Apoptotic Death of Renal Tubular Cells in Experimental Sepsis

Messaris, Evangelos; Memos, Nikolaos; Chatzigianni, Emmy; Kataki, Agapi; Nikolopoulou, Μarilena; Manouras, Andreas; Albanopoulos, K; Konstadoulakis, Manousos M.; Bramis, John

doi:10.1089/sur.2006.018

Cited by 22 publications

(19 citation statements)

References 18 publications

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“…Recent studies have shown that apoptosis may also be involved in the pathogenesis of sepsis [11]. We observed less cleaved caspase 3 in the tubular cells after CLP in the MyD88 −/− mice compared with those cells from the other mice ( Figures 8a and c ).…”

Section: Resultsmentioning

confidence: 53%

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

et al. 2012

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The aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2−/−, TLR4−/− and MyD88−/− male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis. The TLR2−/−, TLR4−/− and MyD88−/− mice that were subjected to CLP had preserved renal morphology, and fewer areas of hypoxia and apoptosis compared with the wild-type C57BL/6 mice (WT). MyD88−/− mice were completely protected compared with the WT mice. We also observed reduced expression of proinflammatory cytokines in the kidneys of the knockout mice compared with those of the WT mice and subsequent inhibition of increased vascular permeability in the kidneys of the knockout mice. The WT mice had increased GR1+low cells migration compared with the knockout mice and decreased in GR1+high cells migration into the peritoneal cavity. The TLR2−/−, TLR4−/−, and MyD88−/− mice had lower neutrophil infiltration in the kidneys. Depletion of neutrophils in the WT mice led to protection of renal function and less inflammation in the kidneys of these mice. Innate immunity participates in polymicrobial sepsis-induced AKI, mainly through the MyD88 pathway, by leading to an increased migration of neutrophils to the kidney, increased production of proinflammatory cytokines, vascular permeability, hypoxia and apoptosis of tubular cells.

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Section: Resultsmentioning

confidence: 53%

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

et al. 2012

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“…These data might suggest the possible contribution of renal tubular cell apoptosis in development of septic AKI. The possible contribution of various types of proinflammatory cytokines or endotoxin or lipopolysaccharide in sepsis on tubular cell apoptosis has been previously demonstrated (24). Using human proximal tubular cells in culture, Jo et al (25) reported that tumor necrosis factor-α, IL-1β, or lipopolysaccharide treatment induced Fas-dependent apoptosis in tubular cells.…”

Section: Discussionmentioning

confidence: 96%

Distinct pathophysiologic mechanisms of septic acute kidney injury

Lee

Choi

et al. 2012

Critical Care Medicine

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“…15 To investigate whether the activation of TLR2 is related to the cell apoptosis, we studied the distribution of Bax and Caspase-3 in the kidney of septic AKI mice. Our results demonstrated that high levels of Bax and Caspase-3 were detected in the LPS-treated mice glomerular cells along the external side of some capillary loops (Figure 3).…”

Section: Induction Of Septic Aki Mice With Lps Treatmentmentioning

confidence: 99%

Overexpression of toll-like receptor 2 in glomerular endothelial cells and podocytes in septic acute kidney injury mouse model

et al. 2015

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Acute kidney injury (AKI) is one of the most common complications in patients with severe sepsis. The development of septic AKI increases patients' mobility and even mortality. Toll-like receptor 2 (TLR2), as a membrane surface receptor for bacterial, fungal, viral and certain endogenous substances, has been described to contribute to the development of septic AKI; however, the renal cell types associating TLR2 overactivation in septic AKI has not been described. In the current study, we investigated the TLR2 activation patterns in the kidney of lipopolysaccharide-induced septic AKI mice. Our results demonstrated that mRNA level of TLR2 significantly increased in the kidney of lipopolysaccharide-treated mice. Immunohistochemistry revealed the overactivation of TLR2 in the glomeruli. Double immunofluorescence analysis shows the precise distribution of TLR2 by showing the colocalization of TLR2 in glomeruli with synaptopodin, a podocyte marker, and Tie2, an endothelial marker. In addition, proapoptotic molecules Bax and Caspase-3 were increased in the glomeruli of lipopolysaccharide-treated mice. Together, the current study indicates that TLR2 is overactivated in the glomerular endothelial cells and podocytes in septic AKI mice, while the abundance of Bax and Caspase-3 were increased in the glomeruli of these mice, it may supply a clue that TLR2 induced these cell apoptosis in AKI. This finding provides an alternative mechanism to understand AKI development and potential targets for treatment.

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Apoptotic Death of Renal Tubular Cells in Experimental Sepsis

Abstract: Apoptosis in renal tissue was significantly more common in animals with sepsis than in controls. The time distribution of cell death markers showed a consistent pattern, making early sepsis the likely initiator of the apoptotic events.

Cited by 22 publications

References 18 publications

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

TLR2, TLR4 and the MYD88 Signaling Pathway Are Crucial for Neutrophil Migration in Acute Kidney Injury Induced by Sepsis

Distinct pathophysiologic mechanisms of septic acute kidney injury

Overexpression of toll-like receptor 2 in glomerular endothelial cells and podocytes in septic acute kidney injury mouse model

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