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Biomedical subjects

M Fukumoto

Publications and source records attributed to M Fukumoto.

At least 91 records · Page 5Linked to original sources

Decreased expression of cold-inducible RNA-binding protein (CIRP) in male germ cells at elevated temperature.

Physiological scrotal hypothermia is necessary for normal spermatogenesis and fertility in mammals. Cirp is a recently identified cold-inducible RNA-binding protein that is inducible at 32 degrees C in mouse somatic cells in vitro. Cirp is constitutively expressed in the testis of mouse and structurally highly similar to RBM1, a candidate for the human azoospermia factor. To elucidate the role played by Cirp in spermatogenesis, we investigated its expression levels during spermatogenesis and after heat stress. In the mouse testis, cirp mRNA was detected in the germ cells, and the level varied depending on the stage of differentiation. Also, a high level of Cirp protein was detected immunohistochemically in the nucleus of primary spermatocytes. Expression of Cirp was decreased in the GC-2spd(ts) mouse germ cell line when culture temperature was raised from 32 degrees C to 37 degrees C. When mouse testis was exposed to heat stress by experimental cryptorchidism or immersion of the lower abdomen in warm (42 degrees C) water, the expression of Cirp was decreased in the testis within 6 hours after either treatment. In human testis with varicocele analyzed immunohistochemically, germ cells expressed less Cirp protein than those in the testis without varicocele. These results demonstrated that CIRP expression is down-regulated at elevated temperature in male germ cells of mice and humans. Analysis of Cirp expression in the testes will help elucidate the molecular mechanisms leading to male infertility.

Adult↗

Cyclin-D1-gene amplification is a more potent prognostic factor than its protein over-expression in human head-and-neck squamous-cell carcinoma.

To evaluate the prognostic significance of cyclin D1 protein/gene expressions in human head-and-neck squamous-cell carcinoma (HNSCC), we examined amplification of the cyclin-D1 gene (CCND1) by the differential PCR method and over-expression of cyclin-D1 protein by immunohistochemistry in 45 paraffin-embedded sections from HNSCC. Amplification of CCND1 was found in 10 (22%) cases and over-expression of cyclin D1 was found in 24 (53%) cases. CCND1 amplification was also found in 3 (25%) of 12 cases of dysplastic lesions adjacent to HNSCC. The overall 5-year survival of patients with CCND1 amplification or with protein over-production was significantly lower than that of patients without (p < 0.0001 and p < 0.05, respectively). However, with multivariate analysis, only amplification of CCND1 retained an independent prognostic value (p = 0.0018). These suggest that CCND1 amplification occurs at early stages of HNSCC tumorigenesis and is a more useful prognostic factor than over-expression of cyclin D1 in HNSCC.

Adult↗

Synergistic effect of MNU and DMBA in mammary carcinogenesis and H-ras activation in female Sprague-Dawley rats.

The combined application of N-methyl-N-nitrosourea (MNU) and 7,12-dimethylbenz[alpha]anthracene (DMBA) was compared with the administration of each carcinogen alone as to the effectiveness of the induction of mammary carcinomas and the influence of H-ras oncogene activation in female Sprague-Dawley rats. At 50 days of age, group 1 received 30 mg/kg MNU intraperitoneally (i.p.), group 2 received 30 mg/kg DMBA i.p., group 3 received 60 mg/kg MNU i.p., group 4 received 60 mg/ kg DMBA i.p., group 5 received 30 mg/kg MNU followed by 30 mg/kg DMBA i.p., group 6 received 30 mg/kg MNU i.p. and then 30 mg/kg DMBA intravenously (i.v.) and group 7 remained untreated. Animals were killed when the largest mammary tumor reached 1-2 cm in diameter or were necropsied when they were 30 weeks of age. MNU i.p. produced no deaths (groups 1 and 3), however, the i.p. administration of DMBA induced death due to peritonitis (groups 2, 4 and 5), whereas the i.v. administration of DMBA suppressed the death (group 6). All of the tumors produced by MNU were adenocarcinomas of mammary origin. In contrast, DMBA produced tumors of other than mammary origin. The combined treatment with DMBA and MNU increased the mammary carcinogenic effect; it significantly increased the mean number of mammary cancers per rat. With either carcinogen alone and in combination, the mammary carcinomas produced identical adenocarcinoma histology. Of the mammary carcinomas induced by the combined application of MNU and DMBA (group 6), all 11 tumors from five rats showed the GGA to GAA transitional mutation in H-ras codon 12 (38%) and all 18 tumors from the other 10 rats remained as wild-type. An H-ras point mutation at codon 61 was not detected.

