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• W2020478425 abstract "Nephrotoxicity of cyclosporine (CsA) is an important factor limiting its effectiveness in transplantation and renal diseases. However, the mechanisms causing this toxicity are not clearly defined. Previous studies of experimental models of CsA nephropathy reported that increased expression of osteopontin (OPN) correlated with the severity of renal macrophage infiltration and fibrosis. In this issue of Kidney International, Mazzali et al tested the hypothesis that OPN was an important mediator of CsA nephropathy through studies of a CsA model in mice with a targeted deletion of the OPN gene1.Mazzali M. Hughes J. Dantas M. et al.Effects of cyclosporine in osteopontin null mice.Kidney Int. 2002; 62: 78-85Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar. These studies showed that mice lacking OPN (OPN-/-) all survived the 2 weeks of CsA treatment and showed less severe CsA nephrotoxicity with less interstitial collagen deposition and cortical infiltration of macrophages and less arteriopathy than control (OPN+/+) mice. Furthermore, half of the OPN+/+ mice died during the period of CsA treatment. Mazzali et al1.Mazzali M. Hughes J. Dantas M. et al.Effects of cyclosporine in osteopontin null mice.Kidney Int. 2002; 62: 78-85Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar correctly conclude that “OPN appears to have a modest role in macrophage recruitment and in the development of fibrosis in the murine CsA nephropathy model.” These studies add to a growing body of information indicating that OPN is a multifunctional molecule with roles in the responses to a multitude of injurious stimuli. The availability of OPN-/- mice for analysis has been an important resource contributing to the development of our current insights about OPN. These actions may be both pro- and anti-inflamatory and their protective capacities have been recently emphasized2.Denhardt D.T. Noda M. O'Regan A.W. et al.Osteopontin as a means to cope with environmental insults: regulation of inflammation, tissue remodeling, and cell survival.J Clin Invest. 2001; 107: 1055-1061Crossref PubMed Scopus (870) Google Scholar. For example, the net effect of OPN in the host response to infections with certain microorganisms is clearly protective3.Nau G.J. Liaw L. Chupp G.L. et al.Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin.Infect Immun. 1999; 67: 4223-4230Crossref PubMed Google Scholar. However, as illustrated in the paper by Mazzali et al1.Mazzali M. Hughes J. Dantas M. et al.Effects of cyclosporine in osteopontin null mice.Kidney Int. 2002; 62: 78-85Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar, OPN may enhance, rather than limit, processes causing tissue pathology within the kidney. The oral cavity is another site of inflamation in patients treated with CsA. Gingivitis is a well-recognized side effect of CsA. OPN was markedly increased in surgically removed hypertrophied gingival tissue from patients treated with CsA (Bahateq M and Farach-Carson MC, personal communication, 2002). Although not explored in detail, detecting the development of ataxia in some OPN+/+ mice (but not in OPN-/- mice) suggests that OPN might also mediate neural toxicity caused by CsA. Evidence that OPN may play an important role in inflammatory responses within the central nervous system has been recently provided by studies of OPN-/- mice in experimental autoimmune encephalomyelitis, (EAE), a model for multiple sclerosis, a disease with increased OPN transcripts4.Chabas D. Baranzini S.E. Mitchell D. et al.The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease.Science. 2001; 294: 1731-1735Crossref PubMed Scopus (725) Google Scholar. Although EAE could be induced in OPN -/- mice, the mice were resistant to progressive EAE and had cytokine profiles that were more favorable to self-limited pathologic changes than the profiles of OPN+/+ mice4.Chabas D. Baranzini S.E. Mitchell D. et al.The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease.Science. 2001; 294: 1731-1735Crossref PubMed Scopus (725) Google Scholar. The authors of this study conclude that OPN “may offer a potential target in blocking development of progressive multiple sclerosis”4.Chabas D. Baranzini S.E. Mitchell D. et al.The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease.Science. 2001; 294: 1731-1735Crossref PubMed Scopus (725) Google Scholar. Insights derived from such studies of OPN in other tissues are likely to become important components of our understanding of the role of OPN in renal diseases." @default.
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• W2020478425 date "2002-07-01" @default.
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• W2020478425 title "Osteopontin in cyclosporine toxicity" @default.
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• W2020478425 doi "https://doi.org/10.1046/j.1523-1755.2002.00440.x" @default.
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