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Title: | Cyclophilin a promotes inflammation in acute kidney injury but not in renal fibrosis. | Authors: | Ma F.Y.;Leong K.G.;Ozols E.;Kanellis J.;Nikolic-Paterson D.J. | Monash Health Department(s): | Nephrology | Institution: | (Leong, Ozols, Kanellis, Nikolic-Paterson, Ma) Department of Nephrology, Monash Health, Monash Medical Centre, Clayton, VIC 3168, Australia (Leong, Ozols, Kanellis, Nikolic-Paterson, Ma) Monash University Centre for Inflammatory Diseases, Monash Medical Centre, Clayton, VIC 3168, Australia | Issue Date: | 18-Jun-2020 | Copyright year: | 2020 | Publisher: | MDPI AG (Postfach, Basel CH-4005, Switzerland. E-mail: rasetti@mdpi.com) | Place of publication: | Switzerland | Publication information: | International Journal of Molecular Sciences. 21 (10) (no pagination), 2020. Article Number: 3667. Date of Publication: 02 May 2020. | Journal: | International Journal of Molecular Sciences | Abstract: | Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease is largely unknown. This study investigates the contribution of CypA in two different types of kidney injury: acute tubular necrosis and progressive interstitial fibrosis. CypA (Ppia) gene deficient and wild type (WT) littermate controls underwent bilateral renal ischaemia/reperfusion injury (IRI) and were killed 24h later or underwent left unilateral ureteric obstruction (UUO) and were killed 7 days later. In the IRI model, CypA-/- mice showed substantial protection against the loss of renal function and from tubular cell damage and death. This was attributed to a significant reduction in neutrophil and macrophage infiltration since CypA-/- tubular cells were not protected from oxidant-induced cell death in vitro. In the UUO model, CypA-/- mice were not protected from leukocyte infiltration or renal interstitial fibrosis. In conclusion, CypA promotes inflammation and acute kidney injury in renal IRI, but does not contribute to inflammation or interstitial fibrosis in a model of progressive kidney fibrosis.Copyright © 2020 by the authors. Licensee MDPI, Basel, Switzerland. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.3390/ijms21103667 | PubMed URL: | 32455976 [http://www.ncbi.nlm.nih.gov/pubmed/?term=32455976] | ISSN: | 1661-6596 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/29288 | Type: | Article | Subjects: | *inflammation interleukin 2/ec [Endogenous Compound] kidney injury molecule 1/ec [Endogenous Compound] Klotho protein/ec [Endogenous Compound] lymphocyte antigen/ec [Endogenous Compound] tumor necrosis factor *acute kidney failure animal cell animal experiment animal model animal tissue article CD3+ T lymphocyte cell damage cell death cell infiltration controlled study female gene deletion histology immunohistochemistry kidney fibrosis kidney function kidney tubule necrosis macrophage male mouse mRNA expression level neutrophil nonhuman protein expression real time polymerase chain reaction reperfusion injury T lymphocyte activation TUNEL assay ureter obstruction alpha smooth muscle actin/ec [Endogenous Compound] angiotensin II CD68 antigen/ec [Endogenous Compound] collagen type 1/ec [Endogenous Compound] creatinine/ec [Endogenous Compound] *cyclophilin A/ec [Endogenous Compound] inducible nitric oxide synthase/ec [Endogenous Compound] inflammation interleukin 2 kidney injury molecule 1 Klotho protein lymphocyte antigen tumor necrosis factor acute kidney failure CD3+ T lymphocyte cell damage cell infiltration gene deletion histology immunohistochemistry kidney fibrosis kidney function kidney tubule necrosis macrophage mRNA expression level neutrophil protein expression real time polymerase chain reaction reperfusion injury T lymphocyte activation TUNEL assay ureter obstruction alpha smooth muscle actin angiotensin II CD68 antigen collagen type 1 creatinine cyclophilin A inducible nitric oxide synthase controlled study female gene deletion histology immunohistochemistry *inflammation kidney fibrosis kidney function kidney tubule necrosis macrophage male mouse mRNA expression level neutrophil nonhuman protein expression real time polymerase chain reaction reperfusion injury T lymphocyte activation TUNEL assay ureter obstruction animal experiment *acute kidney failure animal model animal tissue Article CD3+ T lymphocyte cell damage cell death cell infiltration animal cell |
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