Dynamic Expression of Specific miRNAs during Erythroid Differentiation of Human Embryonic Stem Cells

Hong, Jin; Kim, Jong Soo; Kim, Yong Baek; Kim, Su Jin; Broxmeyer, Hal E.; Kim, Kye Seong

doi:10.1007/s10059-012-0090-6

Cited by 26 publications

(22 citation statements)

References 23 publications

(23 reference statements)

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“…However, little research has been carried out to investigate the possible roles of miRNAs in regulation of the BTB function until now. MiR-142-3p, first identified to exert its function during the development of the lymphoid system [18], was subsequently proved to regulate cell differentiation and serve as a potential tumor suppressor in acute myeloid leukemia, hepatocellular carcinoma, osteosarcoma, nasopharyngeal carcinoma, and pancreatic ductal adenocarcinoma, etc [19-24]. Nevertheless, the microarray using human testis samples showed a relatively high expression level of miR-142-3p but with no significant variation between normal adult testis and testicular tumors [25].…”

Section: Introductionmentioning

confidence: 99%

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

Xu¹,

Wu²,

Fan³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Transforming growth factor-β3 (TGF-β3) has been proved to perturb the blood-testis barrier (BTB) by accelerating junction protein endocytosis in Sertoli cells (SCs) to accommodate the traversing of preleptotene spermatocytes across the BTB around stage VIII in rat. Yet the molecular network underlying the impairment of TGF-β3 on BTB integrity is not fully elucidated. Our study herein was designed to investigate the participation of microRNA-142-3p (miR-142-3p), which has been reported to affect TGF-β3 signaling via different pathways, during BTB dynamics and the corresponding mechanisms. Methods: MiRNA mimic or agomiRNA was co-administered with or without TGF-β3 in the cultured SCs or in the rat testis. The SC permeability barrier function was reflected by measuring the transepithelial resistance (TER) and the permeability of the sodium fluorescein (Na-F). The BTB integrity was detected by the permeation of biotin. A luciferase reporter assay was used to testify the potential target of miR-142-3p, lethal giant larvae 2 (Lgl2). Laser capture microdissection (LCM) was applied to acquire cell components of different stages of seminiferious tubules, followed by detection of the expression levels of miR-142-3p, TGF-β3, and Lgl2 by qPCR. The SC barrier function was also detected as above in the presence of TGF-β3 after Lgl2 knockdown. Results: We revealed a reversion of TGF-β3-induced BTB impairment after miR-142-3p treatment both in vitro and in vivo. Meanwhile, the activation of Cdc42 and reduction in occludin aroused by TGF-β3 were also reversed by miR-142-3p. The predicted binding of miR-142-3p with 3’-untranslated region (3’-UTR) of Lgl2, was verified by the luciferase assay. Moreover, an increased Lgl2 level in TGF-β3-treated SCs was found and correlated stage-specific expressions of TGF-β3, miR-142-3p, and Lgl2 were revealed. Knockdown of Lgl2 in SCs was shown to partially antagonize the BTB disruption mediated by TGF-β3. Conclusions: Collectively, our results suggest a resistance of miR-142-3p on the BTB impairment caused by TGF-β3 during the seminiferous epithelial cycle by targeting Lgl2.

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Section: Introductionmentioning

confidence: 99%

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

Xu¹,

Wu²,

Fan³

et al. 2018

Cell Physiol Biochem

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“…Another interesting hit that is strongly upregulated in p53 wt iPS cells, but very low expressed in p53 KO and mutant iPS cells is miR-142-3p. 84,85 We were unable to identify whether a p53 responsive element is its promoter, suggesting that p53 regulates the expression of this miRNA by an indirect mechanism.…”

Section: Discussionmentioning

confidence: 91%

Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells

et al. 2016

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The tumour suppressor p53 plays an important role in somatic cell reprogramming. While wild-type p53 reduces reprogramming efficiency, mutant p53 exerts a gain of function activity that leads to increased reprogramming efficiency. Furthermore, induced pluripotent stem cells expressing mutant p53 lose their pluripotency in vivo and form malignant tumours when injected in mice. It is therefore of great interest to identify targets of p53 (wild type and mutant) that are responsible for this phenotype during reprogramming, as these could be exploited for therapeutic use, that is, formation of induced pluripotent stem cells with high reprogramming efficiency, but no oncogenic potential. Here we studied the transcriptional changes of microRNA in a series of mouse embryonic fibroblasts that have undergone transition to induced pluripotent stem cells with wild type, knock out or mutant p53 status in order to identify microRNAs whose expression during reprogramming is dependent on p53. We identified a number of microRNAs, with known functions in differentiation and carcinogenesis, the expression of which was dependent on the p53 status of the cells. Furthermore, we detected several uncharacterised microRNAs that were regulated differentially in the different p53 backgrounds, suggesting a novel role of these microRNAs in reprogramming and pluripotency.

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“…Similarly, miR‐451, which was the first miRNA identified in human erythrocytes , was shown to be regulated by GATA‐1 and its depletion in zebrafish led to impaired maturation of erythroid cells into circulating red blood cells, indicating a role for terminal differentiation of erythroid lineages . Moreover, we recently demonstrated that miR‐451 was also upregulated during erythropoietic differentiation from embryonic stem cells, but reciprocally downregulated during megakaryocyte differentiation . This indicates that a set of genes regulated by miR‐451 is involved in lineage determination between erythropoietic and megakaryocytic lineages.…”

Section: Mirnas Fine‐tune Lineage‐specific Differentiationmentioning

confidence: 82%

Concise Review: Exploring miRNAs—Toward a Better Understanding of Hematopoiesis

Hong

Kim

2014

Stem Cells

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Hematopoiesis is governed by a multidimensional regulatory network involving both intrinsic and extrinsic factors that control self-renewal and differentiation of hematopoietic stem cells (HSCs) through the coordination of influences that affect cell fate. Increasing evidence indicates that microRNAs (miRNAs), short noncoding RNAs of approximately 22 nucleotides, play a central role in orchestrating these regulatory mechanisms to modulate the multiple entities of hematopoietic function in a cell-type specific manner, including self-renewal, lineage commitment, and survival of HSCs as well as their microenvironmental crosstalk. Here, we summarize the current understanding regarding the regulatory effects of miRNA on hematopoietic cells, thus enlightening their role in fine-tuning HSC function and hematopoietic homeostasis. STEM CELLS 2015;33:1-7

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Dynamic Expression of Specific miRNAs during Erythroid Differentiation of Human Embryonic Stem Cells

Cited by 26 publications

References 23 publications

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells

Concise Review: Exploring miRNAs—Toward a Better Understanding of Hematopoiesis

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