miR-125b Promotes Early Germ Layer Specification through Lin28/let-7d and Preferential Differentiation of Mesoderm in Human Embryonic Stem Cells

Wong, Sophia; Ritner, Carissa; Ramachandran, Sweta; Aurigui, Julian; Pitt, Cameron; Chandra, Piyanka; Ling, Vivian; Yabut, Odessa; Bernstein, Harold S.

doi:10.1371/journal.pone.0036121

Cited by 44 publications

(36 citation statements)

References 40 publications

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“…The upregulation of miR-125 family members is consistent with its role in the repression of self-renewal of ESCs (Rybak et al, 2008;O'Loghlen et al, 2012), and upregulation of miR-125 family members is indeed involved in the ESC differentiation into other cell linages, such as mesodermal cardiomyocytes (Wong et al, 2012). The robust induction of miR-125 is most likely due to the potent effect of small molecules of BMP inhibitors used in their study (Boissart et al, 2012).…”

Section: Research Articlementioning

confidence: 57%

miR-200 and miR-96 families repress neural induction from human embryonic stem cells

Ma²,

Phillips³

et al. 2013

Development

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SUMMARYThe role of miRNAs in neuroectoderm specification is largely unknown. We screened miRNA profiles that are differentially changed when human embryonic stem cells (hESCs) were differentiated to neuroectodermal precursors (NEP), but not to epidermal (EPI) cells and found that two miRNA families, miR-200 and miR-96, were uniquely downregulated in the NEP cells. We confirmed zinc-finger E-box-binding homeobox (ZEB) transcription factors as a target of the miR-200 family members and identified paired box 6 (PAX6) transcription factor as the new target of miR-96 family members via gain-and loss-of-function analyses. Given the essential roles of ZEBs and PAX6 in neural induction, we propose a model by which miR-200 and miR-96 families coordinate to regulate neural induction.

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Section: Research Articlementioning

confidence: 57%

miR-200 and miR-96 families repress neural induction from human embryonic stem cells

Ma²,

Phillips³

et al. 2013

Development

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“…Although miR-351 is present only in mice and rats, it belongs to the miR-125 family, the human ortholog of miR-351. MiR-125 family performs varied roles in human embryonic stem cell differentiation, cancer, and inflammation (54,56,65). Recent studies have demonstrated that miR-125b inhibited p53-dependent apoptosis pathway and mediated antiapoptotic effect in breast cancer cells by suppression of proapoptotic Bcl-2 antagonist killer 1 (Bak1) expression (32,70).…”

Section: Discussionmentioning

confidence: 99%

MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation

Chen

Melton

Gelfond

et al. 2012

Physiological Genomics

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Chen Y, Melton DW, Gelfond JAL, McManus LM, Shireman PK. MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation. Physiol Genomics 44: 1042-1051, 2012. First published September 11, 2012; doi:10.1152/physiolgenomics.00052.2012.-MicroRNAs (miRNAs) regulate many biological processes including muscle development. However, little is known regarding miRNA regulation of muscle regeneration. Murine tibialis anterior muscle was evaluated after cardiotoxin-induced injury and used for global miRNA expression analysis. From day 1 through day 21 following injury, 298 miRNAs were significantly changed at least at one time point, including 86 miRNAs that were altered Ͼ10-fold compared with uninjured skeletal muscle. Temporal miRNA expression patterns included inflammation-related miRNAs (miR-223 and -147) that increased immediately after injury; this pattern contrasted to that of mature muscle-specific miRNAs (miR-1, -133a, and -499) that abruptly decreased following injury followed by upregulation in later regenerative events. Another cluster of miRNAs were transiently increased in the early days of muscle regeneration including miR-351, a miRNA that was also transiently expressed during myogenic progenitor cell (MPC) differentiation in vitro. Based on computational predictions, further studies demonstrated that E2f3 was a target of miR-351 in myoblasts. Moreover, knockdown of miR-351 expression inhibited MPC proliferation and promoted apoptosis during MPC differentiation, whereas miR-351 overexpression protected MPC from apoptosis during differentiation. Collectively, these observations suggest that miR-351 is involved in both the maintenance of MPC proliferation and the transition into differentiated myotubes. Thus, a novel, timedependent sequence of molecular events during muscle regeneration has been identified; miR-351 inhibits E2f3 expression, a key regulator of cell cycle progression and proliferation, and promotes MPC proliferation and protects early differentiating MPC from apoptosis, important events in the hostile tissue environment after acute muscle injury.microRNA; myogenic progenitor cell; muscle regeneration; muscle differentiation SKELETAL MUSCLES ARE DAMAGED and repaired repeatedly throughout life. The capacity for skeletal muscle growth and regeneration is conferred by satellite cells located between the basal lamina and the sarcolemma of mature myofibers (21). Upon injury, satellite cells reenter the cell cycle, proliferate, and then exit the cell cycle either to renew the quiescent satellite cell pool or to differentiate into mature myofibers (1). Despite recent advances, genes involved in these processes are still largely unknown. Understanding the molecular mechanisms that regulate satellite cell activities could promote development of novel countermeasures to enhance muscle regeneration that is compromised by diseases or aging.Both cell proliferation and differentiation programs are essential for muscle regeneration. The dec...

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“…For example, miR-125b has been shown to regulate let-7 expression via targeting lin-28, an inhibitor of let-7 [71]. …”

Section: Let-7 In Cardiovascular Differentiation Of Embryonic Stem Cellsmentioning

confidence: 99%

Let-7 in Cardiovascular Diseases, Heart Development and Cardiovascular Differentiation from Stem Cells

Bao

Feng

Zhang

et al. 2013

IJMS

159

129

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The let-7 family is the second microRNA found in C. elegans. Recent researches have found it is highly expressed in the cardiovascular system. Studies have revealed the aberrant expression of let-7 members in cardiovascular diseases, such as heart hypertrophy, cardiac fibrosis, dilated cardiomyopathy (DCM), myocardial infarction (MI), arrhythmia, angiogenesis, atherosclerosis, and hypertension. Let-7 also participates in cardiovascular differentiation of embryonic stem cells. TLR4, LOX-1, Bcl-xl and AGO1 are by now the identified target genes of let-7. The circulating let-7b is suspected to be the biomarker of acute MI and let-7i, the biomarker of DCM. Further studies are necessary for identifying the gene targets and signaling pathways of let-7 in cardiovascular diseases. Let-7 might be a potential therapeutic target for cardiovascular diseases. This review focuses on the research progresses regarding the roles of let-7 in cardiovascular development and diseases.

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miR-125b Promotes Early Germ Layer Specification through Lin28/let-7d and Preferential Differentiation of Mesoderm in Human Embryonic Stem Cells

Cited by 44 publications

References 40 publications

miR-200 and miR-96 families repress neural induction from human embryonic stem cells

miR-200 and miR-96 families repress neural induction from human embryonic stem cells

MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation

Let-7 in Cardiovascular Diseases, Heart Development and Cardiovascular Differentiation from Stem Cells

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