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Frail older adults show a distinct plasma microvesicle profile suggesting a prothrombotic and proinflammatory
Diego Arauna1, Gemma Chiva-Blanch2,3,4, Teresa Padró2,5
1Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Thrombosis Research Center, Medical Technology, Universidad de Talca, Talca, Chile.
Abstract:
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.
Insights
Frail older adults exhibit elevated levels of circulating microvesicles (cMVs) derived from platelets, leukocytes, and hematopoietic stem cells. These cMVs may contribute to immune dysregulation and increased thrombosis risk in frailty.
Area of Science:
- Gerontology
- Biomedical Sciences
- Cardiovascular Research
Background:
- Frailty syndrome is a growing concern in aging populations, often linked to atherothrombotic conditions.
- Circulating microvesicles (cMVs) are implicated in the development and progression of atherosclerosis and thrombosis.
- The specific role of cMVs in the pathophysiology of frailty remains to be fully elucidated.
Purpose of the Study:
- To investigate the hypothesis that circulating microvesicles (cMVs) are increased in frail older adults compared to non-frail individuals.
- To identify the cellular origins and characteristics of cMVs associated with frailty.
- To explore the potential contribution of cMVs to the adverse health outcomes linked to frailty.
Main Methods:
- A prevalent-case control study involving 28 frail and 27 non-frail older adults (age > 64 years) was conducted.
- Frailty was assessed using Fried's phenotype criteria.
- Flow cytometry was employed to quantify total cMVs, phosphatidylserine-exposing (AV+) cMVs, and non-exposing (AV-) cMVs, with specific cell surface markers used for identification.
Main Results:
- Frail individuals showed significantly higher concentrations of total cMVs expressing markers for monocytes (CD14+), platelets (CD41a+), and natural killer cells (CD56+).
- Elevated levels of phosphatidylserine-exposing cMVs (AV+) were observed in frail subjects, particularly those derived from monocytes (CD14+), platelets (P2RY12+), and erythrocytes (CD235a+).
- Increased concentrations of AV- cMVs originating from platelets (CD142+/CD41a+), natural killer cells (CD56+), and hematopoietic stem cells (CD34+) were also found in the frail group.
Conclusions:
- Frail older adults have a higher burden of circulating microvesicles derived from platelets, leukocytes, and hematopoietic cells.
- These cMVs may play a role in the immune system deregulation, endothelial damage, and heightened thrombotic risk associated with frailty.
- Further research is warranted to explore the therapeutic potential of targeting cMVs in managing frailty and its complications.
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