Urinary heat shock protein-72 excretion in clinical and experimental renal ischemia

Mueller, Thomas; Bidmon, Bettina; Pichler, Patrick; Arbeiter, Klaus; Ruffingshofer, Dagmar; VanWhy, Scott K.; Aufricht, Christoph

doi:10.1007/s00467-002-1037-5

Cited by 28 publications

(12 citation statements)

References 14 publications

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“…In agreement, we found that patients with severe IgA nephropathy had a predominant interstitial TLR2 expression with occasionally apical staining of tubuli. The apical expression of TLR2 on tubular cells could be optimal for interaction with filtered or leaked stress ligands [30]–[32] or with ligands that are expressed apically [33]. Indeed, we found a profound upregulation of tubular biglycan with expression at the apical side and in the cytoplasm during UUO injury.…”

Section: Discussionmentioning

confidence: 72%

The Role of Toll-Like Receptor 2 in Inflammation and Fibrosis during Progressive Renal Injury

et al. 2009

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Tissue fibrosis and chronic inflammation are common causes of progressive organ damage, including progressive renal disease, leading to loss of physiological functions. Recently, it was shown that Toll-like receptor 2 (TLR2) is expressed in the kidney and activated by endogenous danger signals. The expression and function of TLR2 during renal fibrosis and chronic inflammation has however not yet been elucidated. Therefore, we studied TLR2 expression in human and murine progressive renal diseases and explored its role by inducing obstructive nephropathy in TLR2−/− or TLR2+/+ mice. We found that TLR2 is markedly upregulated on tubular and tubulointerstitial cells in patients with chronic renal injury. In mice with obstructive nephropathy, renal injury was associated with a marked upregulation and change in distribution of TLR2 and upregulation of murine TLR2 danger ligands Gp96, biglycan, and HMGB1. Notably, TLR2 enhanced inflammation as reflected by a significantly reduced influx of neutrophils and production of chemokines and TGF-β in kidneys of TLR2−/− mice compared with TLR2+/+ animals. Although, the obstructed kidneys of TLR2−/− mice had less interstitial myofibroblasts in the later phase of obstructive nephropathy, tubular injury and renal matrix accumulation was similar in both mouse strains. Together, these data demonstrate that TLR2 can initiate renal inflammation during progressive renal injury and that the absence of TLR2 does not affect the development of chronic renal injury and fibrosis.

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Section: Discussionmentioning

confidence: 72%

The Role of Toll-Like Receptor 2 in Inflammation and Fibrosis during Progressive Renal Injury

et al. 2009

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“…The sharp increase in HSP72 urinary excretion is also observed in patients during the first hours after kidney transplantation, in the first urine of renal allografts, reflecting the violation of the integrity of the tubular epithelium and possibly indicating the degree of kidney damage after renal ischemia (Mueller et al 2003). However, Ramires-Sandoval et al (2014) showed that the urinary level of HSP72 did not increase significantly in kidney transplant recipients with prerenal AKI and immunological rejection.…”

Section: Hsp70 As a Biomarker Of Kidney Injurymentioning

confidence: 97%

Heat shock proteins and kidney disease: perspectives of HSP therapy

Chebotareva

Bobkova

Shilov

2017

Cell Stress and Chaperones

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Heat shock proteins (HSPs) mediate a diverse range of cellular functions, prominently including folding and regulatory processes of cellular repair. A major property of these remarkable proteins, dependent on intracellular or extracellular location, is their capacity for immunoregulation that optimizes immune activity while avoiding hyperactivated inflammation. In this review, recent investigations are described, which examine roles of HSPs in protection of kidney tissue from various traumatic influences and demonstrate their potential for clinical management of nephritic disease. The HSP70 class is particularly attractive in this respect due to its multiple protective effects. The review also summarizes current understanding of HSP bioactivity in the pathophysiology of various kidney diseases, including acute kidney injury, diabetic nephropathy, chronic glomerulonephritis, and lupus nephritis-along with other promising strategies for their remediation, such as DNA vaccination.

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“…Moreover, cytoprotective effect of HSP72 is related to its ability to inhibit apoptosis and inhibit synthesis of proinflammatory cytokines . It has been documented that urinary HSP72 is a good marker for loss of tubular cell integrity .…”

Section: Introductionmentioning

confidence: 99%

NLRP3 expression and urinary HSP72 in relation to biomarkers of inflammation and oxidative stress in diabetic nephropathy patients

et al. 2017

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Diabetic nephropathy (DN) is one of the major causes of end-stage renal disease. Nod-like receptors nucleotide-binding domain and leucine-rich repeat pyrin-3 domain (NLRP3) inflammasome displays a considerable role in the chronic inflammatory state observed in diabetic patients. Urinary heat shock protein 72 (uHSP72) is a sensitive and specific biomarker for the early detection of acute kidney injury. The aim of this study was to evaluate NLRP3 relative gene expression, its correlation with inflammatory and oxidative stress markers, and to assess the value of uHSP72 in the early detection of DN in type 2 diabetic patients with different degrees of DN. Forty-five type 2 diabetic patients: 15 normoalbuminuric, 15 microalbuminuric, 15 macroalbuminuric, in addition to 15 healthy controls were enrolled in this study. Clinical examination and routine laboratory investigations were performed. NLRP3 mRNA expression was assessed by real time polymerase chain reaction. Serum 8-hydroxy-2'-deoxyguanosine (8-OHdG), interleukin 1β (IL-1β), and uHSP72 levels were estimated by enzyme-linked immunosorbent assay. Serum chitotriosidase (CHIT1) activity was examined. NLRP3 mRNA relative expression, serum levels of 8-OHdG, IL-1β, and uHSP72, in addition to CHIT 1 activity were significantly increased in the macroalbuminuric patient group as compared to control and the other two diabetic groups. Also, a significant positive correlation was documented between the previously mentioned parameters and urinary albumin/creatinine ratio, serum creatinine, and HbA1c. Multiple linear regression analysis using urinary albumin/creatinine ratio as dependent variable confirmed that uHSP72 and NLRP3 mRNA relative expression were the independent predictors of DN (β were 0.432 and 0.448 respectively, P < 0.001). Receiver operating characteristic analyses revealed that both NLRP3 mRNA relative expression and uHSP72 levels were useful biomarkers discriminating DN patients from patients with type 2 diabetes mellitus (AUC were 0.957 and 0.983, respectively). uHSP72 may be considered as a novel potential diagnostic biomarker for the early detection of DN. Moreover, these data support the pivotal role of NLRP3 in the development and progression of DN. © 2017 IUBMB Life, 69(8):623-630, 2017.

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Urinary heat shock protein-72 excretion in clinical and experimental renal ischemia

Cited by 28 publications

References 14 publications

The Role of Toll-Like Receptor 2 in Inflammation and Fibrosis during Progressive Renal Injury

The Role of Toll-Like Receptor 2 in Inflammation and Fibrosis during Progressive Renal Injury

Heat shock proteins and kidney disease: perspectives of HSP therapy

NLRP3 expression and urinary HSP72 in relation to biomarkers of inflammation and oxidative stress in diabetic nephropathy patients

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