scholarly journals Long non-coding RNA MEG3 inhibits neovascularization in diabetic retinopathy by regulating microRNA miR-6720-5p and cytochrome B5 reductase 2

Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 11872-11884
Author(s):  
Jinpeng Chen ◽  
Lin Liao ◽  
Huiyong Xu ◽  
Zheng Zhang ◽  
Jian Zhang
Keyword(s):  
Diabetic Retinopathy ◽  
Cytochrome B5 ◽  
Cytochrome B5 Reductase ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Cytochrome B5 Reductase 2

Long non-coding RNA SNHG16 regulates E2F1 expression by sponging miR-20a-5p and aggravating proliferative diabetic retinopathy

2021 ◽  
Author(s):  
Xiaohua Li ◽  
Chenyu Guo ◽  
Yong Chen ◽  
Feifei Yu
Keyword(s):  
Diabetic Retinopathy ◽  
Microvascular Dysfunction ◽  
Luciferase Reporter ◽  
Non Coding Rna ◽  
Reporter Assays ◽  
Polymerase Chain ◽  
Long Non Coding Rna ◽  
E2f1 Expression

Long non-coding RNAs (lncRNAs) were reported that related to microvascular dysfunction in diabetic retinopathy (DR), but the potential mechanism remains unknown. This study was designed to elucidate the effects of lncRNA SNHG16 in proliferative DR progression. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the levels of SNHG16 and miR-20a-5p from peripheral blood samples of different participants. Pearson’s correlation analysis on the plasma data was applied to detect correlations between SNHG16 and miR-20a-5p. Finally, the interactions of miR-20a-5p and SNHG16 or E2F1 were assessed by luciferase reporter assays. SNHG16 and E2F1 were increased and miR-20a-5p was decreased in proliferative DR both in vivo and in vitro, when compared with control or non-proliferative DR. E2F1 was identified as the target of miR-20a-5p. MiR-20a-5p interacted with SNHG16 and E2F1, and was controlled by SNHG16. The regulation of SNHG16 on E2F1 was mediated by miR-20a-5p. Cells transfected with SNHG16 OE plasmid markedly increased cell apoptosis and vessel-like formation, whereas the miR-20a-5p mimic partially reversed these effects. Transfection with si-E2F1 plasmid rescued SNHG16 overexpression-aggravated proliferative DR. This study indicated that SNHG16 regulated E2F1 expression by sponging miR-20a-5p and aggravating proliferative DR.

scholarly journals The Identification of Cytochrome B5 Reductase 2 and Fructose-1,6-Bisphosphatase 1 Proteins in Non-Small Cell Lung Cancer: Proteomics Approach

2020 ◽  
Vol 13 (12) ◽  
Author(s):  
Zahra Najafi ◽  
Abdolreza Mohamadnia ◽  
Rahim Ahmadi ◽  
Minoo Mahmoodi ◽  
Naghmeh Bahrami ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cytochrome B5 ◽  
Small Cell ◽  
Healthy Individuals ◽  
Small Cell Lung ◽  
Tissue Samples ◽  
Messenger Ribonucleic Acid ◽  
Cytochrome B5 Reductase ◽  
Fructose 1,6 Bisphosphatase ◽  
Cytochrome B5 Reductase 2

Background: Lung cancer is one of the major causes of death worldwide, with more than a million deaths a year. Despite advanced surgical techniques and combined therapies, lung cancer is still a disease with poor prognosis. According to available reports, the number of patients with lung cancer among Iranian men and women is increasing. In a study, 4,361 deaths from lung cancer have been recorded in Iran, which are 9.80% and 6.07% of all cancer deaths among men and women, respectively. Objectives: This study aimed at investigating the proteomes in patients with non-small cell lung cancer (NSCLC) and comparing them with those of the healthy individuals to detect protein markers for the diagnosis of the disease in the early stages. Methods: According to the sample size estimation, the tissue samples of 30 patients with NSCLC were compared with 30 healthy tissues. Proteomics and reverse transcriptase polymerase chain reaction (RT-PCR) methods were used. First, the tissue samples were collected under sterile conditions and then protein was extracted. Next, 2-dimensional electrophoresis and mass spectrometry were performed. Finally, with proteomic analysis in patients and healthy individuals, differences in the proteomic pattern of healthy and cancerous tissue were examined. Results: More than 40 differences were revealed in the proteomics pattern of the healthy and cancerous tissues, and 2 different spots were submitted for liquid chromatography-mass spectrometry (LC-MS/ MS). Then cytochrome b5 reductase 2 (CYB5R2) and fructose-1,6-bisphosphate1 were detected. It has been shown that these proteins down-regulated in cancer tissue compared to healthy tissue. It was also shown molecularly that the expression of fructose-1,6-bisphosphatase 1 messenger ribonucleic acid (mRNA) and cytochrome b5 reductase 2 messenger ribonucleic acid (mRNA) in the cancerous tissue was 0.8 and 0.64 times less than their expression in healthy tissues, respectively. Conclusions: The result of this study, which deals with tumor markers of NSCLC, can be considered as a screening diagnostic test for diagnosis of the disease in the early stages. This research could provide the basis for further research to identify the critical effects of these 2 molecules cytochrome b5 reductase 2 and fructose-1,6-bisphosphate on tissue carcinogenesis. It is recommended to do more thorough research.

