ARRB1/β-arrestin-1 mediates neuroprotection through coordination of BECN1-dependent autophagy in cerebral ischemia

Wang, Pei; Xu, Tao; Wei, Kai; Guan, Yongjun; Wang, Xia; Xu, Hui; Su, Ding‐Feng; Pei, Gang; Miao, Chao‐Yu

doi:10.4161/auto.29203

Cited by 126 publications

(104 citation statements)

References 72 publications

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“…The ischemic penumbra was confirmed as illustrated in Figure 1 [17] . The 4th section was stained with 1% TTC for 10 min to determine the infarct area, and the ischemic penumbra in this section was determined.…”

Section: Tissue Samplingsupporting

confidence: 49%

Minocycline Suppresses NLRP3 Inflammasome Activation in Experimental Ischemic Stroke

Xiao²,

Luo³

2016

Neuroimmunomodulation

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Objective: Minocycline, a tetracycline antibiotic, has shown anti-inflammatory effects in cerebral ischemia and neurodegenerative disease; however, the molecular mechanisms underlying this effect have not been clearly identified. Since NLRP3 inflammasome activation controls the maturation and release of proinflammatory cytokines, especially interleukin-1β (IL-1β) and IL-18 in ischemia stroke, we suppose that minocycline may be involved in the regulation of NLRP3 inflammasome activation. Methods: We investigated the effects of minocycline on NLRP3 inflammasome activation using the transient middle cerebral artery occlusion (tMCAO) mouse model and an in vitro oxygen-glucose deprivation/reoxygenation injury model in BV2 microglial cells. Results: We found that minocycline administrated 1 h after reperfusion can improve neurological disorder, reduce infarct volume, and alleviate cerebral edema. Meanwhile, we showed that minocycline prevented the activation of microglias and attenuated NLRP3 inflammasome signaling after tMCAO injury. Furthermore, we found that the pretreatment of minocycline significantly inhibited signal 1 and signal 2 of NLRP3 inflammasome activation in BV2 cells. Conclusion: We demonstrated that minocycline can ameliorate ischemia-induced brain damage via inhibiting NLRP3 inflammasome activation.

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Section: Tissue Samplingsupporting

confidence: 49%

Minocycline Suppresses NLRP3 Inflammasome Activation in Experimental Ischemic Stroke

Xiao²,

Luo³

2016

Neuroimmunomodulation

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“…49 However, such results are anticipated since NAMPT is a stress sensor, and these results cannot answer whether NAMPT is a friend or foe of the ischemic injury and the postischemic vascular repair. Recent experimental studies from our laboratory and others have demonstrated that NAMPT-NAD axis is a potent protective pathway against ischemic injury in brain, 36,[50][51][52][53][54] heart, 55-57 and hindlimb. 58 Importantly, NAMPT and NAMPT-controlled NAD pool also facilitates postischemic vascular repair.…”

Section: Nampt and Nampt-controlled Nad Pool In Ischemic Diseases Andmentioning

confidence: 98%

NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair

Wang

Liu

et al. 2016

Journal of Cardiovascular Pharmacology

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Vascular repair plays important roles in postischemic remodeling and rehabilitation in cardiovascular and cerebrovascular disease, such as stroke and myocardial infarction. Nicotinamide adenine dinucleotide (NAD), a well-known coenzyme involved in electron transport chain for generation of adenosine triphosphate, has emerged as an important controller regulating various biological signaling pathways. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme for NAD biosynthesis in mammals. NAMPT may also act in a nonenzymatic manner, presumably mediated by unknown receptor(s). Rapidly accumulating data in the past decade show that NAMPT and NAMPT-controlled NAD metabolism regulate fundamental biological functions in endothelial cells, vascular smooth muscle cells, and endothelial progenitor cells. The NAD-consuming proteins, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38, may contribute to the regulatory effects of NAMPT-NAD axis in these cells and vascular repair. This review discusses the current data regarding NAMPT and NAMPT-controlled NAD metabolism in vascular repair and the clinical potential translational application of NAMPT-related products in treatment of cardiovascular and cerebrovascular disease.

