A miRNA-tRNA mix-up: tRNA origin of proposed miRNA

Schopman, Nick C.T.; Heynen, Stephan; Haasnoot, Joost; Berkhout, Ben

doi:10.4161/rna.7.5.13141

Cited by 116 publications

(61 citation statements)

References 16 publications

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“…The mir-1274B was originally identified from a genome sequencing project, sharing structure with tRNA (lys3). 62 Recent studies showed that mir-1274B was upregulated in cutaneous malignant melanoma while downregulated in chemoradiotherapy-treated advanced rectal cancer, implying that mir-1274B may be related to tumor growth. 63,64 Report from Shinozuka et al 65 showed that mir-1274B was regulated by SnoN/SKIL and negatively related to esophageal cancer cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

XBP 1-Deficiency Abrogates Neointimal Lesion of Injured Vessels Via Cross Talk With the PDGF Signaling

Zeng

Yang

et al. 2015

ATVB

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Objective-Smooth muscle cell (SMC) migration and proliferation play an essential role in neointimal formation after vascular injury. In this study, we intended to investigate whether the X-box-binding protein 1 (XBP1) was involved in these processes. Approach and Results-In vivo studies on femoral artery injury models revealed that vascular injury triggered an immediate upregulation of XBP1 expression and splicing in vascular SMCs and that XBP1 deficiency in SMCs significantly abrogated neointimal formation in the injured vessels. In vitro studies indicated that platelet-derived growth factor-BB triggered XBP1 splicing in SMCs via the interaction between platelet-derived growth factor receptor β and the inositolrequiring enzyme 1α. The spliced XBP1 (XBP1s) increased SMC migration via PI3K/Akt activation and proliferation via downregulating calponin h1 (CNN1). XBP1s directed the transcription of mir-1274B that targeted CNN1 mRNA degradation. Proteomic analysis of culture media revealed that XBP1s decreased transforming growth factor (TGF)-β family proteins secretion via transcriptional suppression. TGF-β3 but not TGF-β1 or TGF-β2 attenuated XBP1s-induced CNN1 decrease and SMC proliferation. Conclusions-This study demonstrates for the first time that XBP1 is crucial for SMC proliferation via modulating the platelet-derived growth factor/TGF-β pathways, leading to neointimal formation. under stress conditions. [21][22][23] Under ER stress conditions, XBP1 mRNA undergoes unconventional splicing through an ER-resident kinase that possesses ribonuclease activity, the inositol-requiring enzyme 1 α (IRE1α). 24 Our recent studies and reports from other groups showed that physiological stimuli such as vascular endothelial cell growth factor could trigger XBP1 splicing in an ER stress response-independent manner. [25][26][27][28] In endothelial cells (ECs), XBP1 splicing plays diverse roles, including cell proliferation, 26 autophagy response, 29 and apoptosis. 30 In SMCs, bone morphogenetic protein-2 was reported to activate XBP1 splicing, 31 but the exact role of XBP1 in SMCs still remains unclear. In this study, we demonstrated that XBP1 splicing is crucial in PDGF-BB-induced SMC proliferation and contributes to neointima formation after vascular injury. Materials and MethodsMaterials and Methods are available in the online-only Data Supplement. Results Vascular Injury Increased XBP1 Expression and SplicingIn response to vascular injury, vascular SMCs will be activated undergoing migration, proliferation, and apoptosis. 32 To test whether XBP1 was involved in SMC activation, femoral artery injury model was introduced into the right side of C57Bl/6 mice. The injured vessels were harvested at day 1, and day 3 post surgery, whereas the left uninjured vessels were collected as control. Double immunofluorescence staining with anti-α SMC actin and antispliced XBP1 (XBP1s) or unspliced XBP1 (XBP1u) antibodies were performed on the cryo-sections. As shown in Figure 1A, low levels of XBP1s and XBP1u were detected in the uninjure...

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Section: Discussionmentioning

confidence: 99%

XBP 1-Deficiency Abrogates Neointimal Lesion of Injured Vessels Via Cross Talk With the PDGF Signaling

Zeng

Yang

et al. 2015

ATVB

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“…Schopman et al (59) pointed out the possibility that tRFs may serve as primers for reverse transcriptase but also presented experimental evidence from studies of HIV-1 that did not support this proposal. Efficient HIV-1 reverse transcription requires interactions of tRNA-Lys with the PBS, as well as other regions of the viral genome.…”

Section: Discussionmentioning

confidence: 99%

Small Noncoding RNAs in Cells Transformed by Human T-Cell Leukemia Virus Type 1: a Role for a tRNA Fragment as a Primer for Reverse Transcriptase

Ruggero

Guffanti

Corradin

et al. 2014

J Virol

122

129

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The present study employed mass sequencing of small RNA libraries to identify the repertoire of small noncoding RNAs expressed in normal CD4؉ T cells compared to cells transformed with human T-cell leukemia virus type 1 (HTLV-1), the causative agent of adult T-cell leukemia/lymphoma (ATLL). The results revealed distinct patterns of microRNA expression in HTLV-1-infected CD4؉ T-cell lines with respect to their normal counterparts. In addition, a search for virus-encoded microRNAs yielded 2 sequences that originated from the plus strand of the HTLV-1 genome. Several sequences derived from tRNAs were expressed at substantial levels in both uninfected and infected cells. One of the most abundant tRNA fragments (tRF-3019) was derived from the 3= end of tRNA-proline. tRF-3019 exhibited perfect sequence complementarity to the primer binding site of HTLV-1. The results of an in vitro reverse transcriptase assay verified that tRF-3019 was capable of priming HTLV-1 reverse transcriptase. Both tRNA-proline and tRF-3019 were detected in virus particles isolated from HTLV-1-infected cells. These findings suggest that tRF-3019 may play an important role in priming HTLV-1 reverse transcription and could thus represent a novel target to control HTLV-1 infection. IMPORTANCE Small noncoding RNAs, a growing family of regulatory RNAs that includes microRNAs

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“…These newly discovered small RNAs represent an entirely new set of possible regulatory molecules whose physiological relevance is not currently understood; however, tRFs have been found to participate in gene silencing and are consistently observed on HDL ( 88,92 ). Similar to miRNAs, tRFs have their own numerical nomenclature (e.g., tRF-1001); however, a few tRFs were initially identifi ed as miRNAs (miR-1274A, miR-1274B, miR-1308, miR-866-5p, miR-1280, and miR-720) ( 90,93 ). Using the TaqMan real-time PCR lowdensity array platform to quantify miRNAs on mouse HDL, miR-720 was found to be upregulated 8.75-fold in a mouse model of atherosclerosis, ApoE Ϫ / Ϫ mice on a high-fat diet compared with wild-type c57Bl/6 mice on a chow diet ( 88 ).…”

Section: Hdl Proteomementioning

confidence: 99%