9,10-Dimethyl-1,2-benzanthracene↗

Brca2 is required for embryonic cellular proliferation in the mouse.

Mutations of the tumor suppressor gene BRCA2 are associated with predisposition to breast and other cancers. Homozygous mutant mice in which exons 10 and 11 of the Brca2 gene were deleted by gene targeting (Brca2(10-11)) die before day 9.5 of embryogenesis. Mutant phenotypes range from severely developmentally retarded embryos that do not gastrulate to embryos with reduced size that make mesoderm and survive until 8.5 days of development. Although apoptosis is normal, cellular proliferation is impaired in Brca2(10-11) mutants, both in vivo and in vitro. In addition, the expression of the cyclin-dependent kinase inhibitor p21 is increased. Thus, Brca2(10-11) mutants are similar in phenotype to Brca1(5-6) mutants but less severely affected. Expression of either of these two genes was unaffected in mutant embryos of the other. This study shows that Brca2, like Brca1, is required for cellular proliferation during embryogenesis. The similarity in phenotype between Brca1 and Brca2 mutants suggests that these genes may have cooperative roles or convergent functions during embryogenesis.

Animals↗

Doxorubicin sensitizes human bladder carcinoma cells to Fas-mediated cytotoxicity.

BACKGROUND: The resistance of bladder carcinoma to anticancer chemotherapeutic agents remains a major problem. Hence, several immunotherapeutic approaches have been developed to treat the drug-resistant cancer cells. Fas antigen (Fas) and Fas ligand participate in cytotoxicity mediated by T lymphocytes and natural killer cells. Like Fas ligand, anti-Fas monoclonal antibody (MoAb) induces apoptosis of the cells expressing Fas. This study examined whether bladder carcinoma cells are sensitive to cytotoxicity mediated by anti-Fas MoAb and whether anticancer agents synergize with anti-Fas MoAb in cytotoxicity. METHODS: Cytotoxicity was determined by a 1-day microculture tetrazolium dye assay. Synergy was assessed by isobolographic analysis. RESULTS: The T24 human bladder carcinoma cell line constitutively expressed the Fas on the cell surface; however, T24 line was resistant to anti-Fas MoAb. Treatment of T24 cells with anti-Fas MoAb in combination with mitomycin C, methotrexate, or 5-fluorouracil did not overcome their resistance to these agents. However, treatment of T24 cells with a combination of anti-Fas MoAb and doxorubicin resulted in a synergistic cytotoxic effect. In addition, the doxorubicin-resistant T24 cells were sensitive to treatment with a combination of anti-Fas MoAb and doxorubicin. Synergy was also achieved in three other bladder carcinoma cell lines and four freshly derived human bladder carcinoma cells. Treatment with anti-Fas MoAb in combination with epirubicin or pirarubicin also resulted in a synergistic cytotoxic effect on T24 cells. The mechanisms of synergy were examined. Anti-Fas MoAb did not affect the intracellular accumulation of doxorubicin, the expression of P-glycoprotein, or the expression of the antioxidant glutathione S-transferase-pi mRNA. However, treatment with doxorubicin enhanced the expression of Fas on T24 cells. CONCLUSIONS: This study demonstrated that treatment of bladder carcinoma cells with doxorubicin sensitized the cells to lysis by anti-Fas MoAb. The synergistic effect obtained with established doxorubicin-resistant bladder carcinoma cells and freshly isolated bladder carcinoma cells suggests that drug-resistant bladder carcinoma cells can be sensitized by doxorubicin to Fas- and Fas ligant-mediated cytotoxicity by lymphocytes. Furthermore, the sensitization required low concentrations of doxorubicin, thus supporting the in vivo application of a combination of chemotherapy and immunotherapy in the treatment of drug-resistant and/or immunotherapy-resistant bladder carcinoma.

Antibiotics, Antineoplastic↗

Subcellular distribution of thallium: morphological and quantitative study in rat myocardium.

