miR-223 and miR-142 attenuate hematopoietic cell proliferation, and miR-223 positively regulates miR-142 through LMO2 isoforms and CEBP-β

Sun, Wei; Shen, Wenwen; Yang, Shuang; Hu, Fang; Li, Huihui; Zhu, Tianhui

doi:10.1038/cr.2010.134

Cited by 98 publications

(95 citation statements)

References 40 publications

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“…This result is in agreement with the recent studies showing that cell-secreted MVs, particularly exosomes, serve as physiological carriers of miRNAs to exchange genetic materials and signaling molecules between cells (45,46). As a hematopoietic-specific miRNA with crucial functions in myeloid lineage development (47,48), miR-223 has been shown to target a transcription factor Mef2c (47), CEBP-b (49), glutamate receptors (GluR2 and NR2B) (50), and IGF-1R (51) in other cell types. By the luciferase reporter assay and experimental validation, we confirmed IGF-1R as a target of miR-223 in vascular endothelial cells.…”

Section: Discussionsupporting

confidence: 82%

Platelet-Secreted MicroRNA-223 Promotes Endothelial Cell Apoptosis Induced by Advanced Glycation End Products via Targeting the Insulin-like Growth Factor 1 Receptor

Pan

Liang

Liu

et al. 2014

The Journal of Immunology

214

177

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Platelets play a significant role in atherosclerosis, stroke, and asthma through active interaction with neutrophils, monocytes, and vascular endothelial cells. The mechanism underlying these intercellular interactions, however, is incompletely understood. In this study, we report that platelets can remotely modulate vascular endothelial cell apoptosis through releasing microRNA-223 (miR-223)–containing microvesicles (MVs). First, platelets expressed abundant miRNAs, and miR-223 had the highest level of expression. Platelet miR-223 and other miRNAs can be upregulated by the stimulation with thrombopoietin (TPO) or thrombin. Unlike leukocytes, platelets contained high levels of pre-miRNAs, and upregulation of mature platelet miRNAs by TPO was correlated with decreased pre-miRNAs. Second, under stimulation with TPO, platelets released a large amount of MVs, which also contain higher levels of miR-223. Elevation of miR-223 inside circulating platelet MVs (P-MVs) was also observed in plasma samples from patients with enteritis, hepatitis, nephritis, or atherosclerosis. Third, incubation of P-MVs with HUVECs, which had significantly lower levels of miR-223 than platelets, showed that P-MVs effectively delivered miR-223 into HUVECs. Finally, in HUVECs, exogenous platelet miR-223 decreased the level of insulin-like growth factor 1 receptor and thus promoted HUVEC apoptosis induced by advanced glycation end products. The proapoptotic effect of P-MVs on HUVECs was largely abolished by depleting cellular miR-223 using anti–miR-223 antisense oligonucleotide. In conclusion, our study presents the first evidence, to our knowledge, that platelet-released miR-223 promotes advanced glycation end product–induced vascular endothelial cell apoptosis via targeting insulin-like growth factor 1 receptor.

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Section: Discussionsupporting

confidence: 82%

Platelet-Secreted MicroRNA-223 Promotes Endothelial Cell Apoptosis Induced by Advanced Glycation End Products via Targeting the Insulin-like Growth Factor 1 Receptor

Pan

Liang

Liu

et al. 2014

The Journal of Immunology

214

177

View full text Add to dashboard Cite

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“…To date, very few miRNAs have been shown to play important roles in HSC development in vertebrates in vivo. miR-142-3p is specifically expressed in HSCs (AGM and CHT) and T cells (thymus) in zebrafish, mouse and other species [15][16][17][18][19][20][21]. By knockdown of miR-142a-3p using 2 specific MOs, the numbers of HSCs and T cells were decreased.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, miR-144 and miR-451, as direct targets of the critical hematopoietic master regulator GATA1, are required for erythropoiesis in zebrafish and mouse [11][12][13]. miR-142-3p is an evolutionally conserved miRNA of vertebrates, which is expressed in many different hematopoietic cells [14][15][16][17][18][19][20][21]. Chen et al [15] first reported that miR-142 is expressed in embryonic and adult hematopoietic tissues, including the fetal liver, bone marrow, spleen and thymus, in mice, indicating its role in both embryonic and adult hematopoiesis.…”

