Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

Woller, Sarah A.; Choi, Sung Hyuk; An, Eun Jung; Low, Hann; Schneider, Dina A.; Ramachandran, Roshni; Kim, Jung-Su; Bae, Yun Soo; Sviridov, Dmitri; Corr, Maripat; Yaksh, Tony L.; Miller, Yury I.

doi:10.1016/j.celrep.2018.04.110

Cited by 57 publications

(111 citation statements)

References 58 publications

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“…These cell culture experiments were corroborated with experiments in embryonic zebrafish in which apoa1bp knockdown resulted in ectopic and excessive angiogenesis (22). Similar to the effect of AIBP on endothelial cells, AIBP has been reported to promote cholesterol efflux from THP-1derived and RAW macrophages and microglia (23)(24)(25).…”

Section: Introductionsupporting

confidence: 62%

“…Overexpression of AIBP delivered by an adeno-associated virus reduces atherosclerosis in hypercholesterolemic mouse models (24,39). In addition, spinal delivery of recombinant AIBP prevents neuropathic pain states in mice (25).…”

Section: Discussionmentioning

confidence: 99%

“…Quantitative PCR. Quantitative PCR (qPCR) was performed as previously described (24,25). Total RNA was isolated using Nucleospin RNA columns (Clontech).…”

Section: Methodsmentioning

confidence: 99%

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AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation

et al. 2018

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Acute respiratory distress syndrome (ARDS) is characterized by an excessive pulmonary inflammatory response. Removal of excess cholesterol from the plasma membrane of inflammatory cells helps reduce their activation. The secreted apolipoprotein A-I binding protein (AIBP) has been shown to augment cholesterol efflux from endothelial cells to the plasma lipoprotein HDL. Here, we find that AIBP was expressed in inflammatory cells in the human lung and was secreted into the bronchoalveolar space in mice subjected to inhalation of LPS. AIBP bound surfactant protein B and increased cholesterol efflux from alveolar macrophages to calfactant, a therapeutic surfactant formulation. In vitro, AIBP in the presence of surfactant reduced LPS-induced p65, ERK1/2 and p38 phosphorylation, and IL-6 secretion by alveolar macrophages. In vivo, inhalation of AIBP significantly reduced LPS-induced airspace neutrophilia, alveolar capillary leak, and secretion of IL-6. These results suggest that, similar to HDL in plasma, surfactant serves as a cholesterol acceptor in the lung. Furthermore, lung injury increases pulmonary AIBP expression, which likely serves to promote cholesterol efflux to surfactant and reduce inflammation.

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Section: Introductionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation

et al. 2018

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“…54,55 This is in line with the data that TLR-4 interacts with ApoA-I binding protein, recently shown in a pain model. 11 Oral D-4F is safe and well tolerated by high-risk cardiovascular patients. The daily application of single doses of D-4F reduced their HDL-inflammatory index.…”

Section: Discussionmentioning

confidence: 99%

D-4F, an ApoA-I mimetic peptide ameliorating TRPA1-mediated nocifensive behaviour in a model of neurogenic inflammation

et al. 2020

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Background: High doses of capsaicin are recommended for the treatment of neuropathic pain. However, low doses evoke mechanical hypersensitivity. Activation of the capsaicin chemosensor transient receptor potential vanilloid 1 (TRPV1) induces neurogenic inflammation. In addition to the release of pro-inflammatory mediators, reactive oxygen species are produced. These highly reactive molecules generate oxidised phospholipids and 4-hydroxynonenal (4-HNE) which then directly activate TRP ankyrin 1 (TRPA1). The apolipoprotein A-I mimetic peptide D-4F neutralises oxidised phospholipids. Here, we asked whether D-4F ameliorates neurogenic hypersensitivity in rodents by targeting reactive oxygen species and 4-HNE in the capsaicin-evoked pain model. Results: Co-application of D-4F ameliorated capsaicin-induced mechanical hypersensitivity and allodynia as well as persistent heat hypersensitivity measured by Randell-Selitto, von Frey and Hargreaves test, respectively. In addition, mechanical hypersensitivity was blocked after co-injection of D-4F with the reactive oxygen species analogue H 2 O 2 or 4-HNE. In vitro studies on dorsal root ganglion neurons and stably transfected cell lines revealed a TRPA1-dependent inhibition of the calcium influx when agonists were pre-incubated with D-4F. The capsaicin-induced calcium influx in TRPV1-expressing cell lines and dorsal root ganglion neurons sustained in the presence of D-4F. Conclusions: D-4F is a promising compound to ameliorate TRPA1-dependent hypersensitivity during neurogenic inflammation.

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“…Most amyloidogenic proteins concentrate and sometimes processed in lipid rafts, initiating the rollover of neurodegeneration (10). Raft mitigation strategy using βcyclodextrins and Apolipoprotein A-I Binding Protein (AIBP) were successfully tested in restricting inflammation, neuropathic pain, atherosclerosis and HIV infection (11)(12)(13)(14), but delicate balance must be preserved not to affect physiological pathways relying on lipid rafts.…”

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confidence: 99%

Biology of Lipid Rafts: Introduction to the Thematic Review Series

Sviridov

Miller

2020

Journal of Lipid Research

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Lipid rafts are organized plasma membrane microdomains, which provide a distinct level of regulation of cellular metabolism and response to extracellular stimuli, affecting a diverse range of physiologic and pathologic processes. This Thematic Review Series focuses on Biology of Lipid Rafts rather than on their composition or structure. The aim is to provide an overview of ideas on how lipid rafts are involved in regulation of different pathways and how they interact with other layers of metabolic regulation. Articles in the series will review the involvement of lipid rafts in regulation of hematopoiesis, production of extracellular vesicles, host interaction with infection, and the development and progression of cancer, neuroinflammation, and neurodegeneration, as well as the current outlook on therapeutic targeting of lipid rafts.

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Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

Cited by 57 publications

References 58 publications

AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation

AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation

D-4F, an ApoA-I mimetic peptide ameliorating TRPA1-mediated nocifensive behaviour in a model of neurogenic inflammation

Biology of Lipid Rafts: Introduction to the Thematic Review Series

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