The inflammatory component in progressive renal disease—are interventions possible?

Noronha, Irene L.; Fujihara, Clarice Kazue; Zatz, Roberto

doi:10.1093/ndt/17.3.363

Cited by 94 publications

(122 citation statements)

References 34 publications

Supporting

Mentioning

109

Contrasting

Unclassified

Order By: Relevance

“…Inflammatory cells migrate to the interstitium driven by the up-regulated expression of chemoattractant molecules (chemokines and adhesion molecules) produced by activated tubular cells, which further lead to local tissue injury (Noronha et al, 2002). In this work, we demonstrated that kidneys from UUO rats exhibited high levels of ICAM-1 and CCL2 mRNA during the injury, corresponding to the accumulation of macrophages in the interstitium.…”

Section: Figurementioning

confidence: 66%

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Chiang

Sheu

Lin

et al. 2011

British J Pharmacology

View full text Add to dashboard Cite

BACKGROUND AND PURPOSE Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. The present study investigated, in vivo and in vitro, the anti-fibrotic and anti-inflammatory effects, particularly on the epithelial to mesenchymal transition of renal tubular cells, exerted by honokiol, a phytochemical used in traditional medicine, and mechanisms underlying these effects. EXPERIMENTAL APPROACH Anti-fibrotic effects in vivo were assayed in a rat model of renal fibrosis [the unilateral ureteral obstruction (UUO) model]. A rat tubular epithelial cell line (NRK-52E) was stimulated by transforming growth factor-beta 1 (TGF-beta 1) and treated with honokiol to explore possible mechanisms of these anti-fibrotic effects. Gene or protein expression was analysed by Northern or Western blotting. Transcriptional regulation was investigated using luciferase activity driven by a connective tissue growth factor (CTGF) promoter. KEY RESULTS Honokiol slowed development of renal fibrosis both in vivo and in vitro. Honokiol treatment attenuated tubulointerstitial fibrosis and expression of pro-fibrotic factors in the UUO model. Honokiol also decreased expression of the mRNA for the chemokine CCL2 and for the intracellular adhesion molecule-1, as well as accumulation of type I (alpha 1) collagen and fibronectin in UUO kidneys. Phosphorylation of Smad-2/3 induced by TGF-beta 1 and CTGF luciferase activity in renal tubular cells were also inhibited by honokiol. CONCLUSIONS AND IMPLICATIONS Honokiol suppressed expression of pro-fibrotic and pro-inflammatory factors and of extracellular matrix proteins. Honokiol may become a therapeutic agent to prevent renal fibrosis

show abstract

Section: Figurementioning

confidence: 66%

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Chiang

Sheu

Lin

et al. 2011

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Proinflammatory cytokines lead to the transition of epithelial cells to mesenchymal cells or, more specifically, myofibroblasts. Inflammatory cells may secrete several factors, such as TGF-b, platelet-derived growth factor, endothelial-derived growth factor, and fibroblast growth factor 2, that may lead to a phenomenon called EMT [44]. TGF-b is the main molecule that triggers EMT through the activation of multiple factors such as Smads and Snails.…”

Section: Discussionmentioning

confidence: 99%

“…TGF-b is the main molecule that triggers EMT through the activation of multiple factors such as Smads and Snails. Among the factors that lead to EMT, proteinuria, chronic hypoxia, oxidative stress, and inflammatory cytokines have been described [43][44][45][46]. All these factors are presented during CKD.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Attenuate Renal Fibrosis Through Immune Modulation and Remodeling Properties in a Rat Remnant Kidney Model

et al. 2009

View full text Add to dashboard Cite

Mesenchymal stem cells (MSCs) have regenerative properties in acute kidney injury, but their role in chronic kidney diseases is still unknown. More specifically, it is not known whether MSCs halt fibrosis. The purpose of this work was to investigate the role of MSCs in fibrogenesis using a model of chronic renal failure. MSCs were obtained from the tibias and femurs of male Wistar-EPM rats. Female Wistar rats were subjected to the remnant model, and 2|3|10 5 MSCs were intravenously administrated to each rat every other week for 8 weeks or only once and followed for 12 weeks. SRY gene expression was observed in female rats treated with male MSCs, and immune localization of CD73 1 CD90 1 cells at 8 weeks was also assessed. Serum and urine analyses showed an amelioration of functional parameters in MSC-treated animals at 8 weeks, but not at 12 weeks. Masson's trichrome and Sirius red staining demonstrated reduced levels of fibrosis in MSC-treated animals. These results were corroborated by reduced vimentin, type I collagen, transforming growth factor b, fibroblast specific protein 1 (FSP-1), monocyte chemoattractant protein 1, and Smad3 mRNA expression and a smooth muscle actin and FSP-1 protein expression. Renal interleukin (IL)-6 and tumor necrosis factor a mRNA expression levels were significantly decreased after MSC treatment, whereas IL-4 and IL-10 expression levels were increased. All serum cytokine expression levels were decreased in MSC-treated animals. Taken together, these results suggested that MSC therapy can indeed modulate the inflammatory response that follows the initial phase of a chronic renal injury. The immunosuppressive and remodeling properties of MSCs may be involved in the decreased fibrosis in the kidney.

show abstract

“…Chronic kidney disease (CKD) is associated with inflammation and hemodynamic changes that result in scarring of the renal tubules and interstitial spaces, and ultimately, the development of end-stage renal disease [1]. CKD is frequently diagnosed and currently represents the leading cause of death among patients with diabetes and hypertension [1].…”

Section: Introductionmentioning

confidence: 99%

“…CKD is frequently diagnosed and currently represents the leading cause of death among patients with diabetes and hypertension [1].…”

Section: Introductionmentioning

confidence: 99%

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Zhang¹,

Yang²,

Li³

et al. 2017

Trop. J. Pharm Res

View full text Add to dashboard Cite

show abstract

The inflammatory component in progressive renal disease—are interventions possible?

Cited by 94 publications

References 34 publications

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Mesenchymal Stem Cells Attenuate Renal Fibrosis Through Immune Modulation and Remodeling Properties in a Rat Remnant Kidney Model

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Contact Info

Product

Resources

About