Nicotinamide phosphoribosyltransferase/sirtuin 1 pathway is involved in human immunodeficiency virus type 1 Tat‐mediated long terminal repeat transactivation

Zhang, Hongsheng; Weiwei, Sang; Wang, Yu-Ou; Liu, Wei

doi:10.1002/jcb.22704

Cited by 30 publications

(17 citation statements)

References 36 publications

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“…13 A major factor contributing to the requirement of AMPK to provide PKCemediated ischemic neuroprotection in our experiments may lie in the ability of AMPK to regulate Nampt and NAD levels. Ischemic preconditioning and resveratrol have been shown to enhance levels of Nampt, 33,34 which implicates Nampt as a major player in ischemic neuroprotection. Studies have shown that knockdown of Nampt increases susceptibility to cerebral ischemic infarct, while Nampt overexpression enhances neuronal survival after ischemic injury through AMPK activity.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase C Epsilon Regulates Mitochondrial Pools of Nampt and NAD Following Resveratrol and Ischemic Preconditioning in the Rat Cortex

Morris-Blanco

Cohan

Neumann

et al. 2014

J Cereb Blood Flow Metab

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Preserving mitochondrial pools of nicotinamide adenine dinucleotide (NAD) or nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in NAD production, maintains mitochondrial function and confers neuroprotection after ischemic stress. However, the mechanisms involved in regulating mitochondrial-localized Nampt or NAD have not been defined. In this study, we investigated the roles of protein kinase C epsilon (PKCe) and AMP-activated protein kinase (AMPK) in regulating mitochondrial pools of Nampt and NAD after resveratrol or ischemic preconditioning (IPC) in the cortex and in primary neuronal-glial cortical cultures. Using the specific PKCe agonist ceRACK, we found that PKCe induced robust activation of AMPK in vitro and in vivo and that AMPK was required for PKCe-mediated ischemic neuroprotection. In purified mitochondrial fractions, PKCe enhanced Nampt levels in an AMPK-dependent manner and was required for increased mitochondrial Nampt after IPC or resveratrol treatment. Analysis of intrinsic NAD autofluorescence using two-photon microscopy revealed that PKCe modulated NAD in the mitochondrial fraction. Further assessments of mitochondrial NAD concentrations showed that PKCe has a key role in regulating the mitochondrial NAD þ / nicotinamide adenine dinucleotide reduced (NADH) ratio after IPC and resveratrol treatment in an AMPK-and Nampt-dependent manner. These findings indicate that PKCe is critical to increase or maintain mitochondrial Nampt and NAD after pathways of ischemic neuroprotection in the brain.

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Section: Discussionmentioning

confidence: 99%

Protein Kinase C Epsilon Regulates Mitochondrial Pools of Nampt and NAD Following Resveratrol and Ischemic Preconditioning in the Rat Cortex

Morris-Blanco

Cohan

Neumann

et al. 2014

J Cereb Blood Flow Metab

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“…Multiple studies have demonstrated that HIV-1 Tat protein is a substrate of SIRT1 for deacetylation and functional inhibition or knockdown of SIRT1 is known to enhance Tat’s ability to transactivate HIV-1 (Pinzone et al, 2013; Zhang et al, 2010; Zhang and Wu, 2009). By contrast, in SIRT1-null mouse cells, where there is no SIRT1 expression, Tat transactivation is defective but can be rescued by expression of SIRT1 (Pagans et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications

Das¹,

Dobrowolski²,

Shahir³

et al. 2015

Virology

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HIV patients with severe periodontitis have high levels of residual virus in their saliva and plasma despite effective therapy (HAART). Multiple short chain fatty acids (SCFAs) from periodontal pathogens reactivate HIV-1 in both Jurkat and primary T-cell models of latency. SCFAs not only activate positive transcription elongation factor b (P-TEFb), which is an essential cellular cofactor for Tat, but can also reverse chromatin blocks by inducing histone modifications. SCFAs simultaneously increase histone acetylation by inhibiting class-1/2 histone deacetylases (HDACs) and decrease repressive histone tri-methylation at the proviral LTR by downregulating expression of the class-3 HDAC sirtuin-1 (SIRT1), and the histone methyltransferases enhancer of Zeste homolog 2 (EZH2) and suppressor of variegation 3–9 homolog 1 (SUV39H1). Our findings provide a mechanistic link between periodontal disease and enhanced HIV-1 replication, and suggest that treatment of periodontal disease, or blocking the activities of SCFAs, will have a therapeutic benefit for HIV patients.

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“…All immunoblots were visualized using the Odyssey infrared imaging system (LI-COR Biosciences) according to the manufacturer's instructions. Densitometry was performed using Li-Cor Odyssey instrument software (Zhang et al, 2010).…”

Section: Immunoblottingmentioning

confidence: 99%

EGCG inhibits Tat-induced LTR transactivation: Role of Nrf2, AKT, AMPK signaling pathway

Zhang

Weiwei

et al. 2012

Life Sciences

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Nicotinamide phosphoribosyltransferase/sirtuin 1 pathway is involved in human immunodeficiency virus type 1 Tat‐mediated long terminal repeat transactivation

Cited by 30 publications

References 36 publications

Protein Kinase C Epsilon Regulates Mitochondrial Pools of Nampt and NAD Following Resveratrol and Ischemic Preconditioning in the Rat Cortex

Protein Kinase C Epsilon Regulates Mitochondrial Pools of Nampt and NAD Following Resveratrol and Ischemic Preconditioning in the Rat Cortex

Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications

EGCG inhibits Tat-induced LTR transactivation: Role of Nrf2, AKT, AMPK signaling pathway

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