Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

Lu, Wenjing; Huang, Shengyun; Su, Le; Zhao, Bao; Miao, Jun

doi:10.1038/srep21620

Cited by 54 publications

(45 citation statements)

References 49 publications

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“…Expression of the miR‐744‐5p was detected in human lip tissues and expressed in the maxillary, mandibular, and frontal nasal palate during mouse craniofacial development based on the FaceBase database. The involvement of miR‐744‐5p in wet age‐related macular degeneration has been previously reported (Lu et al, ), and our study provided the first evidence of its association with the risk of NSCL/P.…”

Section: Discussionsupporting

confidence: 82%

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Rs2262251 in lncRNA RP11‐462G12.2 is associated with nonsyndromic cleft lip with/without cleft palate

Wang

et al. 2019

Human Mutation

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Nonsyndromic cleft lip with/without cleft palate (NSCL/P) is one of the most common human congenital defects. Rs2262251 (G>C) in long noncoding RNA (lncRNA) RP11‐462G12.2 is in high linkage disequilibrium with rs8049367, which was identified in our previous genome‐wide association study on NSCL/P, and is a potential causative single‐nucleotide polymorphism (SNP) for NSCL/P. To test these hypotheses, rs2262251 was evaluated in another cohort of 1,314 cases and 1,259 controls. Rs2262251 was associated with NSCL/P risk (p = .003). However, no association was detected for cleft palate only. SNP rs2262251 affected the structure and expression of lncRNA RP11‐462G12.2 in HEK293 and HEPM cells and in lip tissues from patients with NSCL/P. Overexpression of the rs2262251 G allele contributed to reducing the number of cells in the G0/G1 phase, inhibiting cell apoptosis, and promoting cell proliferation in vitro. The rs2262251 C allele regulated the expression of miR‐744‐5p and its target gene IQSEC2, both of which were expressed in human lip tissues, and showed reverse correlation during mouse lip development. Taken together, these findings suggest that rs2262251 is associated with the risk of NSCL/P and participates in a lncRNA–miRNA–mRNA regulatory axis in which miR‐744‐5p and IQSEC2 combine to control NSCL/P development.

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Section: Discussionsupporting

confidence: 82%

“…LncRNAs can act as endogenous miRNA sponges, thereby affecting the expression of these miRNAs (Cesana et al, ; Chen, Liang, Zhang, & Zen, ; Lu, Huang, Su, Zhao, & Miao, ). Here, miR‐744‐5p was identified to interact with the C allele of rs2262251 in lncRNA RP11‐462G12.2 in an allele‐specific manner.…”

Section: Discussionmentioning

confidence: 99%

Rs2262251 in lncRNA RP11‐462G12.2 is associated with nonsyndromic cleft lip with/without cleft palate

Wang

et al. 2019

Human Mutation

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“…lncRNAs, defined as transcripts of greater than 200 nucleotides without protein‐coding function, have generated considerable interest in the past decade . Large numbers of lncRNAs have been identified, and they are implicated in human diseases by regulating oxidative stress, inflammation, apoptosis, cell growth and viability . However, the expression profile and biological function of lncRNAs in BPD are currently unknown.…”

Section: Introductionmentioning

confidence: 99%

“…9 Large numbers of lncRNAs have been identified, and they are implicated in human diseases by regulating oxidative stress, inflammation, apoptosis, cell growth and viability. [10][11][12][13] However, the expression profile and biological function of lncRNAs in BPD are currently unknown.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of long non‐coding RNAs in hyperoxia‐induced bronchopulmonary dysplasia

