microRNA‐19b‐3p‐containing extracellular vesicles derived from macrophages promote the development of atherosclerosis by targeting JAZF1

Wang, Qingshan; Dong, Yuandi; Wang, Haiyang

doi:10.1111/jcmm.16938

Cited by 20 publications

(11 citation statements)

References 27 publications

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“…Macrophages release EVs rich in cholesterol that can be taken up by VSMC [ 148 ]. The contribution of macrophage foam cell-derived EVs to enhance VSMC adhesion and migration was shown by the transfer of integrins and subsequent downstream activation of ERK and Ak strain transforming (AKT) [ 144 ] and the transport of miR-19b-3p and targeting juxtaposed with another zinc finger gene 1 [ 149 ]. Those EVs rich in tissue factor (TF) have the capacity to modulate VSMC migration though PAR interaction [ 150 ].…”

Section: Evs As Pathophysiological Drivers Of Atherothrombosismentioning

confidence: 99%

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Suades

Greco

Padró

et al. 2022

Cells

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Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality all over the world. Extracellular vesicles (EVs), small lipid-bilayer membrane vesicles released by most cellular types, exert pivotal and multifaceted roles in physiology and disease. Emerging evidence emphasizes the importance of EVs in intercellular communication processes with key effects on cell survival, endothelial homeostasis, inflammation, neoangiogenesis, and thrombosis. This review focuses on EVs as effective signaling molecules able to both derail vascular homeostasis and induce vascular dysfunction, inflammation, plaque progression, and thrombus formation as well as drive anti-inflammation, vascular repair, and atheroprotection. We provide a comprehensive and updated summary of the role of EVs in the development or regression of atherosclerotic lesions, highlighting the link between thrombosis and inflammation. Importantly, we also critically describe their potential clinical use as disease biomarkers or therapeutic agents in atherothrombosis.

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Section: Evs As Pathophysiological Drivers Of Atherothrombosismentioning

confidence: 99%

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Suades

Greco

Padró

et al. 2022

Cells

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“…In trophoblast miR-19b-3p overexpression prevents syncytialization of primary human cytotrophoblasts (34), decreased PTEN production in JEG-3 (20) and here we found miR-19b-3p impaired HTR8/ Svneo trophoblast proliferation. In other tissues miR-19b-3p mostly promotes proliferation (35)(36)(37)(38)(39). The inhibition of proliferation by miR-19b-3p mimic seen here may be due to the increase in HOXA9 production also stimulated by the miR-19b-3p mimic: HOXA9 inhibits HTR8/Svneo proliferation (40), migration and invasion (41).…”

Section: Discussionmentioning

confidence: 99%

Endometrial stromal cell miR-19b-3p release is reduced during decidualization implying a role in decidual-trophoblast cross-talk

Menkhorst

Rainczuk

et al. 2023

Front. Endocrinol.

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IntroductionA healthy pregnancy requires successful blastocyst implantation into an adequately prepared or ‘receptive’ endometrium. Decidualization of uterine endometrial stromal fibroblast cells (hESF) is critical for the establishment of a healthy pregnancy. microRNAs (miRs) are critical regulators of cellular function that can be released by a donor cell to influence the physiological state of recipient cells. We aimed to determine how decidualization affects hESF miR release and investigated the function of one decidualization regulated miR, miR-19b-3p, previously shown to be associated with recurrent pregnancy loss.MethodmiR release by hESF was determined by miR microarray on culture media from hESF decidualized in vitro for 3 and 14 days by treatment with oestradiol and medroxyprogesterone acetate. Cellular and whole endometrial/decidual tissue miR expression was quantified by qPCR and localized by in situ hybridization. The function of miR-19b-3p in HTR8/Svneo trophoblast cells was investigated using real time cell analysis (xCELLigence) and gene expression qPCR.ResultsFrom our miR screen we found that essentially all hESF miR release was reduced following in vitro decidualization, significantly so for miR-17-5p, miR-21-3p, miR-34c-3p, miR-106b-5p, miR-138-5p, miR-296-5p, miR-323a-3p, miR-342-3p, miR-491-5p, miR-503-5p and miR-542-5p. qPCR demonstrated that miR-19b-3p, 181a-2-3p and miR-409-5p likewise showed a significant reduction in culture media following decidualization but no change was found in cellular miR expression following decidualization. In situ hybridization localized miR-19b-3p to epithelial and stromal cells in the endometrium and qPCR identified that miR-19b-3p was significantly elevated in the cycling endometrium of patients with a history of early pregnancy loss compared to normally fertile controls. Functionally, overexpression of miR-19b-3p significantly reduced HTR8/Svneo trophoblast proliferation and increased HOXA9 expression.DiscussionOur data demonstrates that decidualization represses miR release by hESFs and overexpression of miR-19b-3p was found in endometrial tissue from patients with a history of early pregnancy loss. miR-19b-3p impaired HTR8/Svneo proliferation implying a role in trophoblast function. Overall we speculate that miR release by hESF may regulate other cell types within the decidua and that appropriate release of miRs by decidualized hESF is essential for healthy implantation and placentation.