scholarly journals Long non-coding RNA nuclear paraspeckle assembly transcript 1 inhibits the apoptosis of retina Müller cells after diabetic retinopathy through regulating miR-497/brain-derived neurotrophic factor axis

2018 ◽  
Vol 15 (3) ◽  
pp. 204-213 ◽  
Author(s):  
Xiu-juan Li
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Retinopathy ◽  
High Glucose ◽  
Neurotrophic Factor ◽  
Müller Cells ◽  
Brain Derived Neurotrophic Factor ◽  
Muller Cells ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background: The role of long non-coding RNA in diabetic retinopathy, a serious complication of diabetes mellitus, has attracted increasing attention in recent years. The purpose of this study was to explore whether long non-coding RNA nuclear paraspeckle assembly transcript 1 was involved in the context of diabetic retinopathy and its underlying mechanisms. Results: Our results revealed that nuclear paraspeckle assembly transcript 1 was significantly downregulated in the retina of diabetes mellitus rats. Meanwhile, miR-497 was significantly increased in diabetes mellitus rats’ retina and high glucose–treated Müller cells, but brain-derived neurotrophic factor was increased. We also found that high glucose–induced apoptosis of Müller cells was accompanied by the significant downregulation of nuclear paraspeckle assembly transcript 1 in vitro. Further study demonstrated that high glucose–promoted Müller cells apoptosis through downregulating nuclear paraspeckle assembly transcript 1 and downregulated nuclear paraspeckle assembly transcript 1 mediated this effect via negative regulating miR-497. Moreover, brain-derived neurotrophic factor was negatively regulated by miR-497 and associated with the apoptosis of Müller cells under high glucose. Conclusion: Our results suggested that under diabetic conditions, downregulated nuclear paraspeckle assembly transcript 1 decreased the expression of brain-derived neurotrophic factor through elevating miR-497, thereby promoting Müller cells apoptosis and aggravating diabetic retinopathy.

Role of Long Non-Coding RNA MALAT1 in the Pathogenesis of Diabetic Retinopathy

2017 ◽  
Vol 41 (5) ◽  
pp. S8
Author(s):  
Saumik Biswas ◽  
Anu Thomas ◽  
Biao Feng ◽  
Shali Chen ◽  
John Gonder ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Transthyretin Upregulates Long Non-Coding RNA MEG3 by Affecting PABPC1 in Diabetic Retinopathy

2019 ◽  
Vol 20 (24) ◽  
pp. 6313 ◽  
Author(s):  
Guangming Fan ◽  
Yu Gu ◽  
Jiaojiao Zhang ◽  
Yu Xin ◽  
Jun Shao ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Retinal Vessel ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Mice Model ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Maternally Expressed Gene 3

The aim of the study was to demonstrate how transthyretin (TTR) could affect long non-coding RNA (lncRNA) of maternally expressed gene 3 (MEG3) and play important roles in diabetic retinopathy (DR). A DR model in C57BL/6 mice was established after intraperitoneal injection of streptozotocin (STZ). After intravitreal injection with TTR pAAV vector, MEG3 short hairpin RNA (shRNA), scrambled shRNA, or MEG3, retinal imaging, retinal trypsin digestion, and fundus vascular permeability tests were performed. Cell counting kit-8 (CCK8), transwell, and Matrigel assays were employed to detect the proliferation and migration of human retinal microvascular endothelial cells (hRECs). The binding between long non-coding RNA of maternally expressed gene 3 (lncRNA-MEG3) and microRNA-223-3p (miR-223-3p) was observed by using luciferase reporter assays, while co-immunoprecipitation (co-IP) was employed to confirm the interaction between TTR and the target. In the DR mice model, retinal vascular leakage and angiogenesis were repressed by overexpressing TTR. In vitro, the added TTR promoted the level of lncRNA-MEG3 by interacting with poly (A) binding protein cytoplasmic 1 (PABPC1), and then repressed proliferation and angiogenesis of hRECs. In vivo, silencing or overexpressing lncRNA-MEG3 significantly affected retinal vascular phenotypes. Additionally, the interaction between lncRNA-MEG3 and miR-223-3p was confirmed, and silencing of miR-223-3p revealed similar effects on hRECs as overexpression of lncRNA-MEG3. In summary, in the DR environment, TTR might affect the lncRNA MEG3/miR-223-3p axis by the direct binding with PABPC1, and finally repress retinal vessel proliferation.

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