Adiponectin protects human neuroblastoma SH-SY5Y cells against MPP+-induced cytotoxicity

Jung, Tae Woo; Lee, Ji Young; Shim, Wan Sub; Kang, Eun Seok; Kim, Jongsun; Ahn, Chul Woo; Lee, Hyun Chul; Soo, Bong

doi:10.1016/j.bbrc.2006.02.186

Cited by 47 publications

(40 citation statements)

References 22 publications

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“…Adiponectin has been ascribed antioxidative properties (Jung et al, 2006); it improves endothelial function in nondiabetic patients with metabolic syndrome (Bahia et al, 2007) and also improves the beneficial effects of antihypertensive agents in hypertensive patients (Yilmaz et al, 2007). These observations serve to define some of the key mechanisms by which HO-1 is involved in the maintenance of microvascular tone and to offer a possible approach as to how these mechanisms might be therapeutically manipulated.…”

Section: F Heme Oxygenase-1 In Myocardial Ischemiareperfusion Injurymentioning

confidence: 99%

Pharmacological and Clinical Aspects of Heme Oxygenase

Abraham

Kappas²

2008

Pharmacol Rev

1,010

988

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Section: F Heme Oxygenase-1 In Myocardial Ischemiareperfusion Injurymentioning

confidence: 99%

Pharmacological and Clinical Aspects of Heme Oxygenase

Abraham

Kappas²

2008

Pharmacol Rev

1,010

988

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“…Adiponectin, in particular the trimeric form, has been demonstrated in human cerebrospinal fluid using gel filtration chromatography (P.E.S., unpublished data). Moreover, adiponectin protects human neuroblastoma SH-SY5Y cells from apoptosis induced by the mitochondrial complex I inhibitor, 1-methyl-4-phenylpyridinium, suggesting a direct action on neurons (81). It is possible adiponectin enters the brain via the circumventricular organs, e.g., area postrema, median eminence, and subfornical organ, located outside the blood-brain barrier.…”

Section: Role Of Leptin In Famine and Feastmentioning

confidence: 99%

Brain Adipocytokine Action and Metabolic Regulation

et al. 2006

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Adipose tissue secretes factors that control various physiological systems. The fall in leptin during fasting mediates hyperphagia and suppresses thermogenesis, thyroid and reproductive hormones, and immune system. On the other hand, rising leptin levels in the fed state stimulate fatty acid oxidation, decrease appetite, and limit weight gain. These divergent effects of leptin occur through neuronal circuits in the hypothalamus and other brain areas. Leptin also regulates the activities of enzymes involved in lipid metabolism, e.g., AMP-activated protein kinase and stearoyl-CoA desaturase-1, and also interacts with insulin signaling in the brain. Adiponectin enhances fatty acid oxidation and insulin sensitivity, in part by stimulating AMP-activated protein kinase phosphorylation and activity in liver and muscle. Moreover, adiponectin decreases body fat by increasing energy expenditure and lipid catabolism. These effects involve peripheral and possibly central mechanisms. Adipose tissue mediates interconversion of steroid hormones and secretes proinflammatory cytokines, vasoactive peptides, and coagulation and complement proteins. Understanding the actions of these "adipocytokines" will provide insight into the pathogenesis and treatment of obesity and related diseases. Diabetes 55 (Suppl. 2): S145-S154, 2006 ADIPOSE TISSUE

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“…Beyond energy regulation, APN may also play other roles in the nervous system. For instance, APN protected human neuroblastoma SH‐SY5Y cells against MPP+‐induced cytotoxicity24 and amyloid β ‐induced neurotoxicity 25. In vivo, APN was protective against kainic acid‐induced excitotoxicity in the mouse hippocampus, a well‐established model of seizure 26.…”

Section: Apn Actions In the Nervous Systemmentioning

confidence: 99%

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Waragai

Ho²,

Takamatsu

et al. 2017

Ann Clin Transl Neurol

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A recent study suggested that insulin resistance may play a central role in the pathogenesis of Alzheimer's disease (AD). In this regard, it is of note that upregulation of plasma adiponectin (APN), a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation, has recently been associated with the severities of amyloid deposits and cognitive deficits in the elderly, suggesting that APN may enhance the risk of AD. These results are unanticipated because AD has been linked to type II diabetes and other metabolic disorders in which hypoadiponectinemia has been firmly established, and because APN ameliorated neuropathological features in a mouse model of neurodegeneration. Therefore, the objective of this study is to discuss the possible mechanisms underlying the biological actions of APN in the context of AD. Given that insulin receptor signaling is required for normal function of the nervous system, we predict that APN may be upregulated to compensate for compromised activity of the insulin receptor signaling pathway. However, increased APN might be sequestered by tau in the brain, leading to neurotoxic protein aggregation in AD. Alternatively, misfolding of APN may result in downregulation of the insulin/APN signal transduction network, leading to decreased neuroprotective and neurotrophic activities. Thus, it is possible that both ‘gain of function’ and ‘loss of function’ of APN may underlie synaptic dysfunction and neuronal cell death in AD. Such a unique biological mechanism underlying APN function in AD may require a novel therapeutic strategy that is distinct from previous treatment for metabolic disorders.

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Adiponectin protects human neuroblastoma SH-SY5Y cells against MPP+-induced cytotoxicity

Cited by 47 publications

References 22 publications

Pharmacological and Clinical Aspects of Heme Oxygenase

Pharmacological and Clinical Aspects of Heme Oxygenase

Brain Adipocytokine Action and Metabolic Regulation

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

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