The miR-143/145 Cluster Is a Novel Transcriptional Target of Jagged-1/Notch Signaling in Vascular Smooth Muscle Cells

Boucher, Joshua M.; Peterson, Sarah; Urs, Sumithra; Zhang, Chunxiang; Liaw, Lucy

doi:10.1074/jbc.m111.221945

Cited by 123 publications

(96 citation statements)

References 42 publications

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“…25 These findings, together with our observations, suggest that miR-145-5p functions to maintain the SM phenotype of JG cells and arteriolar VSMCs. miR-145-5p may promote the contractile phenotype by upregulating myocardin, 25 which forms a complex with the transcription factor SRF to activate SM genes 13 ( Figure 7A). Increasing miR-145-5p expression in fibroblasts in vitro reprograms them into VSMCs, in part by the positive effect of miR-145-5p on myocardin in a feedback loop in which miR-145-5p upregulates myocardin, allowing the formation of the SRF-myocardin complex, and subsequent SRF expression reinforces miR-145-5p to maintain myocardin expression.…”

Section: Discussionsupporting

confidence: 77%

“…12 We found reduced miR-145-5p expression in cKO renal arterioles and JG cells, suggesting that RBP-J regulates miR-145-5p directly through its promoter. In fact, the human miR-145-5p promoter has seven predicted RBP-J binding sites, 25 and studies in human aortic VSMCs showed that activation of the canonical Notch signaling pathway is required to maintain miR-145-5p transcription. 25 These findings, together with our observations, suggest that miR-145-5p functions to maintain the SM phenotype of JG cells and arteriolar VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, the human miR-145-5p promoter has seven predicted RBP-J binding sites, 25 and studies in human aortic VSMCs showed that activation of the canonical Notch signaling pathway is required to maintain miR-145-5p transcription. 25 These findings, together with our observations, suggest that miR-145-5p functions to maintain the SM phenotype of JG cells and arteriolar VSMCs. miR-145-5p may promote the contractile phenotype by upregulating myocardin, 25 which forms a complex with the transcription factor SRF to activate SM genes 13 ( Figure 7A).…”

Section: Discussionmentioning

confidence: 99%

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Recombination Signal Binding Protein for Ig-κJ Region Regulates Juxtaglomerular Cell Phenotype by Activating the Myo-Endocrine Program and Suppressing Ectopic Gene Expression

Castellanos-Rivera¹,

Pentz²,

Lin³

et al. 2015

Journal of the American Society of Nephrology

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Recombination signal binding protein for Ig-kJ region (RBP-J), the major downstream effector of Notch signaling, is necessary to maintain the number of renin-positive juxtaglomerular cells and the plasticity of arteriolar smooth muscle cells to re-express renin when homeostasis is threatened. We hypothesized that RBP-J controls a repertoire of genes that defines the phenotype of the renin cell. Mice bearing a bacterial artificial chromosome reporter with a mutated RBP-J binding site in the renin promoter had markedly reduced reporter expression at the basal state and in response to a homeostatic challenge. Mice with conditional deletion of RBP-J in renin cells had decreased expression of endocrine (renin and Akr1b7) and smooth muscle (Acta2, Myh11, Cnn1, and Smtn) genes and regulators of smooth muscle expression (miR-145, SRF, Nfatc4, and Crip1). To determine whether RBP-J deletion decreased the endowment of renin cells, we traced the fate of these cells in RBP-J conditional deletion mice. Notably, the lineage staining patterns in mutant and control kidneys were identical, although mutant kidneys had fewer or no reninexpressing cells in the juxtaglomerular apparatus. Microarray analysis of mutant arterioles revealed upregulation of genes usually expressed in hematopoietic cells. Thus, these results suggest that RBP-J maintains the identity of the renin cell by not only activating genes characteristic of the myo-endocrine phenotype but also, preventing ectopic gene expression and adoption of an aberrant phenotype, which could have severe consequences for the control of homeostasis.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Recombination Signal Binding Protein for Ig-κJ Region Regulates Juxtaglomerular Cell Phenotype by Activating the Myo-Endocrine Program and Suppressing Ectopic Gene Expression

Castellanos-Rivera¹,

Pentz²,

Lin³

et al. 2015

Journal of the American Society of Nephrology

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“…MiR-143, which was originally detected during adipocyte differentiation (Esau et al 2004), in many studies has emerged as an essential regulator of cellular physiology, particularly in tumorigenesis and cancer (Akao et al 2009;Quintavalle et al 2010;Qian et al 2013). In addition, recent studies show that miR-143 regulates the vascular smooth muscle cell phenotype (Boucher et al 2011). The dysregulation of miR-143 is implicated in a wide range of malignancies, including various forms of lymphoma, carcinomas of the breast, lung and pancreas and cervical cancer (Tripathi et al 2009;Liu et al 2012;Kapoor 2014).…”

Section: Discussionmentioning

confidence: 99%

miR-143 inhibits proliferation and induces apoptosis of mammary epithelial cells in dairy goat

Wang

Hou

et al. 2016

Animal Cells and Systems

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MicroRNAs are a class of post-transcriptional regulators of gene expression in multicellular organisms, which play important roles in cell fate, organ morphogenesis and carcinogenesis. In the present study, we demonstrated the critical roles of miR-143 on mammary epithelial cells of dairy goat. The test results of cell count, methylthiazolyldiphenyl-tetrazolium bromide, Hoechst33342/PI (propidium iodide) and flow cytometry showed miR-143-induced G0/G1 phase arrest, inhibited proliferation and promoted apoptosis of mammary epithelial cells; the qRT-PCR test of marker genes related to cell proliferation and apoptosis, BAX and BCL-2, supported the same conclusions. Our study presents evidence that miR-143 is an important post-transcription regulator involving in mammary cells survival, and it may have a value function in mammary gland development, lactation or involution.ARTICLE HISTORY

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“…On the opposite, TGF 1 (Transforming Growth Factor 1), a strong activator of VSMC differentiation, stimulates both miRNAs expression in a dose-and time-dependent manner [27]. The transcription of miR-143/145 is under the control of two independent signaling pathways: SRF/myocardin/Nkx2.5 and Jag-1/Notch signaling [28]. The expression of miR-143/145 is drastically reduced in several models of vascular disease: carotid artery ligation injury in mouse, carotid balloon-injury in rat, and ApoE Knock-out mice [27].…”

Section: The Mir-143/145 Clustermentioning

confidence: 99%

Implication of MicroRNAs in the Pathophysiology of Cardiac and Vascular Smooth Muscle Cells

Meuth¹,

M'Baya-Moutoula²,

Taibi³

et al. 2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

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The miR-143/145 Cluster Is a Novel Transcriptional Target of Jagged-1/Notch Signaling in Vascular Smooth Muscle Cells

Cited by 123 publications

References 42 publications

Recombination Signal Binding Protein for Ig-κJ Region Regulates Juxtaglomerular Cell Phenotype by Activating the Myo-Endocrine Program and Suppressing Ectopic Gene Expression

Recombination Signal Binding Protein for Ig-κJ Region Regulates Juxtaglomerular Cell Phenotype by Activating the Myo-Endocrine Program and Suppressing Ectopic Gene Expression

miR-143 inhibits proliferation and induces apoptosis of mammary epithelial cells in dairy goat

Implication of MicroRNAs in the Pathophysiology of Cardiac and Vascular Smooth Muscle Cells

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