miR-34a inhibits differentiation of human adipose tissue-derived stem cells by regulating cell cycle and senescence induction

Park, Ho; Park, Hyeon; Pak, Ha-Jin; Yang, Dongyun; Kim, Yun-Hong; Choi, Won-Jun; Park, Se Jin; Cho, Jung-Ah; Lee, Kyo-Won

doi:10.1016/j.diff.2015.10.010

Cited by 39 publications

(29 citation statements)

References 35 publications

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“…For example, overexpression of miR-34a mimics in blood monocytes induces tumor necrosis factor α (TNFα) production by downregulating AXL expression (Kurowska-Stolarska et al, 2010). Another study also showed that the expression levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) are modulated by miR-34a in human adipose tissue-derived stem cells, as they are strongly increased by miR-34a (Park et al, 2015). However, these recent results are still unclear and need further investigations because they showed IL-6 treatment repressing miR-34a expression while miR-34a can also inhibit IL-6 receptor expression (H.…”

Section: Mir-34a and Normal Tissue Radiation-induced Toxicitymentioning

confidence: 99%

Emergence of miR-34a in radiation therapy

Lacombe

Zenhausern

2017

Critical Reviews in Oncology/Hematology

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Expressions of many microRNAs (miRNAs) in response to ionizing radiation (IR) have already been investigated and some of them seem to play an important role in the tumor radioresistance, normal tissue radiotoxicity or as predictive biomarkers to radiation. MiR-34a is an emerging miRNA in recent radiobiology studies. Here, we review this miR-34 family member by detailing its different roles in radiation response and we will discuss about the role that it can play in radiation treatment. Thus, we will show that IR regulates miR-34a by increasing its expression. We will also highlight different biological processes involved in cellular response to IR and regulated by miR-34a in order to demonstrate the role it can play in tumor radio-response or normal tissue radiotoxicity as a radiosensitizer or radioprotector. MiR-34a is poised to assert itself as an important player in radiobiology and should become more and more important in radiation therapy management.

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Section: Mir-34a and Normal Tissue Radiation-induced Toxicitymentioning

confidence: 99%

Emergence of miR-34a in radiation therapy

Lacombe

Zenhausern

2017

Critical Reviews in Oncology/Hematology

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“…It has been shown to repress translation via imperfectly pairing with complementary sites within the 3'UTR of target mRNA (Liu et al 2014, Munoz et al 2015. In diverse cellular programs, miRNA plays a key role and involves in cell growth, differentiation, apoptosis, and many other physiological processes , Park et al 2015. In insects, the studies on miRNAs are mostly focused on the development, behavior, and hostpathogen interactions (Lucas et al 2015).…”

Section: Introductionmentioning

confidence: 99%

MiR-932 Regulates Pyrethroid Resistance inCulex pipiens pallens(Diptera: Culicidae)

Liu¹,

Tian²,

Guo³

et al. 2016

J Med Entomol

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MicroRNAs (miRNAs) play notable role in regulation of gene expression at the posttranscription level, and have been involved in many biological processes, including insecticide resistance. In this study, we investigated the role of miR-932 in the molecular mechanisms of pyrethroid resistance in Culex pipiens pallens (L.). Overexpression of miR-932 in the DS-strain made the mosquitoes more resistant to deltamethrin, while inhibiting the expression of miR-932 in the DR-strain made the mosquitoes more sensitive to deltamethrin. Further, we also identified CpCPR5 as a target gene of miR-932. Sustained overexpression of miR-932 resulted in repression of CpCPR5, and that knockdown of miR-932 increased CpCPR5 expression. In addition, knockdown of CpCPR5 decreased the sensitivity of mosquitoes to deltamethrin in the DS-strain. In conclusion, our study finds a molecular link between miR-932 and CpCPR5 and provides a novel insight into the mechanism of insecticide resistance.Key words: Culex pipiens pallens, pyrethroid, microRNA, CpCPR5Mosquitoes transmit a lot of pathogens, causing severe diseases such as malaria, dengue fever, West Nile fever, encephalitis, and filariasis, which threat public health worldwide (Andriessen et al. 2015, Fortuna et al. 2015, Paredes-Esquivel et al. 2015. Recent estimates show that there are about 400 million infections of dengue fever annually around the world (Sood et al. 2015). According to the WHO world malaria report, there are still 214 million new infections worldwide in 2015. Therefore, it is imperative for controlling and preventing mosquito-borne diseases. However, due to the lack of effective vaccines and drugs, vector control mostly relies on insecticides to reduce the number of mosquitoes (Glunt et al. 2015). But continuous and lasting application of insecticides has led to a constant increasing resistance, which makes antivector strategies more challenging (Rasic et al. 2015). Insecticide resistance arises from complex polygenic inheritance and many genes involved , Bonizzoni et al. 2015. These genes can be regulated at transcriptional and posttranscriptional levels and microRNA (miRNA) is known to be a posttranscriptional gene regulator (Wang et al. 2016).MiRNA is a class of small noncoding RNA, with about 22 nucleotides in length. It has been shown to repress translation via imperfectly pairing with complementary sites within the 3'UTR of target mRNA (Liu et al. 2014, Munoz et al. 2015. In diverse cellular programs, miRNA plays a key role and involves in cell growth, differentiation, apoptosis, and many other physiological processes , Park et al. 2015. In insects, the studies on miRNAs are mostly focused on the development, behavior, and hostpathogen interactions (Lucas et al. 2015). Recent evidence has shown that a few miRNAs participate in the regulation of insecticide resistance in mosquitoes, but the exact role of miRNA in pyrethroid resistance is still under little attention yet .Here, according to our previous study, we identified many different expressed miRNAs...

