Elevated CSF and plasma microparticles in a rat model of streptozotocin-induced cognitive impairment

Hosseinzadeh, Soheila; Zahmatkesh, Maryam; Zarrindast, Mohammad‐Reza; Hassanzadeh, Gholamreza; Karimian, Morteza; Sarrafnejad, Abdolfattah

doi:10.1016/j.bbr.2013.09.019

Cited by 23 publications

(7 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The overall numbers of platelet-derived MV detected are in agreement with another recent study carried out in streptozotocin-treated rats ( 26 ) . Interestingly, another study that subjected younger rats (13 weeks old rather than 26 weeks old) to hypoxia described much higher numbers of platelet-derived MV, both in control and in hypoxia-exposed animals ( 27 ) .…”

Section: Discussionsupporting

confidence: 92%

Long-term high fat feeding of rats results in increased numbers of circulating microvesicles with pro-inflammatory effects on endothelial cells

et al. 2015

View full text Add to dashboard Cite

Obesity and type 2 diabetes lead to dramatically increased risks of atherosclerosis and CHD. Multiple mechanisms converge to promote atherosclerosis by increasing endothelial oxidative stress and up-regulating expression of pro-inflammatory molecules. Microvesicles (MV) are small (,1 mm) circulating particles that transport proteins and genetic material, through which they are able to mediate cellcell communication and influence gene expression. Since MV are increased in plasma of obese, insulin-resistant and diabetic individuals, who often exhibit chronic vascular inflammation, and long-term feeding of a high-fat diet (HFD) to rats is a well-described model of obesity and insulin resistance, we hypothesised that this may be a useful model to study the impact of MV on endothelial inflammation. The number and cellular origin of MV from HFD-fed obese rats were characterised by flow cytometry. Total MV were significantly increased after feeding HFD compared to feeding chow (P,0·001), with significantly elevated numbers of MV derived from leucocyte, endothelial and platelet compartments (P, 0·01 for each cell type). MV were isolated from plasma and their ability to induce reactive oxygen species (ROS) formation and vascular cell adhesion molecule (VCAM)-1 expression was measured in primary rat cardiac endothelial cells in vitro. MV from HFD-fed rats induced significant ROS (P,0·001) and VCAM-1 expression (P¼0·0275), indicative of a pro-inflammatory MV phenotype in this model of obesity. These findings confirm that this is a useful model to further study the mechanisms by which diet can influence MV release and subsequent effects on cardio-metabolic health.

show abstract

Section: Discussionsupporting

confidence: 92%

Long-term high fat feeding of rats results in increased numbers of circulating microvesicles with pro-inflammatory effects on endothelial cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…An increase in EV's endothelial markers (CD31+ CD41-, CD144) found in the present study in patients with moderate and severe AD has also been documented in other studies [29] and probably corresponds to endothelial damage and bloodbrain barrier (BBB) destruction [49,50], which could be related to vascular damage [51,52]. Moreover, there are studies reporting endothelial damage secondary to shedding of specific EVs [53].…”

Section: Discussionsupporting

confidence: 83%

“…Fluorescein isothiocyanate (FITC) Annexin V is a protein, binding to negatively charged phospholipids (Bender MedSystems, Austria) and characterizing not only injured cells but also live cells such as cancer cells and thus being considered a universal marker for microvesicles [29].…”

Section: Exosome and MV Markersmentioning

confidence: 99%

Extracellular Vesicles of Alzheimer’s Disease Patients as a Biomarker for Disease Progression

et al. 2020

View full text Add to dashboard Cite

Alzheimer's disease (AD) is a progressive neurodegenerative brain pathology and the most common form of dementia. Evidence suggests that extracellular vesicles (EVs) containing cytokines and microRNA are involved in inflammation regulation. The current study aimed to explore a potential impact of AD patients' EVs on disease progression. Blood samples were collected after obtaining signed informed consent (No. 0462-14-RMB) from 42 AD patients at three stages of disease severity and from 19 healthy controls (HC). EV size and concentration were studied by nanotracking analysis. EV membrane antigens were defined by flow cytometry and Western blot; EV protein contents were screened by protein array; the miRNA content was screened by nanostring technology and validated by RT-PCR. HC and AD patients' EVs consisted of a mixture of small (< 100 nm) and larger vesicles. The myelin oligodendrocyte glycoprotein (MOG) expression on EVs correlated with disease severity. EVs of patients with moderate and severe AD had significantly higher levels of MOG, compared with mild AD patients. Levels of EVs expressing the axonal glycoprotein CD171 were significantly higher in severe AD patients than in HC. Increase in endothelial EVs was observed in AD patients. An above twofold increase was found in the content of inflammatory cytokines and > 50% decrease in growth factors in AD patients' EVs compared with HC-EVs. Levels of let-7g-5p, miR126-3p, miR142-3p, miR-146a-5p, and mir223-3p correlated with disease severity. Neural damage, specific miRNA downregulation, and inflammatory cytokine upregulation, found in patients' EVs, might be used as a biomarker reflecting AD severity.

show abstract

“…As EMVs have the capability to travel further via the blood or cerebrospinal fluid, misfolded proteins may spread via this pathway in a prion-like manner [165,166,167,168,169,170]. In addition, functional effects of such a protein transport have been indicated for Aβ, which progressively accumulates in EMVs with age, while the β-site cleavage of amyloid precursor protein (APP) has been reported to occur inside EMVs [171]. Also, the phosphorylation of tau differs in exosomes compared to total cell lysates, indicating functional consequences for its seeding capability [157].…”

Section: Emvs In Neurodegenerative Diseasesmentioning

confidence: 99%

Peptidylarginine Deiminases—Roles in Cancer and Neurodegeneration and Possible Avenues for Therapeutic Intervention via Modulation of Exosome and Microvesicle (EMV) Release?

Lange

Gallagher

Kholia

et al. 2017

IJMS

View full text Add to dashboard Cite

Exosomes and microvesicles (EMVs) are lipid bilayer-enclosed structures released from cells and participate in cell-to-cell communication via transport of biological molecules. EMVs play important roles in various pathologies, including cancer and neurodegeneration. The regulation of EMV biogenesis is thus of great importance and novel ways for manipulating their release from cells have recently been highlighted. One of the pathways involved in EMV shedding is driven by peptidylarginine deiminase (PAD) mediated post-translational protein deimination, which is calcium-dependent and affects cytoskeletal rearrangement amongst other things. Increased PAD expression is observed in various cancers and neurodegeneration and may contribute to increased EMV shedding and disease progression. Here, we review the roles of PADs and EMVs in cancer and neurodegeneration.

show abstract

Elevated CSF and plasma microparticles in a rat model of streptozotocin-induced cognitive impairment

Cited by 23 publications

References 64 publications

Long-term high fat feeding of rats results in increased numbers of circulating microvesicles with pro-inflammatory effects on endothelial cells

Long-term high fat feeding of rats results in increased numbers of circulating microvesicles with pro-inflammatory effects on endothelial cells

Extracellular Vesicles of Alzheimer’s Disease Patients as a Biomarker for Disease Progression

Peptidylarginine Deiminases—Roles in Cancer and Neurodegeneration and Possible Avenues for Therapeutic Intervention via Modulation of Exosome and Microvesicle (EMV) Release?

Contact Info

Product

Resources

About