<scp>HIV</scp>‐1 Tat C modulates <scp>NOX</scp>2 and <scp>NOX</scp>4 expressions through miR‐17 in a human microglial cell line

Jadhav, Vaishnavi; Krause, Karl‐Heinz; Singh, Sunit K.

doi:10.1111/jnc.12933

Cited by 46 publications

(42 citation statements)

References 69 publications

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“…The cell line expresses microglial and macrophage surface markers [16]. Similar to primary microglia, these cells show a distinct response of cytokines and chemokines in contact to pathogens [17] and were already described in the context of HIV [18]. Cells were cultured in Minimum Essential Media (MEM) (Thermo Fisher Scientific, Darmstadt, Germany), supplemented with 10% fetal calf serum (FCS) (Sigma-Aldrich, Taufkirchen, Germany) and 100 units/ml (U/ml) penicillin/streptomycin (Pen/Strep, Invitrogen, Darmstadt, Germany) in T-75 flasks (PRIMARIA™ Tissue Culture Flask, Becton Dickinson, Heidelberg, Germany).…”

Section: Methodsmentioning

confidence: 99%

Teriflunomide and monomethylfumarate target HIV-induced neuroinflammation and neurotoxicity

Ambrosius

Faissner

Guse

et al. 2017

J Neuroinflammation

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HIV-associated neurocognitive disorders (HAND) affect about 50% of infected patients despite combined antiretroviral therapy (cART). Ongoing compartmentalized inflammation mediated by microglia which are activated by HIV-infected monocytes has been postulated to contribute to neurotoxicity independent from viral replication. Here, we investigated effects of teriflunomide and monomethylfumarate on monocyte/microglial activation and neurotoxicity. Human monocytoid cells (U937) transduced with a minimal HIV-Vector were co-cultured with human microglial cells (HMC3). Secretion of pro-inflammatory/neurotoxic cytokines (CXCL10, CCL5, and CCL2: p < 0.001; IL-6: p < 0.01) by co-cultures was strongly increased compared to microglia in contact with HIV-particles alone. Upon treatment with teriflunomide, cytokine secretion was decreased (CXCL10, 3-fold; CCL2, 2.5-fold; IL-6, 2.2-fold; p < 0.001) and monomethylfumarate treatment led to 2.9-fold lower CXCL10 secretion (p < 0.001). Reduced toxicity of co-culture conditioned media on human fetal neurons by teriflunomide (29%, p < 0.01) and monomethylfumarate (27%, p < 0.05) indicated functional relevance. Modulation of innate immune functions by teriflunomide and monomethylfumarate may target neurotoxic inflammation in the context of HAND.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0829-2) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Teriflunomide and monomethylfumarate target HIV-induced neuroinflammation and neurotoxicity

Ambrosius

Faissner

Guse

et al. 2017

J Neuroinflammation

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“…Tat also stimulates the production of CCL2/MCP‐1, IL‐1β, TNFα and inducible nitric oxide synthase (iNOS) in a cyclooxygenase (Cox)−2‐dependent manner, downstream of NF‐κB activation (Flora et al, ). Finally, activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases also promotes the secretion of various pro‐inflammatory cytokines and associated neurotoxicity following Tat exposure (Bokhari et al, ; Jadhav et al, ; Turchan‐Cholewo et al, ).…”

Section: The Effect Of Viral Proteins On Microglial Functionmentioning

confidence: 99%

Fate of microglia during HIV‐1 infection: From activation to senescence?

