Expression of the small heat‐shock protein Hsp‐16‐2 in<i>Caenorhabditis elegans</i>is suppressed by<i>Ginkgo biloba</i>extract EGb 761

Strayer, Amy L; Wu, Zhixin; Christen, Yves; Link, Christopher D.; Luo, Yuan

doi:10.1096/fj.03-0376fje

Cited by 124 publications

(90 citation statements)

References 43 publications

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“…Recent reports demonstrate that A␤-induced, and a pro-aggregationprotein-induced paralysis in transgenic C. elegans were reduced by slowing aging (Cohen et al, 2006), or by coexpression of a stress response protein, the small heat shock protein 16 (sHSP-16) (Link et al, 2006) in the worms, respectively. EGb 761 attenuated the expression of sHSP-16 protein in the wild-type worms exposed to oxidative stress (Strayer et al, 2003). A possible explanation is that EGb 761 might act in a manner similar to that of sHSP-16 in protecting against the deleterious process, which would lead to a decreased need for sHSP-16 expression.…”

Section: Egb 761 and Ginkgolide A Inhibit A␤ Oligomerizationmentioning

confidence: 99%

Amyloid-β-Induced Pathological Behaviors Are Suppressed byGinkgo bilobaExtract EGb 761 and Ginkgolides in TransgenicCaenorhabditis elegans

Wu¹,

Wu²,

Butko³

et al. 2006

J. Neurosci.

378

366

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Amyloid-␤ (A␤) toxicity has been postulated to initiate synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (AD). We previously demonstrated that the standardized Ginkgo biloba extract EGb 761, commonly used to enhance memory and by AD patients for dementia, inhibits A␤-induced apoptosis in neuroblastoma cells. In this study, we use EGb 761 and its single constituents to associate A␤ species with A␤-induced pathological behaviors in a model organism, Caenorhabditis elegans. We report that EGb 761 and one of its components, ginkgolide A, alleviates A␤-induced pathological behaviors, including paralysis, and reduces chemotaxis behavior and 5-HT hypersensitivity in a transgenic C. elegans. We also show that EGb 761 inhibits A␤ oligomerization and A␤ deposits in the worms. Moreover, reducing oxidative stress is not the mechanism by which EGb 761 and ginkgolide A suppress A␤-induced paralysis because the antioxidant L-ascorbic acid reduced intracellular levels of hydrogen peroxide to the same extent as EGb 761, but was not nearly as effective in suppressing paralysis in the transgenic C. elegans. These findings suggest that (1) EGb 761 suppresses A␤-related pathological behaviors, (2) the protection against A␤ toxicity by EGb 761 is mediated primarily by modulating A␤ oligomeric species, and (3) ginkgolide A has therapeutic potential for prevention and treatment of AD.

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Section: Egb 761 and Ginkgolide A Inhibit A␤ Oligomerizationmentioning

confidence: 99%

Amyloid-β-Induced Pathological Behaviors Are Suppressed byGinkgo bilobaExtract EGb 761 and Ginkgolides in TransgenicCaenorhabditis elegans

Wu¹,

Wu²,

Butko³

et al. 2006

J. Neurosci.

378

366

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“…The heat shock assay was performed as described previously (Pietsch et al 2009;Strayer et al 2003) with some modifications. CBE-pretreated L4/young adult stage worms and controls were transferred to CBE supplemented (2 mg/mL) plates and regular NGM plates, respectively.…”

Section: Stress Assaysmentioning

confidence: 99%

The longevity effect of cranberry extract in Caenorhabditis elegans is modulated by daf-16 and osr-1

Guha

Cao

Kane

et al. 2012

AGE

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Nutraceuticals are known to have numerous health and disease preventing properties. Recent studies suggest that extracts containing cranberry may have anti-aging benefits. However, little is known about whether and how cranberry by itself promotes longevity and healthspan in any organism. Here we examined the effect of a cranberry only extract on lifespan and healthspan in Caenorhabditis elegans. Supplementation of the diet with cranberry extract (CBE) increased the lifespan in C. elegans in a concentration-dependent manner. Cranberry also increased tolerance of C. elegans to heat shock, but not to oxidative stress or ultraviolet irradiation. In addition, we tested the effect of cranberry on brood size and motility and found that cranberry did not influence these behaviors. Our mechanistic studies indicated that lifespan extension induced by CBE requires the insulin/IGF signaling pathway and DAF-16. We also found that cranberry promotes longevity through osmotic stress resistant-1 (OSR-1) and one of its downstream effectors, UNC-43, but not through SEK-1, a component of the p38 MAP kinase pathway. However, SIR-2.1 and JNK signaling pathways are not required for cranberry to promote longevity. Our findings suggest that cranberry supplementation confers increased longevity and stress resistance in C. elegans through pathways modulated by daf-16 and osr-1. This study reveals the anti-aging property of widely consumed cranberry and elucidates the underpinning mechanisms.

