Differential gene expression mediated by 15-hydroxyeicosatetraenoic acid in LPS-stimulated RAW 264.7 cells

Schrimpe, Alexandra C.; Wright, David W.

doi:10.1186/1475-2875-8-195

Cited by 7 publications

(7 citation statements)

References 40 publications

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“…antigen-processing gene family, including HLA-E, TAP1, TAP2, and TAPBP [29,30]. Considering that the transcription of TAPBP is upregulated by 15(S)-HETE [29,30], the mechanism of induction of the TAPBP gene may differ between AERD and ATA in the presence of aspirin.…”

Section: Discussionmentioning

confidence: 99%

Association analysis of tapasin polymorphisms with aspirin-exacerbated respiratory disease in asthmatics

Cho

Park²,

Park³

et al. 2013

Pharmacogenetics and Genomics

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Section: Discussionmentioning

confidence: 99%

Association analysis of tapasin polymorphisms with aspirin-exacerbated respiratory disease in asthmatics

Cho

Park²,

Park³

et al. 2013

Pharmacogenetics and Genomics

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“…This effect was related to the lipid moiety of Hz, since lipid-free synthetic Hz (β-hematin) did not modulate MMP-9 expression. The Hz-dependent enhancement of MMP-9 transcription and protein release was mimicked by 4-hydroxy-2-nonenal (4-HNE) [ 178 ], a molecule generated by Hz from polyunsaturated fatty acids [ 179 ].…”

Section: Introductionmentioning

confidence: 99%

Host matrix metalloproteinases in cerebral malaria: new kids on the block against blood–brain barrier integrity?

Polimeni

Prato

2014

Fluids Barriers CNS

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Cerebral malaria (CM) is a life-threatening complication of falciparum malaria, associated with high mortality rates, as well as neurological impairment in surviving patients. Despite disease severity, the etiology of CM remains elusive. Interestingly, although the Plasmodium parasite is sequestered in cerebral microvessels, it does not enter the brain parenchyma: so how does Plasmodium induce neuronal dysfunction? Several independent research groups have suggested a mechanism in which increased blood–brain barrier (BBB) permeability might allow toxic molecules from the parasite or the host to enter the brain. However, the reported severity of BBB damage in CM is variable depending on the model system, ranging from mild impairment to full BBB breakdown. Moreover, the factors responsible for increased BBB permeability are still unknown. Here we review the prevailing theories on CM pathophysiology and discuss new evidence from animal and human CM models implicating BBB damage. Finally, we will review the newly-described role of matrix metalloproteinases (MMPs) and BBB integrity. MMPs comprise a family of proteolytic enzymes involved in modulating inflammatory response, disrupting tight junctions, and degrading sub-endothelial basal lamina. As such, MMPs represent potential innovative drug targets for CM.

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“…23 Dynamic measurements were achieved using a multianalyte microphysiometer (MAMP) that simultaneously measures multiple extracellular analytes involved in metabolism in real-time. 24 Measuring the response of multiple cells normalizes cellular variability and local fluctuations, improving the study of complete cellular dynamics measured over time.…”

Section: Introductionmentioning

confidence: 99%

Metabolic Impact of 4-Hydroxynonenal on Macrophage-Like RAW 264.7 Function and Activation

Harry

Hiatt

Kimmel

et al. 2012

Chem. Res. Toxicol.

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Metabolic profiling of macrophage metabolic response upon exposure to 4-hydroxynonenal (HNE) demonstrates that HNE does not simply inactivate superoxide generating enzymes but could also be responsible for the impairment of downfield signaling pathways. Multianalyte microphysiometry (MAMP) was employed to simultaneously measure perturbations in extracellular acidification, lactate production and oxygen consumption for the examination of aerobic and anaerobic pathways. Combining the activation of oxidative burst with phorbol myristate acetate (PMA) and the immunosuppression with HNE, the complex nature of HNE toxicity was determined to be concentration- and time-dependent. Further analysis was utilized to assess the temporal effect of HNE on reactive oxygen species (ROS) production and on protein kinase C (PKC). Increased levels of HNE with decreasing PKC activity suggest PKC is a target for HNE adductation prior to oxidative burst. Additionally, localization of PKC to the cell membrane was prevented with the introduction of HNE, demonstrating a consequence of HNE adductation on NADPH activation. The impairment of ROS by HNE suggests HNE has a greater role in foam cell formation and tissue damage than is already known. Although work has been performed to understand the effect of HNE’s regulation of specific signaling pathways, details regarding its involvement in cellular metabolism as a whole are generally unknown. This study examines the impact of HNE on macrophage oxidative burst and identifies PKC as a key protein for HNE suppression and eventual metabolic response.

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Differential gene expression mediated by 15-hydroxyeicosatetraenoic acid in LPS-stimulated RAW 264.7 cells

Cited by 7 publications

References 40 publications

Association analysis of tapasin polymorphisms with aspirin-exacerbated respiratory disease in asthmatics

Association analysis of tapasin polymorphisms with aspirin-exacerbated respiratory disease in asthmatics

Host matrix metalloproteinases in cerebral malaria: new kids on the block against blood–brain barrier integrity?

Metabolic Impact of 4-Hydroxynonenal on Macrophage-Like RAW 264.7 Function and Activation

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