UNLABELLED: The purpose of this study is to determine the subcellular distribution of thallium (SDTl) by electron microscopy and a newly designed fixation method that makes insoluble grains of Tl visible. METHODS: To obtain the high dose necessary for electron microscopic visualization, we employed TlCl instead of 201TlCl. EM was performed in fixed rat myocardium resected at 20 min (early phase) and 3 hr (delay phase) after intravenous injection of TlCl. To fix Tl in the cell, we used orthovanadate in our fixative. Atomic absorption spectroscopy (AAS) of Tl and quantification of subcellular distribution of 201Tl (SD201Tl) were studied to prove the propriety of our fixation. RESULTS: AAS detected Tl in the Tl-loaded specimen but not in the control, indicating that Tl was the origin of the grains observed in the former. In the early phase, numerous grains were observed in mitochondria, sarcoplasmic reticulum (SR), myofibrils, and nuclei, but no such grains were visible in controls. In the delay phase, grains were retained in mitochondria, SR and nuclei, but not in myofibrils. Electron microscopic SDTl(%) correlated with SD201Tl(%) calculated from isolated fractions. CONCLUSION: In both the early and delay phases, mitochondria are the major site of Tl and 201Tl uptake.

Animals↗

Messenger ribonucleic acid expression of LH/hCG receptor gene in human ovarian carcinomas.

The mRNA expression of luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors was analysed by the RT-nested PCR method in five normal ovarian tissues, 62 ovarian tumours (5 benign, 7 borderline and 43 malignant epithelial tumours, 3 sex cord-stromal tumours and 4 germ cell tumours) and in 2 ovarian cancer cell lines. In normal ovaries, two cDNA fragments of different sizes were detected using primers designed to amplify a region including exon 9. Sequencing revealed that the larger fragment was derived from a full-length receptor, while the smaller fragment was a splice variant lacking exon 9. In ovarian tumours, the larger fragment of LH/hCG receptors was detected in 40% of the epithelial ovarian carcinomas, none of the germ cell tumours, all of the sex cord-stromal tumours and one of the 2 ovarian cancer cell lines. Immunohistochemistry confirmed the localisation of LH/hCG receptor protein in the tumour cells which correlated with mRNA expression. Patients with full-length LH/hCG receptors in carcinomas showed a better prognosis compared with those without the receptors.

Biomarkers, Tumor↗

An autopsy case of angioimmunoblastic T-cell lymphoma with a high content of epithelioid cells in the lymph node: immunohistochemical and genomic analyses.

A 79-year-old female developed red papulonodular eruptions on her extremities, facial erythema, generalized lymphadenopathy and high fever. Histopathology of an affected lymph node showed the features of angioimmunoblastic T-cell lymphoma with a high content of epithelioid cells. She died about two years after the onset despite therapy. Genomic Southern blotting and immunostaining of the lymph nodes were performed twice. In August of 1993, Southern blotting did not show any rearrangement of the immunoglobulin or the T-cell receptor (TCR) gene. Small or medium-sized lymphoid cells were positive for CD4 or CD8 (CD4:CD8 = 2:1). However, in September of 1994 (at autopsy), rearrangements of TCK C beta 1, J beta 2 and J gamma genes were observed. Small or medium-sized lymphoid cells were positive for CD4, but negative for CD8. Several large cells were positive for Latent Membrane Protein 1 (LMP1) of the Epstein-Barr virus (EBV). Our results proved that selective oligoclonal proliferation of tumor cells (probably CD4+) accompanied the disease progress.

Aged↗

Overexpression of integrin-associated protein (CD47) in rat kidney treated with a renal carcinogen, ferric nitrilotriacetate.

An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces renal proximal tubular necrosis, a consequence of free radical-associated damage, that ultimately leads to a polycystic change of the renal cortex and a high incidence of renal cell carcinoma (RCC) in rodents. The differential display technique was used to search for inducible genes in the kidney of male Wistar rats treated with Fe-NTA and in the induced RCCs. Six fragments were selected that showed specific quantitative changes in mRNA. Two of them exhibited similar patterns in northern blots as well. One fragment showed a high homology (89%) to murine integrin-associated protein (IAP; CD47). We thus cloned rat IAP cDNA including the entire coding region for use in further analysis. Rat IAP cDNA showed a 21-amino-acid deletion that was also observed in human, but not in mouse. Northern blots revealed that IAP was consistently overexpressed in non-tumorous parts of the kidney (2.4-fold increase, n = 9, P < 0.0001) as compared with matched controls 1 to 2 years after Fe-NTA treatment. IAP overexpression of more than 2.9-fold was found in 25% (2/8) of RCCs studied, and was limited to cases of a high histological grade and lung metastasis. Unexpectedly, IAP expression was higher in the non-tumorous part of the kidney after Fe-NTA treatment (2.8-fold) than in RCC (1.5-fold) in each case (n = 4, P < 0.05). Abundant expression of IAP mRNA in the renal tubular epithelium after Fe-NTA treatment and RCC cells was observed by in situ hybridization. The results suggest that IAP overexpression may be associated with Fe-NTA-induced renal cortical tubular damage and regeneration that lead to a polycystic state, and with tumor progression and metastasis of the induced RCCs.

