondromatosis of the temporomandibular joint.

Animals↗
PubMed1998

Suppressive effect of the angiogenesis inhibitor TNP-470 on the development of carcinogen-induced hepatic nodules in rats.

Tumor metastasis can be prevented by inhibiting angiogenesis. In the present study, we have demonstrated that the angiogenesis inhibitor TNP-470 also suppresses the development of primary hepatic nodules. Hepatocarcinogenesis was performed by the feeding of 2-acetylaminofluorene to hepatectomized rats during 8-14 weeks of age. Predominantly arterial-to-portal circulation and sinusoidal capillarization were determined by the staining of nodules with arterially infused ink and immunostaining for factor VIII-related antigen, respectively. Intraperitoneal administration of 30 mg/kg b.w. of TNP-470 twice a week significantly reduced the number of hepatic nodules. Among the nodules, hyperplastic nodules stained with ink, atypical hyperplastic nodules and hepatocellular carcinoma, all of which possess structurally altered sinusoidal endothelial cells or capillary-type endothelial cells, were dramatically decreased in number. Suppression was observed equally in nodules of all sizes. TNP-470 was more effective when administered during 8-20 weeks than during 14-26 weeks. In contrast, ink-non-stained hyperplastic nodules, which have normal sinusoidal endothelial cells, were not affected at all. The present results indicate that TNP-470 suppresses the development of primary hepatic nodules whose microvessels are capillaries or transitional forms from sinusoids to capillaries.

2-Acetylaminofluorene↗
PubMed1998

Clinicopathological criteria for multicentricity of hepatocellular carcinoma and risk factors for such carcinogenesis.

Multicentric occurrence is an important characteristic of hepatocellular carcinoma. We evaluated clinicopathological criteria for multicentric hepatocellular carcinoma and identified risk factors for such carcinogenesis. Subjects were 251 consecutive patients undergoing liver resection for hepatocellular carcinoma. One kind of multicentric hepatocellular carcinoma had at least one tumor consisting of well-differentiated hepatocellular carcinoma, together with moderately or poorly differentiated hepatocellular carcinoma located in a separate region. The other kind had an area of well-differentiated component around hepatocellular carcinoma with less differentiation in all occurrences. The outcome of patients with tumors classified in this way was studied. Univariate and multivariate analyses were done to identify risk factors for multicentric hepatocellular carcinoma. The cumulative survival rate was significantly higher in patients with multicentric hepatocellular carcinoma than in patients with hepatocellular carcinoma associated with intrahepatic metastasis. Analysis by Cox's proportional hazard model showed that multicentricity was not a factor in the outcome. The risk of multicentric occurrence increases with progression of chronic liver disease. Univariate analysis showed hepatitis C virus marker and hepatitis B core antibody to be risk factors. By multivariate analysis, the odds ratio for multicentric occurrence in patients infected with hepatitis C virus and with serum hepatitis B virus core antibody compared with patients without either hepatitis C virus or hepatitis B virus was 10.86. This ratio in patients with hepatitis C virus alone was 4.30. These criteria for multicentric hepatocellular carcinoma seem to be clinically useful. Hepatitis C virus infection with or without former infection by hepatitis B virus is a strong risk factor for multicentric hepatocarcinogenesis.

Aged↗
PubMed1998

Hyperplastic foci in chronic liver disease: their proliferative activity assessed by nucleolar organizing region.

In the cirrhotic and precirrhotic liver, there may be small foci with increased cellularity and amphophilic cytoplasm. These are microscopic lesions that do not form macroscopically detectable nodules, which differ from the macroscopically apparent nodules of dysplastic nodules. In the present study, we assessed the proliferating activity of 12 hyperplastic foci in 11 patients with cirrhosis or chronic hepatitis, by staining for agyrophilic nucleolar organizing regions (AgNOR). The mean AgNOR count per nucleus in the hyperplastic foci ranged from 0.96 to 1.36 (mean, 1.13; SD 0.12), and from 0.81 to 1.06 (mean, 0.94; SD 0.08) in the controls. The AgNOR count in the hyperplastic foci was significantly higher than that in the controls (P < 0.01). Small hyperplastic foci show increased proliferative activity. Further study on these foci is required to clarify their relation to hepatocarcinogenesis.