Bao

Cheng

et al. 2016

Cell Biochemistry & Function

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Bronchopulmonary dysplasia (BPD) is a common complication of premature birth that seriously affects the survival rate and quality of life among preterm neonates. Long non-coding RNAs (lncRNAs) have been implicated in many human diseases. However, the role of lncRNAs in the pathogenesis of BPD remains poorly understood. Here, we exposed neonatal C57BL/6J mice to 95% concentrations of ambient oxygen and established a mouse lung injury model that mimicked human BPD. Next, we compared lncRNA and messenger RNA (mRNA) expression profiles between BPD and normal lung tissues using a high-throughput mouse lncRNA + mRNA array system. Compared with the control group, 882 lncRNAs were upregulated, and 887 lncRNAs were downregulated in BPD lung tissues. We validated some candidate BPD-associated lncRNAs by real-time quantitative reverse-transcription polymerase chain reaction analysis in eight pairs of BPD and normal lung tissues. Gene ontology, pathway and bioinformatics analyses revealed that a downregulated lncRNA, namely AK033210, associated with tenascin C may be involved in the pathogenesis of BPD. To the best of our knowledge, our study is the first to reveal differential lncRNA expression in BPD, which provides a foundation for further understanding of the molecular mechanism of BPD development. Copyright © 2016 John Wiley & Sons, Ltd.

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“…Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts longer than 200 nucleotides [6] that were previously considered “transcription noise”, but studies have increasingly demonstrated that lncRNA transcripts are widely involved in almost every aspect of cellular biological functions, such as cell proliferation [7, 8], differentiation [9, 10], metabolism [11], and apoptosis [12]. Accumulating evidence suggests that the aberrant expression of lncRNAs plays an important role in the regulation of pancreatic β-cell function.…”

Section: Introductionmentioning

confidence: 99%

Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet β-Cell Function

Ruan¹,

Lin²,

Ma³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The islet is an important endocrine organ to secrete insulin to regulate the metabolism of glucose and maintain the stability of blood glucose. Long noncoding RNAs (lncRNAs) are involved in a variety of biological functions and play key roles in many diseases, including type 2 diabetes (T2D). The aim of this study was to determine whether lncRNA-p3134 is associated with glucose metabolism and insulin signaling in pancreatic β cells. Methods: LncRNA microarray technology was used to identify the differentially expressed circulating lncRNAs in T2D patients. RT-PCR analyses were performed to determine the expression of lncRNA-p3134 in 30 pairs of diabetic and non-diabetic patients. The correlation of lncRNA-p3134 to clinical data from T2D patients was analyzed. LncRNA-p3134 was overexpressed in Min6 cells and db/db mice by adenovirus-mediated technology. CCK-8, TUNEL, Western blot, glucose-stimulated insulin secretion (GSIS), ELISAs and immunochemistry were performed to determine the effect of lncRNA-p3134 on proliferation, apoptosis and insulin secretion both in vitro and vivo. Results: The circulating level of lncRNA-p3134 was higher in diabetic patients than in non-diabetic controls and was correlated with fasting blood glucose and HOMA-β levels. The lncRNA-p3134 had risen by 4 times in serum exosomes but nearly unchanged in exosome-free samples. The secretion of lncRNA-p3134 was dynamically modulated by glucose in both Min6 cells and isolated mouse islet cells. LncRNA-p3134 positively regulate GSIS through promoting of key regulators (Pdx-1, MafA, GLUT2 and Tcf7l2) in β cells. In addition, the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells. The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve β-cell function. Furthermore, a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. After blocking the PI3K/AKT signals with their specific inhibitor, the effect of overexpressed lncRNA-p3134 on insulin secretion was obviously attenuated. Conclusion: Taken together, the results of this study provide new insights into lncRNA-p3134 regulation in pancreatic β cells and provide a better understanding of novel mechanism of glucose homeostasis.

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Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

Cited by 54 publications

References 49 publications

Rs2262251 in lncRNA RP11‐462G12.2 is associated with nonsyndromic cleft lip with/without cleft palate

Rs2262251 in lncRNA RP11‐462G12.2 is associated with nonsyndromic cleft lip with/without cleft palate

Differential expression of long non‐coding RNAs in hyperoxia‐induced bronchopulmonary dysplasia

Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet β-Cell Function

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