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“…EG1653 and TJ375 strains have been regularly used, respectively, to quantify the expression of UNC-49 (Abraham et al 2011;Byrd et al 2001;Garafalo et al 2015;Knobel et al 2001;Rowland et al 2006) and HSP-16.2 (Abbas and Wink 2010;Lamark and Johansen 2012;Leroy et al 2012;Rea et al 2005;Shore et al 2012;Strayer et al 2003;Wang et al 2012;Wu et al 2006) based on the quantitation of their GFP fluorescence intensities.…”

Section: Strains and Culture Conditionsmentioning

confidence: 99%

“…As green fluorescent protein (GFP) is excited in blue light range, a triple band filter that allows for that excitation range was employed. Fluorescent images were processed with software Image Pro Plus 6.0 (Media Cybernetics, Bethesda, MD, USA) (Strayer et al 2003). Briefly, images were converted to grayscale at 16 bits, and afterwards, optical density calibration was undertaken.…”

Section: Fluorescence Microscopymentioning

confidence: 99%

“…Genetic manipulations to overexpress individual chaperones, like Hsp90 and Hsp70, resulted in a subtle extension of life span (Morley and Morimoto 2004); however, the small chaperone Hsp16 seemed to be more efficient in worms (Soti and Csermely 2007), particularly HSP-16.2 that is often used as an indicator of increases in thermal and oxidative stress (Hartwig et al 2009;Rea et al 2005;Strayer et al 2003;Wiegant et al 2009;Wu et al 2006;Xiao et al 2009). …”

Section: Introductionmentioning

confidence: 99%

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Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

Camargo

Elizalde

Trujillo

et al. 2016

Cell Stress and Chaperones

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The mechanisms underlying oxidative stress (OS) resistance are not completely clear. Caenorhabditis elegans (C. elegans) is a good organism model to study OS because it displays stress responses similar to those in mammals. Among these mechanisms, the insulin/IGF-1 signaling (IIS) pathway is thought to affect GABAergic neurotransmission. The aim of this study was to determine the influence of heat shock stress (HS) on GABAergic activity in C. elegans. For this purpose, we tested the effect of exposure to picrotoxin (PTX), gammaaminobutyric acid (GABA), hydrogen peroxide, and HS on the occurrence of a shrinking response (SR) after nose touch stimulus in N2 (WT) worms. Moreover, the effect of HS on the expression of UNC-49 (GABA A receptor ortholog) in the EG1653 strain and the effect of GABA and PTX exposure on HSP-16.2 expression in the TJ375 strain were analyzed. PTX 1 mM-or H 2 O 2 0.7 mM-exposed worms displayed a SR in about 80 % of trials. GABA exposure did not cause a SR. HS prompted the occurrence of a SR as did PTX 1 mM or H 2 O 2 0.7 mM exposure. In addition, HS increased UNC-49 expression, and PTX augmented HSP-16.2 expression. Thus, the results of the present study suggest that oxidative stress, through either H 2 O 2 exposure or application of heat shock, inactivates the GABAergic system, which subsequently would affect the oxidative stress response, perhaps by enhancing the activity of transcription factors DAF-16 and HSF-1, both regulated by the IIS pathway and related to hsp-16.2 expression.

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Expression of the small heat‐shock protein Hsp‐16‐2 inCaenorhabditis elegansis suppressed byGinkgo bilobaextract EGb 761

Cited by 124 publications

References 43 publications

Amyloid-β-Induced Pathological Behaviors Are Suppressed byGinkgo bilobaExtract EGb 761 and Ginkgolides in TransgenicCaenorhabditis elegans

Amyloid-β-Induced Pathological Behaviors Are Suppressed byGinkgo bilobaExtract EGb 761 and Ginkgolides in TransgenicCaenorhabditis elegans

The longevity effect of cranberry extract in Caenorhabditis elegans is modulated by daf-16 and osr-1

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

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