Chen

Partridge

Sell

et al. 2016

Glia

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Microglia support productive human immunodeficiency virus type 1 (HIV-1) infection and disturbed microglial function could contribute to the development of HIV-associated neurocognitive disorders (HAND). Better understanding of how HIV-1 infection and viral protein exposure modulate microglial function during the course of infection could lead to the identification of novel therapeutic targets for both the eradication of HIV-1 reservoir and treatment of neurocognitive deficits. This review first describes microglial origins and function in the normal central nervous system (CNS), and the changes that occur during aging. We then critically discuss how HIV-1 infection and exposure to viral proteins such as Tat and gp120 affect various aspects of microglial homeostasis including activation, cellular metabolism and cell cycle regulation, through pathways implicated in cellular stress responses including p38 mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB). We thus propose that the functions of human microglia evolve during both healthy and pathological aging. Aging-associated dysfunction of microglia comprises phenotypes resembling cellular senescence, which could contribute to cognitive impairments observed in various neurodegenerative diseases. In addition, microglia seem to develop characteristics that could be related to cellular senescence post-HIV-1 infection and after exposure to HIV-1 viral proteins. However, despite its potential role as a component of HAND and likely other neurocognitive disorders, microglia senescence has not been well characterized and should be the focus of future studies, which could have high translational relevance.

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“…All these cell lines were developed through SV40 immortalization of human primary microglial cells, whereas a fraction of SV40-immortalized adult microglial cells were further engineered to express the human telomerase reverse transcriptase (hTERT) and reduce the proliferation rate [19]. To the best of our knowledge, two cell lines are commercially available, the human microglial clone 3 cell line, HMC3 [17,[20][21][22] and the "Immortalized Human Microglia -SV40", developed and distributed by Applied Biological Materials (Vancouver, Canada) [23][24][25][26][27][28]. The HMC3 has been recently authenticated by the American Type Culture Collection (ATCC®), a leading nonprofit organization in the authentication and distribution of biologic material, microorganisms, and standards.…”

Section: Introductionmentioning

confidence: 99%

The human microglial HMC3 cell line: where do we stand? A systematic literature review

Russo

Cappoli

Coletta

et al. 2018

J Neuroinflammation

180

130

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Microglia, unique myeloid cells residing in the brain parenchyma, represent the first line of immune defense within the central nervous system. In addition to their immune functions, microglial cells play an important role in other cerebral processes, including the regulation of synaptic architecture and neurogenesis. Chronic microglial activation is regarded as detrimental, and it is considered a pathogenic mechanism common to several neurological disorders. Microglial activation and function have been extensively studied in rodent experimental models, whereas the characterization of human cells has been limited due to the restricted availability of primary sources of human microglia. To overcome this problem, human immortalized microglial cell lines have been developed. The human microglial clone 3 cell line, HMC3, was established in 1995, through SV40-dependent immortalization of human embryonic microglial cells. It has been recently authenticated by the American Type Culture Collection (ATCC®) and distributed under the name of HMC3 (ATCC®CRL-3304). The HMC3 cells have been used in six research studies, two of which also indicated by ATCC® as reference articles. However, a more accurate literature revision suggests that clone 3 was initially distributed under the name of CHME3. In this regard, several studies have been published, thus contributing to a more extensive characterization of this cell line. Remarkably, the same cell line has been used in different laboratories with other denominations, i.e., CHME-5 cells and C13-NJ cells. In view of the fact that “being now authenticated by ATCC®” may imply a wider distribution of the cells, we aimed at reviewing data obtained with the human microglia cell line clone 3, making the readers aware of this complicated nomenclature. In addition, we also included original data, generated in our laboratory with the HMC3 (ATCC®CRL-3304) cells, providing information on the current state of the culture together with supplementary details on the culturing procedures to obtain and maintain viable cells.

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HIV‐1 Tat C modulates NOX2 and NOX4 expressions through miR‐17 in a human microglial cell line

Cited by 46 publications

References 69 publications

Teriflunomide and monomethylfumarate target HIV-induced neuroinflammation and neurotoxicity

Teriflunomide and monomethylfumarate target HIV-induced neuroinflammation and neurotoxicity

Fate of microglia during HIV‐1 infection: From activation to senescence?

The human microglial HMC3 cell line: where do we stand? A systematic literature review

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