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Title: | IL-10 induces mesangial cell proliferation via a PDGF-dependent mechanism. | Authors: | Hurst L.A.;Atkins R.C.;Chadban S.J.;Nikolic-Paterson D.J. ;Robertson T.E. | Institution: | (Robertson, Nikolic-Paterson, Hurst, Atkins, Chadban) Department of Nephrology, Monash Medical Centre, Clayton, Vic., Australia (Nikolic-Paterson, Atkins, Chadban) Monash University, Department of Medicine, Monash Medical Centre, Clayton, Vic., Australia (Chadban) Renal Medicine, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Australia | Issue Date: | 18-Oct-2012 | Copyright year: | 2002 | Publisher: | Blackwell Publishing Ltd (9600 Garsington Road, Oxford OX4 2XG, United Kingdom) | Place of publication: | United Kingdom | Publication information: | Clinical and Experimental Immunology. 130 (2) (pp 241-244), 2002. Date of Publication: 2002. | Abstract: | Interleukin-10 (IL-10) is a mesangial cell growth factor in vivo and in vitro. However, the mechanism by which IL-10 exerts its mitogenic activity is not known. The aim of this study was to determine whether IL-10 induces mesangial cell proliferation in a PDGF-dependent or independent fashion. A well-characterized rat mesangial cell line (1097) was used in a series of cell proliferation experiments in which cells were serum-starved and then incubated with recombinant IL-10 in the presence or absence of STI 571 (a specific inhibitor of signalling via the PDGF-alpha and beta receptors) or a neutralizing anti-PDGF-AB antibody. IL-10 induced significant mesangial cell proliferation at 24 and 48 h after cytokine addition. This response was inhibited totally by the addition of STI-571, demonstrating that IL-10 mitogenic activity has an absolute requirement for signalling through the PDGF receptor. In further studies, it was found that STI-571 could be added 24 h after IL-10 stimulation and still exert a profound inhibition of IL-10 mitogenic activity. The ability of a neutralizing anti-PDGF-AB antibody to inhibit completely IL-10-induced mesangial cell proliferation confirmed that IL-10 acts via induction of an autocrine PDGF response rather than the possibility that IL-10 may transactivate the PDGF receptor in a PDGF-independent fashion. In conclusion, this study has demonstrated that IL-10 induces mesangial cell proliferation via an autocrine PDGF-mediated mechanism. Thus, therapies which antagonize PDGF signalling will also inhibit any contribution of IL-10 to mesangial proliferation. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1046/j.1365-2249.2002.01975.x | PubMed URL: | 12390311 [http://www.ncbi.nlm.nih.gov/pubmed/?term=12390311] | ISSN: | 0009-9104 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/33055 | Type: | Article |
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