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“…Enhanced expression of miR-34a induces apoptosis, cell cycle arrest and differentiation, or reduces migration [30, 31]. Reducing the expression of the pro-apoptotic miR-34a improves survival of bone marrow stem cells in vitro and enhances the therapeutic benefit of cell therapy in mice after acute myocardial infarction [32].…”

Section: Discussionmentioning

confidence: 99%

“…Oxygen concentration in medullary compartments of the kidney is normally low [30], and in kidneys with severe RVD accompanied by inflammation, the degree and extent of hypoxia increase [6, 31]. These studies suggest that functional responses of AMSC under hypoxic conditions may favorably influence their efficacy for renal repair.…”

Section: Discussionmentioning

confidence: 99%

Adipose-derived mesenchymal stem cells from patients with atherosclerotic renovascular disease have increased DNA damage and reduced angiogenesis that can be modified by hypoxia

et al. 2016

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BackgroundAdipose-derived MSC (AMSCs) possess angiogenic and immunomodulatory properties that may modulate kidney regeneration. Whether these properties are retained in older patients with atherosclerotic vascular disease is poorly understood. Hypoxic conditions are known to modify properties and growth characteristics of AMSCs. We tested the hypothesis that AMSCs from older patients with atherosclerotic renovascular disease (RVD) differ from normal kidney donors, and whether hypoxia changes their functional and molecular properties to promote angiogenesis.MethodsAMSCs from 11 patients with RVD (mean age =74.5 years) and 10 healthy kidney donors (mean age = 51.2 years) were cultured under normoxia (20 % O2) and hypoxia (1 % O2) for 3–4 days until they reached 80 % confluency. We analyzed expression of genes and microRNAs using RNA sequencing and real-time quantitative rt-PCR. Protein expression of selected angiogenic factors (VEGF, IGF, HGF and EGF) were quantified in conditioned media using ELISAs. Apoptosis was tested using Annexin IV staining.ResultsNormoxic AMSC from RVD patients grew normally, but exhibited increased DNA damage and reduced migration. VEGF protein secretion was significantly lower in the RVD AMSCs (0.08 vs 2.4 ng/mL/ cell, p <0.05) while HGF was higher. Both trends were reversed during growth under hypoxic conditions. Hypoxia upregulated pro-angiogenic mRNAs expression in AMSCs (VEGF, FGF, STC and ANGPTL4), and downregulated expression of many miRNAs (e.g., miR-15a, miR-16, miR-93, miR-424, 126, 132, 221) except miR-210.ConclusionsThus, although AMSC from patients with RVD had increased DNA damage and reduced migration, hypoxia stimulated pro-angiogenic responses via increased expression of angiogenic genes, VEGF secretion and induction of the hypoxia-inducible miR-210, while downregulating angiogenesis-related miRNAs.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-016-0389-x) contains supplementary material, which is available to authorized users.

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miR-34a inhibits differentiation of human adipose tissue-derived stem cells by regulating cell cycle and senescence induction

Cited by 39 publications

References 35 publications

Emergence of miR-34a in radiation therapy

Emergence of miR-34a in radiation therapy

MiR-932 Regulates Pyrethroid Resistance inCulex pipiens pallens(Diptera: Culicidae)

Adipose-derived mesenchymal stem cells from patients with atherosclerotic renovascular disease have increased DNA damage and reduced angiogenesis that can be modified by hypoxia

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