Amino Acid Sequence↗

A case of dyshormonogenetic goiter complicated with growth hormone deficiency.

A 17-year-old male patient with dyshormonogenetic goiter complicated with follicular adenoma and growth hormone deficiency is described. He had short stature (-2.3 SD), diffuse goiter and a particularly large nodule in the right lobe of the thyroid gland. The endocrinological studies revealed slight hypothyroidism. He underwent surgical removal of the tumor, diagnosed histopathologically as follicular adenoma, embryonal type; and the diffuse goiter was diagnosed as dyshormonogenetic goiter. It was speculated that long-term hypersecretion of thyroid stimulating hormone (TSH) caused adenoma in the thyroid gland. Although the goiter disappeared after oral thyroxine replacement therapy, his height gain remained poor. Then, he was diagnosed partial growth hormone deficiency, and growth hormone therapy improved his height gain. It has been reported that a high percentage of patients with congenital hypothyroidism have additional anomalies. This is, however, the first reported case of dyshormonogenetic goiter complicated with growth hormone deficiency.

Adenoma↗

Early-childhood progressive myoclonus epilepsy presenting as partial seizures in dentatorubral-pallidoluysian atrophy.

PURPOSE: We explored the characteristics of epileptic seizures of progressive myoclonus epilepsy (PME) in 2 brothers with dentatorubral-pallidoluysian atrophy (DRPLA). METHODS: We obtained the case history of the siblings and ictal and interictal EEGs. Postmortem examination or demonstration of elongated CAG repeat in the gene for DRPLA was used to confirm the diagnosis. RESULTS: Two Japanese siblings developed PME characterized by versive or himiclonic seizures with or without secondarily generalized tonic-clonic convulsions. The elder brother regressed mentally and exhibited increasing spasticity after age 1 year. Myoclonus and seizures developed at age 4 years. The younger brother had shown psychomotor retardation before age 4 years, when he began to deteriorate further neurologically as the elder brother had. He also developed myoclonus and seizures at that age. Seizures in both patients remained partial until their deaths at ages 19 and 15 years, respectively. Ictal EEG verified partial onset of seizure evolving to generalized tonic-clonic seizure (GTCS). Interictal EEGs showed multifocal paroxysmal discharges with little or no diffuse paroxysms. Postmortem examination or genetic study confirmed the diagnosis of DRPLA. CONCLUSIONS: Seizures of patients with DRPLA may present as partial seizures in children with early-onset PME.

Adolescent↗

Examination of diarrheagenicity of cytolethal distending toxin: suckling mouse response to the products of the cdtABC genes of Shigella dysenteriae.

Some strains of Escherichia coli, Shigella spp., and Campylobacter spp. that have been implicated in diarrheal disease produce cytolethal distending toxin (CDT). CDT induces unique morphological changes in Chinese hamster ovary cells, but its association with diarrheal disease is unclear. We studied the diarrheagenicity of CDT using the cdt genes that we originally cloned from Shigella dysenteriae. The cdt genes were subcloned into a high-copy-number plasmid in E. coli JM109 to achieve high-level CDT production into the culture supernatant. An isogenic CDT- derivative was constructed by deletion of the 0.9-kb sequence internal to the cdt genes. A suckling mouse model was established, in which the intragastrically administered culture supernatant of the CDT+ E. coli strain induced excretion of loose and/or watery feces more often than did that of the CDT- strain in 24 h. The partially purified CDT preparation induced profuse watery diarrhea by 12 h in this model. High-level intestinal fluid accumulation in 4 h appeared to be related to the watery diarrhea. The results indicate that CDT is diarrheagenic to suckling mice and suggest that diarrheagenicity is dependent on CDT level. The preparations containing wild-type CDT induced tissue damage (necrosis and reparative hyperplasia) in the descending colon, whereas the tissues of the small intestines remained apparently intact. Association between the colonic damage and diarrhea is unclear and needs further investigation.