Adult↗
PubMed1998

Dual regulatory effects of interferon-alpha, -beta, and -gamma on interleukin-8 gene expression by human gingival fibroblasts in culture upon stimulation with lipopolysaccharide from Prevotella intermedia, interleukin-1alpha, or tumor necrosis factor-alpha.

In a previous study, we demonstrated that the amount of interleukin (IL)-8 mRNA expressed by human gingival fibroblasts stimulated with lipopolysaccharide (LPS) from Prevotella intermedia ATCC 25611 is increased by pre-treatment with beta or gamma interferon (IFN-beta or -gamma). In the present study, we identified the regulatory effects of these IFNs on IL-8 mRNA expression and IL-8 production by human gingival fibroblasts. Priming with IFN-alpha (alpha), -beta, or -gamma upregulated the IL-8 mRNA expression in response to P. intermedia LPS, whereas co-stimulation with these IFNs reduced the amount of mRNA expressed by the cells. The regulation of IL-8 mRNA expression induced by recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) or rHuIL-1alpha was similar to that induced by LPS. The IL-8 mRNA expression in response to P. intermedia LPS was enhanced by IFN-gamma independently of de novo protein synthesis, and was regulated, at least in part, at the transcriptional level. The IL-8 mRNA accumulation in response to P. intermedia LPS was inhibited by tosylphenyl-alanyl chloromethyl-ketone, an inhibitor of NF-kappaB activation, although the NF-kappaB activation itself was not altered by IFN-gamma. These findings suggest that IFNs might be capable of both enhancing and inhibiting inflammatory responses in periodontal tissues through the dual regulation of IL-8 production by gingival fibroblasts in response to bacterial components and cytokines.

Blotting, Northern↗
PubMed1998

[A case of segmental sunset glow fundus following a choroidal tumor-like lesion].

This paper presents a very rare case of segmental sunset glow fundus following a choroidal tumor-like lesion in a 59-year-old woman. She complained of metamorphopsia in her left eye. Funduscopic examination disclosed a pale yellowish choroidal tumefaction, superotemporal to the macula. She was initially thought to have a choroidal tumor. However, in spite of systemic investigation, a diagnosis could not be made. Gradually the lesion became flattened but spread to the periphery. Iridocyclitis with Koeppe's nodule occurred but regressed after treatment with a topical steroid. Three months after the initial onset of the lesion, funduscopy showed a red area, the "sunset glow", in the superior temporal quadrant. This case resembles Harada disease because of the red coloration in the fundus, iridocyclitis with Koeppe's nodule, and human leukocyte antigen (HLA)-DR4 positivity. But other findings were not compatible with the criteria of Harada disease. It seems that the present lesion has not been reported in the past.

Choroid↗
PubMed1998

[Study on blood glucose control of subjects with borderline type abnormality in 75 G oral glucose tolerance test values. The establishment of a high risk group on the basis of yearly observations].

SUBJECTS AND METHODS: 227 of subjects with a 2-hour plasma glucose concentration of 120-199 mg/dl were selected from 413 participants who had two or more 75 g OGTT in health examinations from 1987-1995. From these subjects we established 8 groups according to initial 2-hour plasma glucose concentration 120-199 mg/dl stratified by 10 mg/dl, and calculated the total percentages of participants whose 2-hour plasma glucose concentration reached 200 mg/dl or greater over a 1-8 years (2.7 +/- 1.7 years, mean +/- SD) observation period. In 36 subjects who were tested annually over a four year period (4 times), the mean values of their 4 values were analyzed for relationships to coefficients of variation of the 2-hour plasma glucose. RESULTS: By stratified groups (from lowest to highest) of those with an initial plasma glucose concentration of 120-159 mg/dl, 7.4%, 12.1%, 16.1%, and 15.0% attained values of 200 mg/dl and higher, respectively in 1-8 years. On the other hand, 29.6%, 29.6%, 39.1%, and 47.4% of those with an initial plasma glucose concentration of 160-199 mg/dl moved to a diabetic type after 1-8 years, respectively. The percentages of those who ended up with levels of 200 mg/dl and greater at 2-hours tended to increase in subjects whose initial 2-hour plasma glucose concentration was over 160 mg/dl in comparison with patients below that initial level. CONCLUSIONS: From these results, it appears that subjects with 160-199 mg/dl 2-hour glucose concentration, which is considered a borderline status, are at high risk for future abnormal levels (> 200 mg/dl at 2-hours) and should be managed as a high risk level group for prevention of diabetes.

