PMID- 36299680 OWN - NLM STAT- MEDLINE DCOM- 20221028 LR - 20231211 IS - 1748-6718 (Electronic) IS - 1748-670X (Print) IS - 1748-670X (Linking) VI - 2022 DP - 2022 TI - Identification of lncRNAs Associated with the Pathogenesis of Diabetic Retinopathy: From Sequencing Analysis to Validation via In Vivo and In Vitro Experiments. PG - 1755945 LID - 10.1155/2022/1755945 [doi] LID - 1755945 AB - This study is aimed at screening for differentially expressed long noncoding RNAs (lncRNAs) associated with the pathogenesis of diabetic retinopathy and verifying the role of lncZNRD1 in high glucose-induced injury of retinal microvascular endothelial cells. The retinal tissues of normal and diabetic rats were collected for high-throughput sequencing of differentially expressed lncRNAs. Retinal microvascular endothelial cells were treated with 50 mM glucose for 4 h, 8 h, 24 h, 48 h, and 72 h. Our results showed that compared with the control group, there were 736 differentially expressed lncRNAs in the retina tissue of the model group, including 226 upregulated genes and 736 downregulated genes. Based on the differentially expressed lncRNAs, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the ErbB signaling pathway, transforming growth factor- (TGF-) beta signaling pathway, PI3K - Akt signaling pathway, cyclic adenosine 3,5-monophosphate (cAMP) signaling pathway, mitogen-activated protein kinase (MAPK) signaling pathway, and hypoxia-inducible factor-1 (HIF-1) signaling pathway were likely involved in the regulation of diabetic retinopathy. Compared with the control group, the expression of lncZNRD1-AS1 was significantly increased in retinal microvascular endothelial cells after treatment with high glucose for 24 h. Silencing lncZNRD1 promoted high glucose-induced apoptosis of microvascular endothelial cells. Additionally, silencing lncZNRD1 increased the expression levels of ALDH7A1 and ALDH3A2. In conclusion, lncZNRD1-AS1 demonstrated potentially beneficial function against high glucose-induced retina cell injury by regulating ALDH7A1 and ALDH3A2 expressions. CI - Copyright (c) 2022 Cheng-ping Luo et al. FAU - Luo, Cheng-Ping AU - Luo CP AD - Music College of Jiangxi Normal University, Nanchang 330022, China. FAU - Chen, Jia AU - Chen J AD - Department of Ophthalmology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China. FAU - Zou, Yu-Ling AU - Zou YL AUID- ORCID: 0000-0001-5926-8982 AD - Department of Ophthalmology, The Affiliated Eye Hospital of Nanchang University, Nanchang 330006, China. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20221017 PL - United States TA - Comput Math Methods Med JT - Computational and mathematical methods in medicine JID - 101277751 RN - 0 (RNA, Long Noncoding) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - IY9XDZ35W2 (Glucose) RN - EC 2.7.1.- (Phosphatidylinositol 3-Kinases) RN - EC 2.7.11.24 (Mitogen-Activated Protein Kinases) RN - K72T3FS567 (Adenosine) SB - IM RIN - Comput Math Methods Med. 2023 Nov 29;2023:9793672. PMID: 38077900 MH - Rats MH - Animals MH - *RNA, Long Noncoding/genetics/metabolism MH - *Diabetic Retinopathy/genetics MH - Endothelial Cells/metabolism/pathology MH - Proto-Oncogene Proteins c-akt/metabolism MH - *Diabetes Mellitus, Experimental/complications/genetics/metabolism MH - Glucose MH - Phosphatidylinositol 3-Kinases/metabolism MH - Mitogen-Activated Protein Kinases/metabolism MH - Adenosine/metabolism PMC - PMC9592201 COIS- The authors declare that they have no competing interests. EDAT- 2022/10/28 06:00 MHDA- 2022/10/29 06:00 PMCR- 2022/10/17 CRDT- 2022/10/27 02:30 PHST- 2022/08/03 00:00 [received] PHST- 2022/09/15 00:00 [revised] PHST- 2022/09/20 00:00 [accepted] PHST- 2022/10/27 02:30 [entrez] PHST- 2022/10/28 06:00 [pubmed] PHST- 2022/10/29 06:00 [medline] PHST- 2022/10/17 00:00 [pmc-release] AID - 10.1155/2022/1755945 [doi] PST - epublish SO - Comput Math Methods Med. 2022 Oct 17;2022:1755945. doi: 10.1155/2022/1755945. eCollection 2022.