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Involvement of TGF-beta signal for peritoneal sclerosing in continuous ambulatory peritoneal dialysis.
J Nephrol. 2003 Jan-Feb; 16(1):95-102.JN

Abstract

BACKGROUND

Functional failure of the peritoneal membrane is the most serious problem in long-term continuous ambulatory peritoneal dialysis (CAPD). Transforming growth factor-beta (TGF-ss) is one of the key mediators of fibrosis in some organs, and is thought to be involved in peritoneal alterations. In this study, we examined the role of TGF-beta1/TGF-ss receptors for human peritoneal mesothelial cells (HPMCs) and fibroblasts, and their interactions in CAPD patients.

METHODS

HPMCs were cultured for 48 h in a medium containing normal- dose glucose (7 mM), high-dose glucose (30 mM) and mannitol as an osmotic agent, equal to 30 mM glucose. Cell proliferation was observed using the Tetra Color One assay. The concentration of TGF-beta1 in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). The expression of TGF-ss receptor types I and II was observed by flow cytometry. HPMCs and fibroblasts were co-cultured and assayed using transwell inserts in order to identify the effects of the high-concentration glucose solution.

RESULTS

HPMC proliferation was inhibited by the high concentration of glucose but not by mannitol. The inhibition was abrogated by the neutralizing antibody for TGF-beta1. TGF-beta1 was induced by a high concentration of glucose but not by mannitol. The expression of both TGF-ss receptors was augmented in culture with the high concentration of glucose but not with mannitol. In the co-culture assay, the number of HPMCs was decreased and fibroblasts were significantly increased in culture with the high concentration of glucose.

CONCLUSIONS

A high concentration of glucose induced a large amount of TGF-beta1 and enhanced the expression of TGF-ss receptors. HPMCs were sensitive to TGF-beta1 in response to a high concentration of glucose. These data suggest that TGF-beta1 from HPMCs exposed to a high concentration of glucose down-regulates the proliferation of HPMCs and accelerates peritoneal fibrosis.

Authors+Show Affiliations

Department of Internal Medicine, Division of Hematology, Nephrology and Rheumatology, Kinki University School of Medicine, Osaka, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12649540

Citation

Naiki, Yoshito, et al. "Involvement of TGF-beta Signal for Peritoneal Sclerosing in Continuous Ambulatory Peritoneal Dialysis." Journal of Nephrology, vol. 16, no. 1, 2003, pp. 95-102.
Naiki Y, Maeda Y, Matsuo K, et al. Involvement of TGF-beta signal for peritoneal sclerosing in continuous ambulatory peritoneal dialysis. J Nephrol. 2003;16(1):95-102.
Naiki, Y., Maeda, Y., Matsuo, K., Yonekawa, S., Sakaguchi, M., Iwamoto, I., Hasegawa, H., & Kanamaru, A. (2003). Involvement of TGF-beta signal for peritoneal sclerosing in continuous ambulatory peritoneal dialysis. Journal of Nephrology, 16(1), 95-102.
Naiki Y, et al. Involvement of TGF-beta Signal for Peritoneal Sclerosing in Continuous Ambulatory Peritoneal Dialysis. J Nephrol. 2003 Jan-Feb;16(1):95-102. PubMed PMID: 12649540.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of TGF-beta signal for peritoneal sclerosing in continuous ambulatory peritoneal dialysis. AU - Naiki,Yoshito, AU - Maeda,Yasuhiro, AU - Matsuo,Koki, AU - Yonekawa,Satoru, AU - Sakaguchi,Mika, AU - Iwamoto,Ichiro, AU - Hasegawa,Hirofumi, AU - Kanamaru,Akihisa, PY - 2002/07/11/received PY - 2002/11/17/accepted PY - 2002/11/06/revised PY - 2003/3/22/pubmed PY - 2003/7/24/medline PY - 2003/3/22/entrez SP - 95 EP - 102 JF - Journal of nephrology JO - J Nephrol VL - 16 IS - 1 N2 - BACKGROUND: Functional failure of the peritoneal membrane is the most serious problem in long-term continuous ambulatory peritoneal dialysis (CAPD). Transforming growth factor-beta (TGF-ss) is one of the key mediators of fibrosis in some organs, and is thought to be involved in peritoneal alterations. In this study, we examined the role of TGF-beta1/TGF-ss receptors for human peritoneal mesothelial cells (HPMCs) and fibroblasts, and their interactions in CAPD patients. METHODS: HPMCs were cultured for 48 h in a medium containing normal- dose glucose (7 mM), high-dose glucose (30 mM) and mannitol as an osmotic agent, equal to 30 mM glucose. Cell proliferation was observed using the Tetra Color One assay. The concentration of TGF-beta1 in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). The expression of TGF-ss receptor types I and II was observed by flow cytometry. HPMCs and fibroblasts were co-cultured and assayed using transwell inserts in order to identify the effects of the high-concentration glucose solution. RESULTS: HPMC proliferation was inhibited by the high concentration of glucose but not by mannitol. The inhibition was abrogated by the neutralizing antibody for TGF-beta1. TGF-beta1 was induced by a high concentration of glucose but not by mannitol. The expression of both TGF-ss receptors was augmented in culture with the high concentration of glucose but not with mannitol. In the co-culture assay, the number of HPMCs was decreased and fibroblasts were significantly increased in culture with the high concentration of glucose. CONCLUSIONS: A high concentration of glucose induced a large amount of TGF-beta1 and enhanced the expression of TGF-ss receptors. HPMCs were sensitive to TGF-beta1 in response to a high concentration of glucose. These data suggest that TGF-beta1 from HPMCs exposed to a high concentration of glucose down-regulates the proliferation of HPMCs and accelerates peritoneal fibrosis. SN - 1121-8428 UR - https://www.unboundmedicine.com/medline/citation/12649540/Involvement_of_TGF_beta_signal_for_peritoneal_sclerosing_in_continuous_ambulatory_peritoneal_dialysis_ DB - PRIME DP - Unbound Medicine ER -