Blood Glucose↗
PubMed1997

Analysis of hyperplastic foci in livers with hepatocellular carcinomas by flow cytometry and AgNOR staining.

The phase S ratio in cell cycles were analyzed in livers with hyperplastic foci (HPF) and in livers without HPF by nuclear DNA determinations using flow cytometry, and by staining with argyrophilic proteins of the nucleolar organizer region (AgNOR). Flow cytometric analysis was done on 50 fresh frozen specimens of livers resected from 50 patients with hepatocellular carcinoma (HCC). Paraffin sections from the same patients were analyzed using AgNOR staining. There were 25 cases each with and without HPF. We examined the stage of fibrosis and the grade of inflammatory activity according to the modified Scheuer and Desmet scale. The incidence of HCC recurrence among these patients was also studied. The average phase S ratio of the livers of the patients with HPF was 6.5 +/- 3.2%, and that of the livers of the patients without HPF was 4.0 +/- 2.5%. The ratio differed significantly between the two groups (P < 0.01). The average AgNOR score for HPF lesions of the HPF-positive cases was 1.60 +/- 0.34, that for non-HPF lesions in the HPF-positive cases was 1.29 +/- 0.12, and that for the HPF-negative cases was 1.19 +/- 0.14. Significant differences were found between the average AgNOR scores for HPF lesions of the HPF-positive cases and the non-HPF lesions of the HPF-positive cases (P < 0.01), as well as between the non-HPF lesions in the HPF-positive cases and the HPF-negative cases (P < 0.05). Severe fibrosis (stage 3) and cirrhosis (stage 4) were found in 76% of HPF-positive cases and 48% of HPF-negative cases. The livers of HPF-positive patients were significantly more cirrhotic than those of HPF-negative patients (P < 0.05). The association between HPF and the inflammatory grade was not significant (P > 0.05). The incidence of HCC recurrence among HPF-positive cases was significantly higher than that among the HPF-negative cases (P < 0.05). The average phase S ratio of the recurrent HPF-positive patients was 7.48 +/- 3.48%, significantly higher than that of HPF negative cases (5.57 +/- 3.06%, P < 0.05). Hyperplastic foci of the liver was shown to be a highly proliferative lesion. The proliferative activity of the non-HPF lesions in the HPF-positive patients was also higher than that of the HPF-negative patients. Hyperplastic foci tended to be present in cirrhotic livers, but it was not associated with the grade of inflammatory activity of the liver. Hyperplastic foci may represent an important predictor of recurrence after hepatic resection.

Adult↗
PubMed1997

Heart disease deaths on death certificates re-evaluated by clinical records in a Japanese city.

In order to estimate the number of deaths from ischemic heart disease (IHD) in a Japanese city, we reevaluated heart disease deaths among residents aged 25-74 years by examining their clinical records. During the 2-year period from 1987 to 1988, 271 deaths among this population were attributed to heart disease. The recorded underlying cause of death was IHD in 96 cases, heart failure in 123 cases, and other heart disease in 52 cases. Re-evaluation of the cause of death yielded 57 cases of acute myocardial infarction (AMI), 85 cases of sudden death, 37 cases of heart disease other than IHD, and 63 cases of non-heart disease. In the remaining cases, there was insufficient information for evaluation. According to some autopsy studies, about 50% of sudden deaths are due to IHD. Thus, 50% of the number of sudden death cases may be added to the total number of IHD deaths. Accordingly, the total number of IHD deaths may have been 100, ie, 57 cases of AMI plus 43 cases of sudden death. The difference between the number of IHD deaths after re-evaluation and the number for which IHD was recorded as the underlying cause was small, with the former only 4% higher than the latter. The number of false-positives was equal to the number of false-negatives, and hence the number of IHD deaths recorded in this area seems to be close to the actual figure. We speculate that more accurate death certification will result in a decrease in the total number of deaths attributable to heart disease, as in 23% of deaths attributed to heart disease the underlying cause of death was not in fact heart disease.

