Accumulation of Innate Amyloid Beta Peptide in Glioblastoma Tumors

Kucheryavykh, Lilia; Ortiz-Rivera, Jescelica; Kucheryavykh, Yuriy V.; Zayas‐Santiago, Astrid; Díaz-García, Amanda; Inyushin, Mikhail

doi:10.3390/ijms20102482

Cited by 17 publications

(19 citation statements)

References 59 publications

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“…Antibodies against GFAP label glioma cells as well as astrocytes, which become reactive near the tumor, with high expression of GFAP [37]. In addition, we recently showed that glioma cells expressing low levels of GFAP accumulate Aβ in mice [32]. Therefore, we decided to apply antibodies against GFAP, thereby labeling glioma cells and astrocytes, as well as an antibody specifically against NeuN, in order to distinguish between these two cell types.…”

Section: Tumor Cells Of Glial Origin and Some Astrocytes Close To Blomentioning

confidence: 99%

Accumulation of amyloid beta in human glioblastomas

Zayas‐Santiago

Díaz-García

Nuñez-Rodríguez

et al. 2020

Clinical and Experimental Immunology

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Many cancer types are intrinsically associated with specific types of amyloidosis, in which amyloid is accumulated locally inside tumors or systemically. Usually, this condition relates to the hyperproduction of specific amylogenic proteins. Recently, we found that the accumulation of amyloid beta (Aβ) peptide immunofluorescence is linked to glioma cells in mouse tumors. Here we report that amyloid-specific histochemical dyes reveal amyloid accumulation in all human glioma samples. Application of two different antibodies against Aβ peptide (a polyclonal antibody against human Aβ1-42 and a monoclonal pan-specific mAb-2 antibody against Aβ) showed that the amyloid in glioma samples contains Aβ. Amyloid was linked to glioma cells expressing glial-specific fibrillary acidic protein (GFAP) and to glioma blood vessels. Astrocytes close to the glioma site and to affected vessels also accumulated Aβ. We discuss whether amyloid is produced by glioma cells or is the result of systemic production of Aβ in response to glioma development due to an innate immunity reaction. We conclude that amyloid build-up in glioma tumors is a part of the tumor environment, and may be used as a target for developing a novel class of anti-tumor drugs and as an antigen for glioma visualization.

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Section: Tumor Cells Of Glial Origin and Some Astrocytes Close To Blomentioning

confidence: 99%

Accumulation of amyloid beta in human glioblastomas

Zayas‐Santiago

Díaz-García

Nuñez-Rodríguez

et al. 2020

Clinical and Experimental Immunology

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“…Immunostaining was performed using a previously established protocol [37,38]. First, the 40 µm sections were treated for 20 min with a permeabilization solution consisting of 0.03% Triton X-100 (Sigma-Aldrich, St. Louis, MO, USA) and 1% dimethyl sulfoxide (DMSO; MP Biomedicals, Santa Ana, CA, USA) in 0.1 M PBS under gentle agitation (40 rpm).…”

Section: Methodsmentioning

confidence: 99%

Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion

et al. 2019

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It is well known that amyloid beta (Aβ) peptides are generated in blood vessels, released into the brain during thrombosis, and temporarily accumulate in this organ after injury. Here we demonstrate that 24 h after transient middle cerebral artery occlusion (tMCAO), one of the standard models of focal ischemic stroke, Aβ peptide accumulates in the brain, concentrating on the blood vessel walls. Because Aβ oligomers are known to induce significant damage to brain cells, they act as an additional damaging factor during ischemic stroke. Considering that they have been shown to form ion channels in cells, affecting osmotic balance, we used an Aβ peptide channel blocker, tromethamine (2-amino-2-(hydroxymethyl) propane-1,3-diol), to prevent this additional injury. Tromethamine injected 0.1 g/100 g body weight intraperitoneally at 5 min before tMCAO decreased water content in the damaged hemisphere, as measured by dry brain weight. Congo red staining, which binds only to Aβ oligomer plaques (amyloid), showed that there was no significant presence of plaques. Therefore, we suggest that Aβ peptide oligomers are responsible for some of the brain damage during stroke and that blockage of the ion channels that they form could be beneficial in treating this complex neurological syndrome.

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“…It was discovered that plasma levels of Aβ peptides in pancreatic, as well as in esophageal, colorectal, hepatic, and lung cancer patients were significantly higher than in healthy controls ( 24 , 25 ). In glioblastoma, Aβ was found in both oligomeric and aggregated forms to be associated with glioma cells as well as localized in the tumor extracellular space, and it was proposed that blood could be the source of this peptide ( 26 , 27 ). It was shown that platelets are activated near cancer tumors, playing the role of “first responders” during cancer development and metastasis ( 28 ).…”

Section: Aβ Peptide Accumulation Is Associated With a Variety Of Disementioning

confidence: 99%

On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications

et al. 2020

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As do many other immunity-related blood cells, platelets release antimicrobial peptides that kill bacteria, fungi, and even certain viruses. Here we review the literature suggesting that there is a similarity between the antimicrobials released by other blood cells and the amyloid-related Aβ peptide released by platelets. Analyzing the literature, we also propose that platelet-generated Aβ amyloidosis may be more common than currently recognized. This systemic Aβ from a platelet source may participate in various forms of amyloidosis in pathologies ranging from brain cancer, glaucoma, skin Aβ accumulation, and preeclampsia to Alzheimer’s disease and late-stage Parkinson’s disease. We also discuss the advantages and disadvantages of specific animal models for studying platelet-related Aβ. This field is undergoing rapid change, as it evaluates competing ideas in the light of new experimental observations. We summarized both in order to clarify the role of platelet-generated Aβ peptides in amyloidosis-related health disorders, which may be helpful to researchers interested in this growing area of investigation.

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Accumulation of Innate Amyloid Beta Peptide in Glioblastoma Tumors

Cited by 17 publications

References 59 publications

Accumulation of amyloid beta in human glioblastomas

Accumulation of amyloid beta in human glioblastomas

Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion

On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications

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