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Frail older adults show a distinct plasma microvesicle profile suggesting a prothrombotic and proinflammatory phenotype

In a global context of advanced aging, geriatric diseases such as frailty syndrome face challenges in the search for biomarkers and preventive strategies. Frailty has been associated with atherothrombotic pathologies. Circulating microvesicles (cMVs), phospholipid‐rich vesicles with a size of 0.1–1....

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Published in:Journal of cellular physiology 2021-03, Vol.236 (3), p.2099-2108
Main Authors: Arauna, Diego, Chiva‐Blanch, Gemma, Padró, Teresa, Fuentes, Eduardo, Palomo, Iván, Badimon, Lina
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creator Arauna, Diego
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description In a global context of advanced aging, geriatric diseases such as frailty syndrome face challenges in the search for biomarkers and preventive strategies. Frailty has been associated with atherothrombotic pathologies. Circulating microvesicles (cMVs), phospholipid‐rich vesicles with a size of 0.1–1.0 μm, have been shown to participate in atherothrombosis onset and progression. We have hypothesized that cMVs from platelets, and vascular and immune cells, are increased in frail older adults. To verify this, a prevalent‐case control study was designed with 28 frail older and 27 nonfrail older adults older than 64 years. Frailty was defined by Fried's phenotype. Total cMVs, annexin V positive (AV+)‐cMVs, and annexin V negative (AV−)‐cMVs derived from blood and vascular cells were measured by flow cytometry. In the analysis of total cMVs, the frail group presented higher levels of CD14+/CD142+ (p = .042), CD41a+/CD142+ (p = .041), and CD56+ (p = .025), CD14+cMVs (p = .043), and CD16+/CD14+ (p = .019) cMVs levels. Within the phosphatidylserine‐exposing cMVs (AV+), the frail group showed higher CD14+/AV+ (p = .044), CD9+/AV+ (p = .031), P2RY12+/AV+ (p = .028), and CD235a+/AV+ (p = .043) cMVs concentrations. Finally, within AV− cMVs, the frail group showed higher CD142+/CD41a+/AV− cMVs concentrations originated from platelets (p = .027), CD56+/AV− originated from natural killer cells (p = .022), and CD34+/AV− cMVs from hematopoietic stem cells (p = .037). In summary, frail older adults present higher concentrations of platelet‐, leukocyte‐, and hematopoietic cell‐derived cMVs compared to robust age‐matched older adults. These cMVs may be involved in the deregulation of the immune system, endothelial damage, and increased risk of thrombosis associated with frailty. (a) In the present study, we show for the first time a complete study about the production profile of circulating microvesicles (cMVs) from circulating cells in frail older adults, according to Fried's criteria. (b) We provide evidence that frail older adults present higher concentrations of platelet‐, leukocyte‐, and hematopoietic cell‐derived cMVs compared to robust age‐matched older adults. (c) The findings from this study provide a better understanding of the potential role of the cMVs production in the deregulation of the immune system, endothelial damage, and increased risk of thrombosis associated with frail older adults.
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Frailty has been associated with atherothrombotic pathologies. Circulating microvesicles (cMVs), phospholipid‐rich vesicles with a size of 0.1–1.0 μm, have been shown to participate in atherothrombosis onset and progression. We have hypothesized that cMVs from platelets, and vascular and immune cells, are increased in frail older adults. To verify this, a prevalent‐case control study was designed with 28 frail older and 27 nonfrail older adults older than 64 years. Frailty was defined by Fried's phenotype. Total cMVs, annexin V positive (AV+)‐cMVs, and annexin V negative (AV−)‐cMVs derived from blood and vascular cells were measured by flow cytometry. In the analysis of total cMVs, the frail group presented higher levels of CD14+/CD142+ (p = .042), CD41a+/CD142+ (p = .041), and CD56+ (p = .025), CD14+cMVs (p = .043), and CD16+/CD14+ (p = .019) cMVs levels. 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Frailty has been associated with atherothrombotic pathologies. Circulating microvesicles (cMVs), phospholipid‐rich vesicles with a size of 0.1–1.0 μm, have been shown to participate in atherothrombosis onset and progression. We have hypothesized that cMVs from platelets, and vascular and immune cells, are increased in frail older adults. To verify this, a prevalent‐case control study was designed with 28 frail older and 27 nonfrail older adults older than 64 years. Frailty was defined by Fried's phenotype. Total cMVs, annexin V positive (AV+)‐cMVs, and annexin V negative (AV−)‐cMVs derived from blood and vascular cells were measured by flow cytometry. In the analysis of total cMVs, the frail group presented higher levels of CD14+/CD142+ (p = .042), CD41a+/CD142+ (p = .041), and CD56+ (p = .025), CD14+cMVs (p = .043), and CD16+/CD14+ (p = .019) cMVs levels. Within the phosphatidylserine‐exposing cMVs (AV+), the frail group showed higher CD14+/AV+ (p = .044), CD9+/AV+ (p = .031), P2RY12+/AV+ (p = .028), and CD235a+/AV+ (p = .043) cMVs concentrations. Finally, within AV− cMVs, the frail group showed higher CD142+/CD41a+/AV− cMVs concentrations originated from platelets (p = .027), CD56+/AV− originated from natural killer cells (p = .022), and CD34+/AV− cMVs from hematopoietic stem cells (p = .037). In summary, frail older adults present higher concentrations of platelet‐, leukocyte‐, and hematopoietic cell‐derived cMVs compared to robust age‐matched older adults. These cMVs may be involved in the deregulation of the immune system, endothelial damage, and increased risk of thrombosis associated with frailty. (a) In the present study, we show for the first time a complete study about the production profile of circulating microvesicles (cMVs) from circulating cells in frail older adults, according to Fried's criteria. (b) We provide evidence that frail older adults present higher concentrations of platelet‐, leukocyte‐, and hematopoietic cell‐derived cMVs compared to robust age‐matched older adults. (c) The findings from this study provide a better understanding of the potential role of the cMVs production in the deregulation of the immune system, endothelial damage, and increased risk of thrombosis associated with frail older adults.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32749745</pmid><doi>10.1002/jcp.29996</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-0099-4108</orcidid><orcidid>https://orcid.org/0000-0002-9162-2459</orcidid><orcidid>https://orcid.org/0000-0003-1921-954X</orcidid><orcidid>https://orcid.org/0000-0001-6093-0160</orcidid><orcidid>https://orcid.org/0000-0001-7132-991X</orcidid></addata></record>
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source Wiley-Blackwell Journals
subjects Adults
Age related diseases
Aging
Aging (natural)
Annexin V
Biomarkers
CD14 antigen
CD16 antigen
CD34 antigen
CD56 antigen
CD9 antigen
Deregulation
Flow cytometry
Frailty
frailty syndrome
Hematopoietic stem cells
Immune system
Inflammation
Leukocytes
microvesicles
Natural killer cells
older adults
Older people
Phenotypes
Phosphatidylserine
Phospholipids
Platelets
Stem cells
Thromboembolism
Thrombosis
title Frail older adults show a distinct plasma microvesicle profile suggesting a prothrombotic and proinflammatory phenotype
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