Adult↗
PubMed1997

[Reevaluation of heart disease deaths on death certificates and trends for ischemic heart disease mortality during the last five years in Oita city].

To evaluate heart disease deaths and clarify trends for ischemic heart disease (IHD) mortality during the last five years in Oita City, we reevaluated causes of death on death certificates. In 1993, there were 253,000 people aged 25-74 in Oita City. In this population age group, there were 1,996 deaths from January 1992 through December 1993. Our subjects were 982 deaths recorded as caused by heart disease and IHD related diseases. Subjects were reevaluated on the basis of physician's interview, clinical records and police records. This IHD reevaluation was conducted by the WHO MONICA criteria. The death certificates identified 321 heart disease deaths, of which there were 80 (24.9%) acute myocardial infarctions (AMI), 22 (6.9%) other IHD, 180 (56.1%) heart failures, and 39 (12.1%) other heart diseases. The remaining 61 deaths were caused by other diseases. After reevaluation, 40 'definite' AMI and 60 'possible' AMI were recognized through the MONICA criteria, 86 sudden deaths (SD) which were defined as, 'death within 24 hours of the onset of acute symptoms and without clear signs suggesting what disease was the cause,' were also classified. Assuming that 50% of SD were due to IHD, according to some postmortem autopsy studies, aged-standardized IHD mortality per 100,000 for males was 38.3 per year and for females 17.3 per year in this period. Both mortality rates, 31% for males and 38% for females, were higher than IHD mortality statistics. Moreover, in comparison with IHD mortality estimated by reevaluation of heart disease in Oita City in 1987-88, age-standardized IHD mortality per 100,000 for males has remained basically stable, increasing from 37.8 to 38.4 during the last five years. On the other hand, mortality for females has increased from 11.2 to 17.3. Our results suggest that mortality from IHD actually was about 30% more than mortality statistics, and does not show a declining trend as mortality statistics have stated.

Adult↗
PubMed1996

Interleukin-1 alpha activates an NF-kappaB-like factor in osteoclast-like cells.

We investigated the NF-kappaB transcription factor in osteoclast-like cells. Osteoclast-like cells were differentiated from mouse bone marrow cells in co-culture with mouse calvaria-derived primary osteoblasts in the presence of 1alpha,25-dihydroxyvitamin D3 and prostaglandin E2 in collagen gel-coated dishes. We enriched osteoclast-like cells from the co-cultures by Pronase treatment. When the enriched osteoclast-like cells were treated with phorbol 12-myristate 13-acetate, interleukin-1 (IL-1), calcitonin, or macrophage colony-stimulating factor, only IL-1 activated an NF-kappaB-like factor, which specifically bound to a kappaB motif DNA sequence, as detected by an electrophoretic mobility shift assay. IL-1 also activated NF-kappaB induction in osteoblasts. However, the NF-kappaB-like factor induced by IL-1-stimulated osteoclast-like cells is of smaller molecular size than the factor in osteoblasts, as shown by an electrophoretic mobility shift assay. The NF-kappaB activity of osteoclast-like cells was recognized completely by antibodies against the p50 subunit, and only partially by antibodies against the p65 subunit of NF-++kappaB. Antibodies against c-Rel, Rel B, and p52 did not recognize the NF-kappaB-like factor. These results suggest that IL-1 activates an NF-kappaB-like factor in osteoclast-like cells, which contains p50 and p65-related proteins.

Animals↗
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↗