Animals↗

Clinical significance of serum p53 antigen in patients with pancreatic carcinomas.

BACKGROUND: Alterations in the p53 gene are often found in pancreatic cancer, and accumulation of the p53 protein has been noted in tumour cells. AIMS: To investigate whether serum p53 protein concentrations could be used as markers for p53 gene mutations in neoplasms of the pancreas. METHODS: Serum p53 protein concentrations were determined by an enzyme linked immunosorbent assay (ELISA) in 104 cases of pancreatic adenocarcinoma, and 61 matched formalin fixed tissue sections were also stained by an anti-p53 DO-7 monoclonal antibody. RESULTS: The mean serum concentration of p53 protein in the adenocarcinoma patients was 0.27 (SEM 0.02) ng/ml, and was significantly higher than in 35 healthy blood donors (0.15 (0.02) ng/ml, SD = 0.11) or in 15 cases of chronic pancreatitis (0.15 (0.02) ng/ml). Adopting an arbitrary cut off value for the serum p53 protein concentration of 0.37 ng/ml, which corresponded to a value 2 SD above the mean value from the healthy blood donors, positive serum p53 protein concentrations were found in 23 out of 104 (22.1%) patients with adenocarcinomas examined, 16 out of 47 (34.0%) patients with carcinomas with distant metastases, but only seven of 57 patients (12.3%) with carcinomas without metastases (p < 0.05). In 11 patients with pancreatic adenocarcinomas, the mean serum p53 protein concentration after tumour resection was 0.21 (0.05) ng/ml, and had decreased compared with the preoperative concentrations (0.25 (0.05) ng/ml) (P < 0.05). There were no significant associations between the serum concentrations of p53 protein and serum concentrations of markers such as CA19-9 or CEA; however, serum concentrations of p53 protein demonstrated a potential role as an additional tumour marker. Immunohistochemical studies disclosed that the p53 protein was expressed in 28 out of 61 pancreatic adenocarcinomas (45.9%). Serum p53 protein concentrations in the positively immunostained cases were significantly higher than in the negatively immunostained cases (0.35 (0.05) ng/ml v 0.15 (0.01) ng/ml; p < 0.005). Furthermore, positive immunostaining for p53 protein was found in eight out of 10 (80%) serum positive p53 protein cases with adenocarcinomas. CONCLUSION: An increase in serum p53 protein concentrations appears during the progression of pancreatic adenocarcinoma and correlates with the accumulation of p53 protein as a result of a mutation of the p53 gene. An analysis of p53 antigen concentrations can detect p53 gene alterations, which could be useful for the selection of treatment regimens.

Adenocarcinoma↗

'Distinct cellular localization' of the messenger ribonucleic acid for prostaglandin E receptor subtypes in the mouse uterus during pseudopregnancy.

As an initial step to clarify the mechanisms of various uterine actions of PGE2, expression patterns of the messenger RNAs (mRNAs) for four subtypes of PGE receptors, EP1, EP2, EP3, and EP4, were investigated in the mouse uterus during pseudopregnancy. Relative expression levels were investigated by Northern blot analysis of mRNA levels in uteri obtained on days 0, 1, 3, 5, 7, and 9 of pseudopregnancy (day 0 = 48 h after PMSG injection), and cellular localization was determined by in situ hybridization in uteri obtained on days 0 and 5. EP2 mRNA was specifically expressed on day 5, and its expression was confined to the luminal epithelium. On the other hand, the level of the EP3 mRNA expression progressively increased until day 5. Cell populations expressing the EP3 mRNA were confined to the longitudinal smooth muscle on day 0, but they changed to the circular smooth muscle on day 5. The expression level of EP4 mRNA was low on days 0 and 1, but it became high on days 3 and 5. On day 0, EP4 mRNA was localized to the luminal epithelium. On day 5, diffuse, but significant, EP4 expression was observed over the endometrial stroma and epithelium. No EP1 mRNA signals were observed. Transient expression of EP2 on day 5 of pseudopregnancy in the luminal epithelium suggests its involvement in blastocyst implantation signaling. EP4 in the endometrial stroma is suggested to be involved in decidual transformation of the stromal cells, whereas EP3 in the myometrium is believed to be involved in regulation of myometrial activity.

Animals↗

Messenger ribonucleic acid expression of heat shock proteins HSP70 and HSP90 in human endometrium and myometrium during the menstrual cycle.

