Micro<scp>RNA</scp> let‐7a regulates angiogenesis by targeting <i><scp>TGFBR</scp>3 </i><scp>mRNA</scp>

Shao, Wei; Zhou, Huixin; Wu, Dazhou; Ni, Huajing; Chen, Zhongliang; Chen, Chengshui; Xiang, Youqun; Dai, Kezhi; Chen, Xiaoming; Li, Xi

doi:10.1111/jcmm.13960

Cited by 30 publications

(23 citation statements)

References 57 publications

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“…Let-7a plays a prominent role in cell growth and differentiation [60], which may contribute to cerebrovascular endothelial function. In addition, overexpression of let-7a regulates angiogenesis by targeting TGFBR3 and reduces endothelial cell migration rate, in vitro [61]. Other studies from our laboratory have noted BBB leakage Fig.…”

Section: Discussionmentioning

confidence: 73%

Serum-borne factors alter cerebrovascular endothelial microRNA expression following particulate matter exposure near an abandoned uranium mine on the Navajo Nation

et al. 2020

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Background: Commercial uranium mining on the Navajo Nation has subjected communities on tribal lands in the Southwestern United States to exposures from residual environmental contamination. Vascular health effects from these ongoing exposures are an active area of study. There is an association between residential mine-site proximity and circulating biomarkers in residents, however, the contribution of mine-site derived wind-blown dusts on vascular and other health outcomes is unknown. To assess neurovascular effects of mine-site derived dusts, we exposed mice using a novel exposure paradigm, the AirCARE1 mobile inhalation laboratory, located 2 km from an abandoned uranium mine, Claim 28 in Blue Gap Tachee, AZ. Mice were exposed to filtered air (FA) (n = 6) or concentrated ambient particulate matter (CAPs) (n = 5) for 2 wks for 4 h per day. Results: To assess miRNA differential expression in cultured mouse cerebrovascular cells following particulate matter (PM) exposure (average: 96.6 ± 60.4 μg/m 3 for all 4 h exposures), the serum cumulative inflammatory potential (SCIP) assay was employed. MiRNA sequencing was then performed in cultured mouse cerebrovascular endothelial cells (mCECs) to evaluate transcriptional changes. Results indicated 27 highly differentially expressed (p < 0.01) murine miRNAs, as measured in the SCIP assay. Gene ontology (GO) pathway analysis revealed notable alterations in GO enrichment related to the cytoplasm, protein binding and the cytosol, while significant KEGG pathways involved pathways in cancer, axon guidance and Wnt signaling. Expression of these 27 identified, differentially expressed murine miRNAs were then evaluated in the serum. Nine of these miRNAs (~30%) were significantly altered in the serum and 8 of those miRNAs demonstrated the same directional change (either upregulation or downregulation) as cellular miRNAs, as measured in the SCIP assay. Significantly upregulated miRNAs in the CAPs exposure group included miRNAs in the let-7a family. Overexpression of mmu-let-7a via transfection experiments, suggested that this miRNA may mediate mCEC barrier integrity following dust exposure.

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Section: Discussionmentioning

confidence: 73%

Serum-borne factors alter cerebrovascular endothelial microRNA expression following particulate matter exposure near an abandoned uranium mine on the Navajo Nation

et al. 2020

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“…Altered miR-146a-5p/miR-132-3p and Let-7a-5p/miR-16-5p are the most relevant ratios to identify patients with vasomotor deficits from those without these deficits and controls. Concordantly, alterations in all these miRNAs have been described in angiogenesis-related diseases [ 110 , 111 , 112 ]. Our data point to increased circulating miR-146a-5p/miR-132-3p ratio as a hallmark of RTT that can identify patients from controls with very good accuracy, while it also serves to stratify RTT severity, being able to discriminate those patients with microcephaly or vasomotor deficits.…”

Section: Discussionmentioning

confidence: 90%

Unraveling Molecular Pathways Altered in MeCP2-Related Syndromes, in the Search for New Potential Avenues for Therapy

et al. 2021

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Methyl-CpG-binding protein 2 (MeCP2) is an X-linked epigenetic modulator whose dosage is critical for neural development and function. Loss-of-function mutations in MECP2 cause Rett Syndrome (RTT, OMIM #312750) while duplications in the Xq28 locus containing MECP2 and Interleukin-1 receptor-associated kinase 1 (IRAK1) cause MECP2 duplication syndrome (MDS, OMIM #300260). Both are rare neurodevelopmental disorders that share clinical symptoms, including intellectual disability, loss of speech, hand stereotypies, vasomotor deficits and seizures. The main objective of this exploratory study is to identify novel signaling pathways and potential quantitative biomarkers that could aid early diagnosis and/or the monitoring of disease progression in clinical trials. We analyzed by RT-PCR gene expression in whole blood and microRNA (miRNA) expression in plasma, in a cohort of 20 females with Rett syndrome, 2 males with MECP2 duplication syndrome and 28 healthy controls, and correlated RNA expression with disease and clinical parameters. We have identified a set of potential biomarker panels for RTT diagnostic and disease stratification of patients with microcephaly and vasomotor deficits. Our study sets the basis for larger studies leading to the identification of specific miRNA signatures for early RTT detection, stratification, disease progression and segregation from other neurodevelopmental disorders. Nevertheless, these data will require verification and validation in further studies with larger sample size including a whole range of ages.

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“…Let-7a inhibits tube formation and reduces the migration rate of HUVECs by directly targeting transforming growth factor beta (TGFβ) receptor III, resulting in a defective TGFβ signaling pathway in these cells [87]. Sureban et al demonstrated that, in pancreatic cancer and HCC, doublecortin-like kinase 1 (DCLK1), a putative marker of intestinal and pancreatic stem cells, regulates the pluripotency and expression of angiogenic factors via miRNA-dependent mechanisms.…”

Section: Let-7amentioning

confidence: 99%

Insights into the Regulation of Tumor Angiogenesis by Micro-RNAs

Leone

Buonavoglia

Fasano

et al. 2019

JCM

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One of the hallmarks of cancer is angiogenesis, a series of events leading to the formation of the abnormal vascular network required for tumor growth, development, progression, and metastasis. MicroRNAs (miRNAs) are short, single-stranded, non-coding RNAs whose functions include modulation of the expression of pro- and anti-angiogenic factors and regulation of the function of vascular endothelial cells. Vascular-associated microRNAs can be either pro- or anti-angiogenic. In cancer, miRNA expression levels are deregulated and typically vary during tumor progression. Experimental data indicate that the tumor phenotype can be modified by targeting miRNA expression. Based on these observations, miRNAs may be promising targets for the development of novel anti-angiogenic therapies. This review discusses the role of various miRNAs and their targets in tumor angiogenesis, describes the strategies and challenges of miRNA-based anti-angiogenic therapies and explores the potential use of miRNAs as biomarkers for anti-angiogenic therapy response.

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MicroRNA let‐7a regulates angiogenesis by targeting TGFBR3 mRNA

Cited by 30 publications

References 57 publications

Serum-borne factors alter cerebrovascular endothelial microRNA expression following particulate matter exposure near an abandoned uranium mine on the Navajo Nation

Serum-borne factors alter cerebrovascular endothelial microRNA expression following particulate matter exposure near an abandoned uranium mine on the Navajo Nation

Unraveling Molecular Pathways Altered in MeCP2-Related Syndromes, in the Search for New Potential Avenues for Therapy

Insights into the Regulation of Tumor Angiogenesis by Micro-RNAs

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