HIV-1 differentially modulates autophagy in neurons and astrocytes

Mehla, Rajeev; Chauhan, Ankur

doi:10.1016/j.jneuroim.2015.06.001

Cited by 24 publications

(19 citation statements)

References 105 publications

(132 reference statements)

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“…Another study performed on human neuronal cultures has shown that X4 HIV-1 suppresses autophagy leading to neuro-glial toxicity, whereas R5 HIV-1 only causes toxicity in neurons. Results of this study suggest that autophagy plays protective role against HIV-1 insult in human neuronal cultures [38]. Similarly, Tat has been found to cause a decrease in Beclin-1, LC3II, and p62 levels in neurons, suggesting that Tat may induce autophagic degradation by inducing fusion of autophagosomes and lysosomes [31].…”

Section: Autophagy and Hiv-1mentioning

confidence: 94%

Role of Autophagy in HIV Pathogenesis and Drug Abuse

et al. 2016

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Autophagy is a highly regulated process in which excessive cytoplasmic materials are captured and degraded during deprivation conditions. The unique nature of autophagy that clears invasive microorganisms has made it an important cellular defense mechanism in a variety of clinical situations. In recent years, it has become increasingly clear that autophagy is extensively involved in the pathology of HIV-1. To ensure survival of the virus, HIV-1 viral proteins modulate and utilize autophagy pathway so that biosynthesis of the virus is maximized. At the same time, the abuse of illicit drugs such as methamphetamine, cocaine, morphine, and alcohol is thought to be a significant risk factor for the acquirement and progression of HIV-1. During drug-induced toxicity, autophagic activity has been proved to be altered in various cell types. Here we review the current literature on the interaction between autophagy, HIV-1, and drug abuse, and discuss the complex role of autophagy during HIV-1 pathogenesis in co-exposure to illicit drugs.

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Section: Autophagy and Hiv-1mentioning

confidence: 94%

Role of Autophagy in HIV Pathogenesis and Drug Abuse

et al. 2016

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“…Through this mechanism, production of mitochondrial ROS is reduced and mitochondrial membrane potential is maintained, which promotes astrocyte survival [93]. Furthermore, the use of autophagy inducers (rapamycin) and inhibitors (3-MA and leupeptin) reduces or promotes human astrocyte cytotoxicity, respectively [94].…”

Section: Autophagy In Astrocytesmentioning

confidence: 99%

Autophagy in Astrocytes: Importance for Metabolism

Ortiz-Rodriguez¹,

Arévalo²

2020

Preprint

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Autophagy is an essential mechanism to maintain cellular homeostasis. Besides its role in controlling the quality of cytoplasmic components, it participates in nutrient obtaining and lipid mobilization under stressful conditions. Furthermore, autophagy is involved in the regulation of systemic metabolic, a function mainly performed by neuronal populations of the arcuate nucleus of the hypothalamus. Several studies have shown that blockade of autophagy in these neurons can affect central regulation of metabolism and impact body energy balance. Moreover, hypothalamic autophagy can be altered during obesity. However, neurons are not the only cell type involved in the central regulation of metabolism. Astrocytes, essential cells for brain homeostasis, are key metabolic regulators. They can sense metabolic signals in the hypothalamus and modulate systemic functions as glucose homeostasis and feeding response. Moreover, the response of astrocytes to obesity has been widely studied. Astrocytes are important mediators of brain inflammation and can be affected by increased levels of saturated fatty acids associated to obesity. Although autophagy plays important roles for astrocyte homeostasis and functioning, the contribution of astrocyte autophagy to systemic metabolism has not been analysed. Furthermore, how obesity can impact astrocyte autophagy is poorly understood. More studies are needed in other to understand the contribution of astrocyte autophagy to metabolism.

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“…The autophagy pathway can be modulated by HIV or Tat exposure, with other HIVproteins also able to modulate autophagy. Other studies have reported that upon HIV treatment, human astrocytes show increased protein expression of Beclin 1 indicative of autophagy initiation in conjunction with elevated LC3 [188]. In addition, it has been reported that Tat is able to stimulate autophagy by increasing the levels of BAG3 in human glial cells shown by increased LC3 II protein via western blot and immunofluorescence [193].…”

Section: Cholewo Et Al On the Effects Of Tat And Morphine On Opioid Rmentioning

confidence: 97%

“…For example, the viral protein Nef was shown to mimic the fusion inhibitor bafilomycin A1 and prevent autophagic degradation which can ultimately lead to increased viral presence [194]. This induction and later blockade has also been shown in astrocytes [188]. Given these results, it can be said that the role of autophagy in HAND is a complicated one with effects being cell type dependent and specific to particular stages of the autophagy pathway.…”

Section: Autophagy In Handmentioning

confidence: 98%

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HIV Tat and Morphine-induced Neurodegeneration in a Beclin 1 Hemizygous Mouse Model

Lapierre¹

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HIV-1 differentially modulates autophagy in neurons and astrocytes

Cited by 24 publications

References 105 publications

Role of Autophagy in HIV Pathogenesis and Drug Abuse

Role of Autophagy in HIV Pathogenesis and Drug Abuse

Autophagy in Astrocytes: Importance for Metabolism

HIV Tat and Morphine-induced Neurodegeneration in a Beclin 1 Hemizygous Mouse Model

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