Alpha-melanocyte-stimulating hormone protects against renal injury after ischemia in mice and rats.

Chiao, Hsi; Kohda, Yukimasa; McLeroy, Paul; Craig, Leonard C.; Housini, Ihsan; Star, Robert A.

doi:10.1172/jci119272

Cited by 267 publications

(214 citation statements)

References 34 publications

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“…Previous animal studies clearly demonstrated that the treatment of AKI should be started well before the rise of Scr and very early after the insult (31)(32)(33)(34). Sensitive biologic markers of renal tubular injury are needed to detect early AKI because current AKI diagnosing and staging criteria are entirely based on an increase in Scr or decrease in urine output.…”

Section: Discussionmentioning

confidence: 99%

Urinary Biomarkers in the Early Detection of Acute Kidney Injury after Cardiac Surgery

Han¹,

Wagener²,

Zhu³

et al. 2009

Clinical Journal of the American Society of Nephrology

353

249

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Section: Discussionmentioning

confidence: 99%

Urinary Biomarkers in the Early Detection of Acute Kidney Injury after Cardiac Surgery

Han¹,

Wagener²,

Zhu³

et al. 2009

Clinical Journal of the American Society of Nephrology

353

249

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show abstract

“…-MSH, an endogenous antiinflammatory cytokine, has been known to reduce cellular infiltrations in various inflammatory conditions such as rat model of arthritis and liver injury from septic shock (20)(21)(22)(23). -MSH also has been reported to have a beneficial effect in ischemia/ reperfusion injury through its inhibitory action on the mouse chemokine KC and ICAM-1 messages and on the induction of iNOS with a resultant decrease in peroxynitrate production (24). In our previous study, intraperitoneally administered -MSH was also effective in attenuating the severity of injury determined by biochemical and histological data.…”

Section: Discussionmentioning

confidence: 99%

“…et al reported a beneficial effect of -MSH in murine model of ischemic acute renal failure (ARF) through an inhibition of mouse chemokine KC and intercellular adhesion molecule-1 (ICAM-1) expression that mediates the adherence of neutrophils to endothelium and the subsequent neutrophil infiltration (24). In addition, we have observed that tubular cell apoptosis also significantly decreased in -MSH treated group in ischemic ARF rat model with concomitant decrease in Fas/FasL protein expression and suggested that the beneficial effects of -MSH might be partially related to its inhibitory action on Fas/FasL system and apoptosis (25).…”

Section: Introductionmentioning

confidence: 99%

α-Melanocyte Stimulating Hormone (MSH) decreases cyclosporine A induced apoptosis in cultured human proximal tubular cells

Lee

Han

et al. 2001

J Korean Med Sci

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The pathogenesis of chronic cyclosporine A (CsA) nephrotoxicity has not been elucidated, but apoptosis is thought to play an important role in CsA induced tubular atrophy. Recently Fas-Fas ligand system mediated apoptosis has been frequently reported in many epithelial cells as well as in T lymphocytes. We investigated the ability of CsA to induce apoptosis in cultured human proximal tubular epithelial cells and also the effect of alpha-MSH on them. Fas, Fas ligand, and an intracellular adaptor protein, Fas-associating protein with death domain (FADD) expression, and poly-ADP ribose polymerase (PARP) cleavage were also studied. CsA induced apoptosis in cultured tubular epithelial cells demonstrated by increased number of TUNEL positive cells and it was accompanied by a significant increase in Fas mRNA and Fas ligand protein expressions. FADD and the cleavage product of PARP also increased, indicating the activation of caspase. In alpha-MSH co-treated cells, apoptosis markedly decreased with downregulation of Fas, Fas ligand and FADD expressions and also the cleavage product of PARP. In conclusion, these data suggest that tubular cell apoptosis mediated by Fas system may play a role in tubular atrophy in chronic CsA nephrotoxicity and pretreatment of alpha-MSH may have a some inhibitory effect on CsA induced tubular cell apoptosis.

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“…Modulation of the inflammatory response has been shown to improve renal function after I/R. For instance, the anti-inflammatory agent, α-melanocyte stimulating hormone (α-MSH), protects the kidney against ischemic injury but also inhibits neutrophil chemotaxis (135). Similarly, infusion of a tumor necrosis factor (TNF)-α binding protein decreased neutrophil infiltration and preserved renal function, suggesting a deleterious role for the upregulation of TNF-α in renal I/R (136).…”

Section: Activation Of Inflammation and Endothelial-leukocyte Interacmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

238

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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Alpha-melanocyte-stimulating hormone protects against renal injury after ischemia in mice and rats.

Cited by 267 publications

References 34 publications

Urinary Biomarkers in the Early Detection of Acute Kidney Injury after Cardiac Surgery

Urinary Biomarkers in the Early Detection of Acute Kidney Injury after Cardiac Surgery

α-Melanocyte Stimulating Hormone (MSH) decreases cyclosporine A induced apoptosis in cultured human proximal tubular cells

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

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