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“…MicroRNA-19b belongs to the miR-17-92 family of miRNA clusters. It has been shown to be associated with inflammatory conditions including atherosclerosis 18,19 . It is therefore not surprising that it was elevated after HS, but the lack of correlation with syndecan-1 was not anticipated.…”

Section: Discussionmentioning

confidence: 99%

Biomarkers of endothelial cell dysfunction persist beyond resuscitation in patients with hemorrhagic shock

Zeineddin

Chao

et al. 2022

J Trauma Acute Care Surg

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BACKGROUND:It has been shown that binds to and degrades syndecan-1 after hemorrhagic shock (HS) and contributes to endothelial dysfunction in vitro and in vivo. The objective of the current study was to assess longitudinal changes in miR-19b and syndecan-1 in HS patients. METHODS:Blood samples from HS patients (blood pressure <90 mm Hg and ≥2 U blood) were collected upon admission, completion of hemostasis, and after 24 hours for miR-19b (quantitative reverse transcription PCR) and syndecan-1 (enzyme-linked immunosorbent assay) and compared with controls and minimally injured (Injury Severity Score, ≤9). Inflammatory cytokines were measured (Luminex [Thermo Fisher, Waltham, MA]). Correlations between syndecan-1, miR-19b, inflammatory markers, and patient outcomes were performed. Logistic regression models were developed for outcomes. RESULTS:Thirty-four HS patients were studied: age, 46 (19-89) years; male, 82%; penetrating, 35%; Injury Severity Score, 24 ± 10; and blood products at 24 hours, 21 ± 19 U. MicroRNA-19b was increased upon arrival and further increased over time: 4.6 → 6.7 → 24.1-fold change compared with 0.1 and 1.2 for minimally injured patients and controls, respectively. Syndecan-1 was increased to 42.6 → 50 → 51.5 ng/mL over time compared with 14.7 and 23.5 for minimally injured and controls, respectively.Values for both biomarkers remained significantly increased through 24 hours and were associated with a persistent increase in inflammatory cytokines. Admission syndecan-1 significantly predicted mortality, coagulopathy, and massive transfusion. CONCLUSION:We have shown for the first time that miR-19b and syndecan-1 were biomarkers for endothelial dysfunction independent of resuscitation. MicroRNA-19b did not demonstrate a strong correlation with syndecan-1 nor outcomes. Admission syndecan-1, however, remains a strong prognostic marker, but its elevation over time suggests a versatile role following HS that requires further investigation.

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microRNA‐19b‐3p‐containing extracellular vesicles derived from macrophages promote the development of atherosclerosis by targeting JAZF1

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 20 publications

References 27 publications

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis

Endometrial stromal cell miR-19b-3p release is reduced during decidualization implying a role in decidual-trophoblast cross-talk

Biomarkers of endothelial cell dysfunction persist beyond resuscitation in patients with hemorrhagic shock

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