MicroRNAs in body fluids—the mix of hormones and biomarkers

Cortez, María Angélica; Bueso‐Ramos, Carlos E.; Ferdin, Jana; López-Berestein, Gabriel; Sood, Anil K.; Calin, George A.

doi:10.1038/nrclinonc.2011.76

Cited by 1,321 publications

(1,110 citation statements)

References 122 publications

(145 reference statements)

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“…There is evidence implicating these derivatives of sncRNAs in cell‐to‐cell communication both in normal biology and in disease states (Cortez et al ., 2011; Hoy & Buck, 2012; Shah & Calin, 2012; Turchinovich et al ., 2012; Kosaka et al ., 2013). Our deep sequencing studies of serum/plasma have consistently detected tRNA‐derived RNAs of size 30–33 nt (Dhahbi et al ., 2013a,b).…”

Section: Introductionmentioning

confidence: 99%

Circulating microRNA signature of genotype‐by‐age interactions in the long‐lived Ames dwarf mouse

et al. 2015

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SummaryRecent evidence demonstrates that serum levels of specific miRNAs significantly change with age. The ability of circulating sncRNAs to act as signaling molecules and regulate a broad spectrum of cellular functions implicates them as key players in the aging process. To discover circulating sncRNAs that impact aging in the long‐lived Ames dwarf mice, we conducted deep sequencing of small RNAs extracted from serum of young and old mice. Our analysis showed genotype‐specific changes in the circulating levels of 21 miRNAs during aging [genotype‐by‐age interaction (GbA)]. Genotype‐by‐age miRNAs showed four distinct expression patterns and significant overtargeting of transcripts involved in age‐related processes. Functional enrichment analysis of putative and validated miRNA targets highlighted cellular processes such as tumor suppression, anti‐inflammatory response, and modulation of Wnt, insulin, mTOR, and MAPK signaling pathways, among others. The comparative analysis of circulating GbA miRNAs in Ames mice with circulating miRNAs modulated by calorie restriction (CR) in another long‐lived mouse suggests CR‐like and CR‐independent mechanisms contributing to longevity in the Ames mouse. In conclusion, we showed for the first time a signature of circulating miRNAs modulated by age in the long‐lived Ames mouse.

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Section: Introductionmentioning

confidence: 99%

Circulating microRNA signature of genotype‐by‐age interactions in the long‐lived Ames dwarf mouse

et al. 2015

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“…In view of the possibility to use serum miRNAs as disease biomarkers, 31 we performed a miRNA microarray study using serum samples from vitiligo patients (n = 50) and healthy controls (n = 50). The assay identified 48 aberrantly expressed miRNAs (4twofold changes, Po0.01), among which 24 miRNAs (e.g., let-7b) were upregulated, whereas another 24 (e.g., miR-1914) were downregulated (Supplementary Table S1).…”

Section: Resultsmentioning

confidence: 99%

Oxidative stress-induced overexpression of miR-25: the mechanism underlying the degeneration of melanocytes in vitiligo

et al. 2015

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Oxidative stress has a critical role in the pathogenesis of vitiligo. However, the specific molecular mechanism involved in oxidative stress-induced melanocyte death is not well characterized. Given the powerful role of microRNAs (miRNAs) in the regulation of cell survival as well as the fact that the generation of miRNAs can be affected by oxidative stress, we hypothesized that miRNAs may participate in vitiligo pathogenesis by modulating the expression of vital genes in melanocytes. In the present study, we initially found that miR-25 was increased in both serum and lesion samples from vitiligo patients, and its serum level was correlated with the activity of vitiligo. Moreover, restoration of miR-25 promoted the H 2 O 2 -induced melanocyte destruction and led to the dysfunction of melanocytes. Further experiments proved that MITF, a master regulator in melanocyte survival and function, accounted for the miR-25-caused damaging impact on melanocytes. Notably, other than the direct role on melanocytes, we observed that miR-25 inhibited the production and secretion of SCF and bFGF from keratinocytes, thus impairing their paracrine protective effect on the survival of melanocytes under oxidative stress. At last, we verified that oxidative stress could induce the overexpression of miR-25 in both melanocytes and keratinocytes possibly by demethylating the promoter region of miR-25. Taken together, our study demonstrates that oxidative stress-induced overexpression of miR-25 in vitiligo has a crucial role in promoting the degeneration of melanocytes by not only suppressing MITF in melanocytes but also impairing the paracrine protective effect of keratinocytes. Therefore, it is worthy to investigate the possibility of miR-25 as a potential drug target for anti-oxidative therapy in vitiligo. Vitiligo is a disfiguring dermatosis with an incidence rate of approximately 0.5-1.0% in the populations worldwide. 1 Characterized by patchy depigmentation of the skin, the disease can affect the patients' self-image, or even cause depression, thus substantially decreasing life quality among vitiligo patients. 2 Although several etiological theories, including genetic predisposition, 3-5 autoimmunity, 6,7 melanocytorrhagy 8,9 and toxic metabolites 10 have been proposed to participate in the pathogenesis of vitiligo, the exact mechanism of melanocyte degeneration in depigmented lesions still remains unclear.The generation of oxidative stress has long been demonstrated to have a crucial role in the onset and progression of vitiligo. 11,12 Owing to the pro-oxidant state generated during melanin synthesis, melanocytes are particularly vulnerable to oxidative stress. 13 In vitiligo, accumulation of toxic intermediates such as 6-and 7-BH4 and catecholamine, 14,15 concomitant with reduced levels and activity of catalase and several other antioxidant enzymes [16][17][18] have been demonstrated in patients' epidermis. Because of these intracellular metabolic disorder and compromised intrinsic antioxidant defenses, hydrogen peroxide (H 2 O ...

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“…Our method makes it possible to profile miRNA expression from tiny samples such as puncture biopsies. Recently, existence of miRNA in serum suggested that serum miRNAs may serve as potential convenient biomarkers for the detection and screen of various cancers and other diseases (19,20). The serum RNA yield is 1-2 lg/10 mL according a previous study (21).…”

Section: Discussionmentioning

confidence: 99%

A simple and fast method for profiling microRNA expression from low‐input total RNA by microarray

Zhao

Wei

et al. 2012

IUBMB Life

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SummaryAnalysis of mature microRNA (miRNA) expression is important to understand its physiological functions and pathological implications. Microarray is a powerful technology to profile global miRNA expression. In this study, we developed a rapid miRNA labeling method by which miRNA was directly labeled in total RNA for microarray detection. This method consists of RNA tailing by poly(A) polymerase, reverse transcription, and template-switching by moloney murine leukemia virus (MMLV) reverse transcriptase. After these reactions, the small RNA cDNA was ready for labeling for microarray detection. The whole process of prearray sample preparation was dramatically shortened to 2 h. Furthermore, this method allows very limited starting total RNA (100 ng) for microarray analysis. Our data showed that the results from our method were highly consistent with that of real-time polymerase chain reaction (PCR). IUBMBIUBMB Life, 64(7): [612][613][614][615][616] 2012

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MicroRNAs in body fluids—the mix of hormones and biomarkers

Cited by 1,321 publications

References 122 publications

Circulating microRNA signature of genotype‐by‐age interactions in the long‐lived Ames dwarf mouse

Circulating microRNA signature of genotype‐by‐age interactions in the long‐lived Ames dwarf mouse

Oxidative stress-induced overexpression of miR-25: the mechanism underlying the degeneration of melanocytes in vitiligo

A simple and fast method for profiling microRNA expression from low‐input total RNA by microarray

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