Horizontal MicroRNA Transfer by Platelets – Evidence and Implications

Mußbacher, Marion; Pirabe, Anita; Brunnthaler, Laura; Schrottmaier, Waltraud C.; Assinger, Alice

doi:10.3389/fphys.2021.678362

Cited by 16 publications

(9 citation statements)

References 120 publications

(154 reference statements)

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“…In recent years, it has been found that platelet-derived miRNAs can be released into the peripheral blood via encapsulation in PMPs ( 35 ). In contact with the neighboring cells, the internalized PMPs deliver miRNAs, which regulate the function of the recipient cell by post-transcriptional reprogramming ( 36 ). MiR-223, which is abundantly expressed in human platelets, is encapsulated in PMPs and released upon thrombin stimulation ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease

et al. 2022

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BackgroundKawasaki disease (KD) is an acute vasculitis that may result in permanent coronary artery damage with unknown etiology. Endothelial cell (EC) dysfunction and platelet hyperactivity are the hallmarks of KD. Platelets are involved in the development of endothelial dysfunction. MiR-223 transferred by platelet microparticles (PMPs) has been found to involve in the functional regulation of endothelial cells in sepsis. However, the role of platelet-derived miR-223 in endothelial dysfunction has not yet been investigated in KD.ObjectivesWe seek to investigate the role of platelet-derived miR-223 in endothelial dysfunction of KD vasculopathy.Methods and resultsForty-five acute KD patients and 45 matched controls were randomly recruited in the study. When co-cultured with human coronary artery endothelial cells (HCAECs), KD platelets with higher levels of miR-223 were incorporated into HCAECs, resulting in the horizontal transfer of miR-223. Using KD platelets, PMPs, and platelet-releasate from the same amount of blood co-cultured with HCAECs, we found the increased expression of miR-223 in HCAECs was primarily derived from KD platelets, rather than PMPs or free miRNAs from platelet- releasate. KD platelet-derived miR-223 attenuated TNF-α induced intercellular cell adhesion molecule-1 (ICAM-1) expression in HCAECs. KD platelet-derived miR-223 also suppressed the monocyte adhesion to HCAECs. In vivo, platelet-specific miR-223 knockout (PF4-cre: miR-223flox/flox) C57BL/6 mice and miR-223flox/flox C57BL/6 mice were used. Using Lactobacillus casei cell wall extract (LCWE) to establish KD murine model, we showed that in LCWE-injected PF4-cre: miR-223flox/flox mice, deficiency of platelet-miR-223 exacerbates the medial thickening of the abdominal aorta, increased ICAM-1 expression with concomitant CD45+ inflammatory cells infiltration into the endothelium compared to LCWE-injected miR-223flox/flox mice.ConclusionsThe horizontal transfer of platelet-derived miR-223 suppresses the expression of ICAM-1 in HCAECs, which at least in part attenuates leukocyte adhesion, thereby reducing endothelial damage in KD vasculitis

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Section: Discussionmentioning

confidence: 99%

Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease

et al. 2022

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“…38–40 During their biogenesis, platelets are packaged with a finite quantity of megakaryocytic RNA, which following their release into the circulation is either translated, degraded or released. 41 , 42 Being anucleate, platelets are unable to transcribe new RNA and therefore RNA levels decline across platelet life span. This phenomenon has been well established and as such has allowed the monitoring of platelet turnover in patient groups through measurement of the immature platelet fractions within full blood counts.…”

Section: Omic Alterations In An Aged Plateletmentioning

confidence: 99%

What can we learn from senescent platelets, their transcriptomes and proteomes?

et al. 2023

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Research into the natural aging process of platelets has garnered much research interest in recent years, and there have long been associations drawn between the proportion of newly formed platelets in the circulation and the risk of thrombosis. However, these observations have largely been demonstrated in patient groups in which there may be underlying systemic changes that effect platelet function. Recent advances in technology have allowed in-depth analysis of differently aged platelets isolated from the peripheral blood of healthy individuals and have demonstrated that aged platelets, often referred to as senescent platelets, undergo extensive changes in the transcriptome and proteome. Ultimately, these changes result in platelets whose functions have deteriorated such that they cannot partake in hemostatic responses to the same extent as newly formed platelets. Here, we review transcriptomic and proteomic research in platelet aging in the context of health and how this research sheds light upon alterations in platelet structure and function.

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“…In addition, the pharmacokinetics related to the time between drug administration and blood sampling need to be considered. Several studies to date aimed to identify an improved biomarker for cardiovascular risk stratification and assessment of platelet reactivity, among them miRNAs are currently becoming the centre of scientific attention [ 47 ]. Indeed, several correlations between miRNA concentrations and platelet reactivity have been found [ 36 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 ] ( Figure 2 ).…”

Section: Mirnas Expression and Platelet Reactivitymentioning

confidence: 99%

Circulating and Platelet MicroRNAs in Cardiovascular Risk Assessment and Antiplatelet Therapy Monitoring

Procyk

Klimczak-Tomaniak

Sygitowicz

et al. 2022

JCM

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Micro-ribonucleic acids (microRNAs) are small molecules that take part in the regulation of gene expression. Their function has been extensively investigated in cardiovascular diseases (CVD). Most recently, miRNA expression levels have been suggested as potential biomarkers of platelet reactivity or response to antiplatelet therapy and tools for risk stratification for recurrence of ischemic evens. Among these, miR-126 and miR-223 have been found to be of particular interest. Despite numerous studies aimed at understanding the prognostic value of miRNA levels, no final conclusions have been drawn thus far regarding their utility in clinical practice. The aim of this review is to critically appraise the evidence on the association between miRNA expression, cardiovascular risk and on-treatment platelet reactivity as well as provide insights on future developments in the field.

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Horizontal MicroRNA Transfer by Platelets – Evidence and Implications

Cited by 16 publications

References 120 publications

Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease

Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease

What can we learn from senescent platelets, their transcriptomes and proteomes?

Circulating and Platelet MicroRNAs in Cardiovascular Risk Assessment and Antiplatelet Therapy Monitoring

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