Section: Introductionmentioning

confidence: 99%

miR-142-3p regulates the formation and differentiation of hematopoietic stem cells in vertebrates

et al. 2013

Cell Res

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Previous studies on developmental hematopoiesis have mainly focused on signaling and transcription factors, while the appreciation of epigenetic regulation including that of microRNAs is recent. Here, we show that in zebrafish and mouse, miR-142-3p is specifically expressed in hematopoietic stem cells (HSCs). Knockdown of miR-142a-3p in zebrafish led to a reduced population of HSCs in the aorta-gonad-mesonephros (AGM) region as well as T-cell defects in the thymus. Mechanistically, miR-142a-3p regulates HSC formation and differentiation through the repression of interferon regulatory factor 7 (irf7)-mediated inflammation signaling. Finally, we show that miR-142-3p is also involved in the development of HSCs in mouse AGM, suggesting that it has a highly conserved role in vertebrates. Together, these findings unveil the pivotal roles that miR-142a-3p plays in the formation and differentiation of HSCs by repressing irf7 signaling.

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“…The expression of miR-142-3p is related to the correct development of hematopoietic lineage-specific cells (25 ), and its expression in tissues is being considered as a marker of acute and chronic inflammation (26 ). Increased expression measures of miR-142-3p have been reported in serum from patients with chronic inflammation, autoimmune attack, and vascular damage (27 ).…”

Section: Morbid Obesitymentioning

confidence: 99%

Targeting the Circulating MicroRNA Signature of Obesity

et al. 2013

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BACKGROUND Genomic studies have yielded important insights into the pathogenesis of obesity. Circulating microRNAs (miRNAs) are valuable biomarkers of systemic diseases and potential therapeutic targets. We sought to define the circulating pattern of miRNAs in obesity and examine changes after weight loss. METHODS We assessed the genomewide circulating miRNA profile cross-sectionally in 32 men and after surgery-induced weight loss in 6 morbidly obese patients. The most relevant miRNAs were cross-sectionally validated in 80 men and longitudinally in 22 patients (after surgery-induced weight loss). We evaluated the effects of diet-induced weight loss in 9 obese patients. Thirty-six circulating miRNAs were associated with anthropometric variables in the initial sample. RESULTS In the validation study, morbidly obese patients showed a marked increase of miR-140-5p, miR-142-3p (both P < 0.0001), and miR-222 (P = 0.0002) and decreased levels of miR-532–5p, miR-125b, miR-130b, miR-221, miR-15a, miR-423-5p, and miR-520c-3p (P < 0.0001 for all). Interestingly, in silico targets leukemia inhibitory factor receptor (LIFR) and transforming growth factor receptor (TGFR) of miR-140-5p, miR-142-3p, miR-15a, and miR-520c-3p circulated in association with their corresponding miRNAs. Moreover, a discriminant function of 3 miRNAs (miR-15a, miR-520c-3p, and miR-423-5p) was specific for morbid obesity, with an accuracy of 93.5%. Surgery-induced (but not diet-induced) weight loss led to a marked decrease of miR-140-5p, miR-122, miR-193a-5p, and miR-16-1 and upregulation of miR-221 and miR-199a-3p (P < 0.0001 for all). CONCLUSIONS Circulating miRNAs are deregulated in severe obesity. Weight loss–induced changes in this profile and the study of in silico targets support this observation and suggest a potential mechanistic relevance.

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miR-223 and miR-142 attenuate hematopoietic cell proliferation, and miR-223 positively regulates miR-142 through LMO2 isoforms and CEBP-β

Cited by 98 publications

References 40 publications

Platelet-Secreted MicroRNA-223 Promotes Endothelial Cell Apoptosis Induced by Advanced Glycation End Products via Targeting the Insulin-like Growth Factor 1 Receptor

Platelet-Secreted MicroRNA-223 Promotes Endothelial Cell Apoptosis Induced by Advanced Glycation End Products via Targeting the Insulin-like Growth Factor 1 Receptor

miR-142-3p regulates the formation and differentiation of hematopoietic stem cells in vertebrates

Targeting the Circulating MicroRNA Signature of Obesity

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