Protective effects of adiponectin against renal ischemia‐reperfusion injury via prostacyclin‐PPARα‐Heme oxygenase‐1 signaling pathway

Cheng, Ching Feng; Lian, Wei; Chen, Sung Ho; Lai, Pei Fen; Li, Hsiao Fen; Lan, Yi; Cheng, Wan; Lin, Heng

doi:10.1002/jcp.22726

Cited by 69 publications

(71 citation statements)

References 36 publications

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“…Because antiapoptotic effects of adiponectin may result from its antiinflammatory or antioxidative effect after I/R primarily through the ADIPOR2-proliferator-activated receptor a-heme oxygenase-1 pathway, 19 inhibiting ADIPOR2 by miR-494 would result in greater inflammation and hence, more damage to the kidneys. With the relationship between IGF1R and the kidneys, IGF1R has been implicated in normal mammalian glomerular integrity, 20 and suppression of IGF1R by miR-494 may inhibit podocyte cell outgrowth, leading to proteinuria.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-494 Reduces ATF3 Expression and Promotes AKI

Lan

Chen

Lai

et al. 2012

Journal of the American Society of Nephrology

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MicroRNA-494 mediates apoptosis and necrosis in several types of cells, but its renal target and potential role in AKI are unknown. Here, we found that microRNA-494 binds to the 39UTR of activating transcription factor 3 (ATF3) and decreases its transcription. In mice, overexpression of microRNA-494 significantly attenuated the level of ATF3 and induced inflammatory mediators, such as IL-6, monocyte chemotactic protein-1, and P-selectin, after renal ischemia/reperfusion, exacerbating apoptosis and further decreasing renal function. Activation of NF-kB mediated this proinflammatory response. In this ischemia/reperfusion model, urinary levels of microRNA-494 increased significantly before the rise in serum creatinine. In humans, urinary microRNA-494 levels were 60-fold higher in patients with AKI than normal controls. In conclusion, upregulation of microRNA-494 contributes to inflammatory or adhesion molecule-induced kidney injury after ischemia/reperfusion by inhibiting expression of ATF3. Furthermore, microRNA-494 may be a specific and noninvasive biomarker for AKI.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-494 Reduces ATF3 Expression and Promotes AKI

Lan

Chen

Lai

et al. 2012

Journal of the American Society of Nephrology

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111

121

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“…The above-mentioned studies should be considered separately from studies investigating the role of adiponectin in the setting of acute renal injury. The latter group of studies includes two trials investigating whether adiponectin can modulate the adverse effects of renal ischemia-reperfusion injury in mice (Cheng et al 2012, Jin et al 2013. These studies yielded conflicting results with regard to the acute responses of various parameters of renal structure and function resulting from acute renal injury.…”

Section: The Role Of Adiponectin In Renal Physiologymentioning

confidence: 99%

The role of adiponectin in renal physiology and development of albuminuria

Christou¹,

Kiortsis²

2014

Journal of Endocrinology

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Adiponectin is secreted by the adipose tissue and is downregulated in states of obesity and insulin resistance. There is a growing body of evidence indicating that adiponectin has renoprotective effects and protects against the development of albuminuria in rodent experiments. Adiponectin crossing the glomerular filtration barrier possibly inhibits inflammation, fibrosis and oxidative stress in kidneys through activation of AMP-activated protein kinase. Moreover, microalbuminuria is a well established early sign of progressive cardiovascular and renal disease, even in subjects with preserved glomerular filtration rate. Studies investigating the relationship between serum adiponectin levels and urinary albumin excretion rate (UAE) have yielded conflicting data and the mechanisms underlying the interplay between adiponectin and albuminuria remain to be elucidated. This article constitutes a critical review attempting to clarify any remaining confusion about this matter. Furthermore, this article examines the clinical significance of adiponectin-albuminuria interplay, suggesting that adiponectin is possibly involved in the development of albuminuria that is associated with obesity, diabetes and cardiovascular disease and may mediate, at least in part, the actions of medical treatments that influence UAE, such as angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, thiazolidinediones, fenofibrate and diet. Further studies to investigate more thoroughly the renoprotective role of adiponectin in the human setting should be carefully planned, focusing on causality and the possible influence of adiponectin on the development of albuminuria in specific clinical settings.

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“…We showed that LA-induced HO-1 expression was dependent on PPARα, whereas SAM induced HO-1 in a PPAR-independent manner. PPARα is a transcription factor responsible for fatty acid oxidation, and the PPARα/HO-1 signaling pathways constitute a protective mechanism against various cellular insults (Cheng et al, 2012;Yu et al, 2010). The precise mechanism responsible for the difference observed in HO-1 induction by LA and SAM awaits future studies.…”

Section: Discussionmentioning

confidence: 99%

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Kim

Hong

Kim

et al. 2013

Molecules and Cells

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* S-adenosyl methionine (SAM) is a key intermediate in themetabolism of sulfur amino acids and is a major methyl donor in the cell. Although the low plasma level of SAM has been associated with atherosclerosis, the effect of SAM administration on atherosclerosis is not known. Endothelial dysfunction is an early prerequisite for atherosclerosis. This study was undertaken to investigate the possible preventive effect of SAM on endothelial dysfunction and the molecular mechanism of its action. SAM treatment prevented endothelial dysfunction in high fat diet (HFD)-fed rats. In cultured human aortic endothelial cells, linoleic acid (LA) increased and SAM decreased cell apoptosis and endoplasmic reticulum stress. Both LA and SAM increased heme oxygenase-1 (HO-1) expression in an NF-E2-related factor 2-dependent manner. However, knockdown of HO-1 reversed only the SAM-induced preventive effect of cell apoptosis. The LA-induced HO-1 expression was dependent on PPARα, whereas SAM induced HO-1 in a PPAR-independent manner. These data demonstrate that SAM treatment prevents endothelial dysfunction in HFDfed animals by inducing HO-1 in vascular endothelial cells. In cultured endothelial cells, SAM-induced HO-1 was responsible for the observed prevention of cell apoptosis. We propose that SAM treatment may represent a new therapeutic strategy for atherosclerosis.

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Protective effects of adiponectin against renal ischemia‐reperfusion injury via prostacyclin‐PPARα‐Heme oxygenase‐1 signaling pathway

Cited by 69 publications

References 36 publications

MicroRNA-494 Reduces ATF3 Expression and Promotes AKI

MicroRNA-494 Reduces ATF3 Expression and Promotes AKI

The role of adiponectin in renal physiology and development of albuminuria

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

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