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“…32 The mechanism by which P7C3 chemicals initiate the neuroprotection has been proposed in a recent study; P7C3 chemicals may function via activating Nampt. 19 However, it is yet unknown for the efficacy of P7C3 chemicals in stroke model.…”

Section: Strokementioning

confidence: 99%

“…11,19 Figure 1. Nicotinamide phosphoribosyltransferase (Nampt) overexpression promotes neurogenesis after ischemic stroke.…”

Section: Cerebral Ischemia Modelmentioning

confidence: 99%

Regenerative Neurogenesis After Ischemic Stroke Promoted by Nicotinamide Phosphoribosyltransferase–Nicotinamide Adenine Dinucleotide Cascade

Zhao

Guan

Zhou

et al. 2015

Stroke

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N icotinamide adenine dinucleotide (NAD) is a coenzyme found in all living cells, and nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for NAD biosynthesis in mammal.1 Nampt catalyzes the reaction between nicotinamide and 5-phosphoribosyl-1-pyrophosphate to yield nicotinamide mononucleotide (NMN), an intermediate in the biosynthesis of NAD.1 Classically, NAD acts as a coenzyme and metabolite playing a fundamental role in electron transfer chain and energy generation (ATP production) through oxidative phosphorylation.2 Recent work has revealed an entirely different role of NAD as a critical signaling regulator.3,4 Moreover, with the identification of a group of NADconsuming proteins, 3 such as the sirtuins, poly(ADP-ribose) polymerases, and cyclic ADP-ribose synthases, Namptregulated NAD pool has drawn much attention as a substrate and a regulator in cell signaling and cellular homeostasis, such as metabolism, 5,6 circadian rhythms, 7 immunity, 8 and cell death. Nampt-NAD cascade plays critical roles in cerebral ischemic injury. Cerebral ischemia caused brain NAD depletion followed by brain cell death. 10 Replenishment of NAD conferred a marked neuroprotection against ischemic cell death. 10 We and other groups have shown that Nampt is mainly localized on neurons rather than glial cells, 11,12 and both intercellular and extracellular Nampt display potent neuroprotection in ischemic stroke models. [11][12][13] We also showed that induction of autophagyBackground and Purpose-Nicotinamide adenine dinucleotide (NAD) is a ubiquitous fundamental metabolite. Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for mammalian NAD salvage synthesis and has been shown to protect against acute ischemic stroke. In this study, we investigated the role of Nampt-NAD cascade in brain regeneration after ischemic stroke. Methods-Nampt transgenic (Nampt-Tg) mice and H247A mutant enzymatic-dead Nampt transgenic (ΔNampt-Tg) mice were subjected with experimental cerebral ischemia by middle cerebral artery occlusion. Activation of neural stem cells, neurogenesis, and neurological function recovery were measured. Besides, nicotinamide mononucleotide and NAD, two chemical enzymatic product of Nampt, were administrated in vivo and in vitro. Results-Compared with wild-type mice, Nampt-Tg mice showed enhanced number of neural stem cells, improved neural functional recovery, increased survival rate, and accelerated body weight gain after middle cerebral artery occlusion, which were not observed in ΔNampt-Tg mice. A delayed nicotinamide mononucleotide administration for 7 days with the first dose at 12 hours post middle cerebral artery occlusion did not protect acute brain infarction and neuronal deficit; however, it still improved postischemic regenerative neurogenesis. Nicotinamide mononucleotide and NAD + promoted proliferation and differentiation of neural stem cells in vitro. Knockdown of NAD-dependent deacetylase sirtuin 1 (SIRT1) and SIRT2 inhibited the progrowth action of Nampt-NAD axis, ...

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ARRB1/β-arrestin-1 mediates neuroprotection through coordination of BECN1-dependent autophagy in cerebral ischemia

Cited by 126 publications

References 72 publications

Minocycline Suppresses NLRP3 Inflammasome Activation in Experimental Ischemic Stroke

Minocycline Suppresses NLRP3 Inflammasome Activation in Experimental Ischemic Stroke

NAMPT and NAMPT-controlled NAD Metabolism in Vascular Repair

Regenerative Neurogenesis After Ischemic Stroke Promoted by Nicotinamide Phosphoribosyltransferase–Nicotinamide Adenine Dinucleotide Cascade

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