Heat shock proteins of 72 and 90 kDa (HSP70, HSP90) are thought to be involved in the functional modulation of sex steroid receptors. To examine the expression and transcriptional regulation of HSP70 and HSP90 in both the endometrium and myometrium, messenger ribonucleic acid (mRNA) and protein level expression of these HSPs during various phases of the menstrual cycle were analyzed by Northern blotting and immunohistochemistry. In the endometrium, HSP70 mRNA levels increased during the secretory phase compared with levels during the proliferative phase; this is consistent with the stronger immunostaining of HSP70 in glandular cells in the secretory phase. In the myometrium, however, mRNA and protein expression of HSP70 were higher in the proliferative phase than in the secretory phase. This indicates that the regulatory mechanism of HSP70 expression during the menstrual cycle differs between the endometrial glandular cells and myometrial smooth muscle cells and may be correlated with the period of sex steroid-related functions of the respective cells. Expression of the HSP90 mRNA and protein in the myometrium was higher in the proliferative phase than in the secretory phase. In the endometrium, HSP90 immunostaining in the glandular cells was also stronger in the proliferative phase, although expression of HSP90 mRNA was not significantly different between the tissues of the two phases.

Adult↗

Monoclonal antibodies against pig ovarian follicular granulosa cells induce apoptotic cell death in cultured granulosa cells.

Two monoclonal antibodies capable of inducing granulosa cell apoptosis were produced against granulosa cells prepared from antral follicles of pig ovaries. The healthy follicles, 4-5 mm in diameter, were dissected from the ovaries of gilts, and then granulosa cells were isolated. BALB/c female mice were immunized with the isolated granulosa cells. Antibodies against the granulosa cells were detected by immunofluorescent staining using frozen ovarian sections. The isolated spleen cells prepared from immunized mice producing antibodies against the granulosa cells were fused with Sp2/O-Ag 14 mouse myeloma cells by standard hybridization techniques. Two hybridoma clones, PFG-1 and PFG-2, which produced specific IgM antibodies against granulosa cells were selected. Western blotting analysis revealed that PFG-1 and PFG-2 antibodies specifically recognized cell-membrane proteins with molecular weights of 55 and 70 kD and isoelectric points of 5.9 and 5.4, respectively. The monoclonal antibodies immunohistochemically reacted with granulosa cells of healthy follicles. When the isolated granulosa cells prepared from healthy follicles were cultured in medium containing 0.1 or 10 micrograms/m/PFG-1 or PFG-2 antibodies, respectively, the cells underwent apoptosis as determined by nuclear morphology, DNA electrophoresis and flow cytometric analysis. In conclusion, these two monoclonal antibodies against granulosa cells have cell-killing activity in cultured granulosa cells.

Animals↗

Lectin histochemistry in rat liver fibrosis induced by heterologous serum sensitization.

The localization of carbohydrates in rat livers with fibrosis induced by heterologous serum was examined by lectin histochemical and biochemical techniques. Twenty-four lectins were used to visualize the different carbohydrates in paraffin sections of normal and fibrotic liver tissues. No differences in staining patterns of these lectins were observed between normal and fibrotic livers in hepatocyte cell membranes including bile canaliculi, sinusoidal endothelial, or bile ductal cells. Kupffer cells strongly stained with Vicia villosa agglutinin (VVA) were seen only in the periportal zone of the normal liver, but they were observed in the periportal zone and scattered throughout the pseudolobular zone in the fibrotic liver. The cytoplasm of some hepatocytes was strongly stained by Bandeiraea simplicifolia lectin-I (BSL-I). BSL-I positive hepatocytes in normal liver were localized in the periportal zone, but those in the fibrotic liver were scattered in the periportal and perifibrous zones. After polyacrylamide gel electrophoresis of liver glycoproteins, differences in molecular sizes of BSL-I positive glycoproteins (79 and 81 kD) were detected by lectin blotting. Cell density of perifibrous BSL-I positive hepatocytes may be useful as a diagnostic parameter for liver fibrosis and/or cirrhosis. Two distinct staining patterns with twelve lectins were observed in fibrotic septa of the fibrotic liver. The fibrotic septa were stained with six characteristic lectins, and the centrilobular septa were stained with all these twelve of lectins. Histopathological assessment of the centrilobular fibrotic septa stained with these characteristic lectins may contribute to the diagnosis and prognosis of hepatic fibrosis.

Animals↗