Biomedical subjects

F Tateyama

Publications and source records attributed to F Tateyama.

3 recordsLinked to original sources

PubMed2001

Interleukin-1beta is an autocrine growth factor of rat glomerular epithelial cells in culture.

BACKGROUND: The proliferation of glomerular epithelial cells (GEC) is usually observed in crescentic glomerulonephritis. However, the regulation of GEC proliferation is not fully understood. Although it is known that interleukin-1beta (IL-1beta) has a mitogenic effect on mesangial cells and is produced by mesangial cells, the effect of this cytokine on GEC proliferation is not known. We investigated whether cultured rat GEC could produce IL-1beta, and the role of IL-1beta on GEC proliferation. METHODS: Cultured rat GEC from 24th to 36th passage were used. GEC proliferation was evaluated with a colorimetric assay using the tetrazolium salt. GEC were incubated in K1 medium for 72 h and IL-1beta in the culture supernatants was measured by specific enzyme-linked immunosorbent assay (ELISA). IL-1beta in GEC supernatants was examined by immunoblot analysis. IL-1beta mRNA expression in GEC was examined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: IL-1beta showed a mitogenic effect on GEC, while interferon-gamma (IFN-gamma) and heparin inhibited GEC proliferation. Moreover, GEC proliferation cultured with K1 medium was partially inhibited by anti-IL-1beta neutralizing antibody. Amounts of IL-1beta in the culture supernatants increased over time (24-72 h). K1 medium increased IL-1beta production by GEC, while IFN-gamma or heparin did not change IL-1beta production. Immunoblot analysis revealed 17 kD protein of IL-1beta in the concentrated GEC supernatants. RT-PCR also demonstrated mRNA expression of IL-1beta in GEC. CONCLUSIONS: Our data indicate that IL-1beta is an autocrine growth factor for GEC and may have an important role in the regulation of GEC proliferation.

3T3 Cells↗

PubMed2000

Platelet-derived growth factor, basic fibroblast growth factor, and interferon gamma increase type IV collagen production in human fetal mesangial cells via a transforming growth factor-beta-dependent mechanism.

BACKGROUND: Glomerulosclerosis is characterized by glomerular accumulation of extracellular matrix following mesangial cell proliferation. The precise pathomechanism of glomerulosclerosis is still undetermined. Platelet-derived growth factor (PDGF) and basic fibroblast growth factor (b-FGF) are known to be mitogenic for mesangial cells, and interferon gamma (IFN-gamma) is known to have an inhibitory effect on mesangial cell proliferation. We attempted to clarify the role of these cytokines on mesangial matrix production using cultured human fetal mesangial cells (HMC). METHODS: HMC were incubated with these cytokines for 24-72 h and the levels of type IV collagen and TGF-beta in the cell supernatants were measured by enzyme immunoassay. RESULTS: PDGF, b-FGF, and IFN-gamma stimulated type IV collagen production by HMC in a dose- and time-dependent manner. The anti-TGF-beta neutralizing antibody clearly inhibited their stimulatory effect on type IV collagen production. PDGF and b-FGF also stimulated TGF-beta production by HMC in a dose-dependent manner, although IFN-gamma did not. CONCLUSION: PDGF, b-FGF, and IFN-gamma stimulate type IV collagen production in cultured HMC via a TGF-beta-dependent mechanism.

Antibodies↗

PubMed2000

C-Type natriuretic peptide inhibits proliferation and monocyte chemoattractant protein-1 secretion in cultured human mesangial cells.

BACKGROUND: Mesangial cell proliferation and matrix accumulation are hallmarks of various progressive glomerular diseases. We examined whether C-type natriuretic peptide (CNP) that is known to regulate the proliferation of vascular smooth muscle cells could modulate these pathological processes using human glomerular mesangial cells (GMCs) in culture. METHODS: Proliferation of GMCs cultured with different concentrations of CNP-22 for 48 h was determined by a colorimetric assay using a tetrazolium salt. Monocyte chemoattractant protein-1 (MCP-1) and type IV collagen secretion into the culture media by GMCs in the presence or absence of CNP-22 were evaluated by ELISA. Expression of mRNA for natriuretic peptide receptor B (NPR-B), a specific receptor for CNP, was examined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: CNP-22 (1-10 microM) inhibited serum-induced GMC growth in a dose-dependent manner. The amount of MCP-1 in the culture supernatant was increased approximately 2.4-fold by 5 microg/ml of lipopolysaccharide. This increase was inhibited by CNP-22 at 0.1-1 microM in a dose-dependent fashion. CNP-22 (10 microM) inhibited GMC type IV collagen secretion stimulated by 20 ng/ml of platelet-derived growth factor. Expression of NPR-B mRNA was confirmed in GMCs by RT-PCR. CONCLUSIONS: CNP suppresses GMC proliferation and MCP-1 and type IV collagen secretion by GMCs. It may have a therapeutic potential against human proliferative glomerular diseases, especially those with the involvement of monocytes.

Cell Division↗