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01000naa a22002652 4500 |
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NLM339429798 |
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DE-627 |
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20231226002858.0 |
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cr uuu---uuuuu |
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231226s2022 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2022.109006
|2 doi
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2 |
|a pubmed24n1131.xml
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|a (DE-627)NLM339429798
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|a (NLM)35413439
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|a (PII)S1521-6616(22)00087-0
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Zhu, Wangliang
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a LncRNA SOX2OT facilitates LPS-induced inflammatory injury by regulating intercellular adhesion molecule 1 (ICAM1) via sponging miR-215-5p
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| 264 |
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1 |
|c 2022
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 17.05.2022
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|a Date Revised 31.05.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2022. Published by Elsevier Inc.
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|a AIM: Long non-coding RNA SOX2 overlapping transcript (SOX2OT) is closely related to heart failure and myocardial damage. We attempted to investigate its role in endotoxin lipopolysaccharide (LPS) injury in cardiomyocytes
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| 520 |
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|a MATERIALS & METHODS: Cell viability, apoptosis rate, and levels of pro-inflammatory cytokines and apoptosis- and oxidative stress-related proteins were measured by MTS assay kit, flow cytometry, western blotting, and commercial kits. Physical interactions were confirmed by dual-luciferase report assay and RNA immunoprecipitation assay
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| 520 |
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|a RESULTS: Silencing SOX2OT and reinforcing miRNA (miR)-215-5p protected human AC16 cardiomyocytes from LPS-induced oxidative and inflammatory injuries by inhibiting intercellular adhesion molecule 1 (ICAM1). SOX2OT directly interacted with miR-215-5p, and miR-215-5p could target ICAM1
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|a CONCLUSION: Inhibiting SOX2OT/miR-215-5p/ICAM1 axis might be a possible approach to treat myocardial damage
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|a LAY ABSTRACT: Lipopolysaccharide (LPS) is an endotoxin from some bacteria including Escherichia coli, and it can cause inflammation in different tissues/cells including myocardia/cardiomyocytes, resulting in diseases such as myocarditis, cardiomyopathy, and cardiac hypertrophy. The underlying mechanism was not completely clarified, but known to include the dysregulation of non-coding RNAs. Herein, we demonstrated the biological role of long non-coding RNA SOX2 overlapping transcript (SOX2OT) in LPS-infected cardiomyocytes. Eventually, we found that inhibiting the expression of SOX2OT could mitigate LPS-induced a series of injuries in human cardiomyocytes, and SOX2OT interacts with a microRNA named as miR-215-5p. Besides, restoring miR-215-5p elicited similar effects to SOX2OT knockdown. Collectively, we concluded that SOX2OT binding to miR-215-5p might protect cardiomyocytes from LPS infection through regulating an important protein named ICAM1. This study suggested SOX2OT/miR-215-5p might be novel potential treatment targets in bacterial infection-related myocardial damages
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|a Journal Article
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|a Cardiomyocytes
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4 |
|a LPS
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| 650 |
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4 |
|a SOX2OT
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| 650 |
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4 |
|a miR-215-5p
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| 650 |
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7 |
|a ICAM1 protein, human
|2 NLM
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| 650 |
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7 |
|a Lipopolysaccharides
|2 NLM
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| 650 |
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7 |
|a MIRN215 microRNA, human
|2 NLM
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| 650 |
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7 |
|a MicroRNAs
|2 NLM
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| 650 |
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7 |
|a RNA, Long Noncoding
|2 NLM
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| 650 |
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7 |
|a long non-coding RNA Sox2ot, human
|2 NLM
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| 650 |
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7 |
|a Intercellular Adhesion Molecule-1
|2 NLM
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| 650 |
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7 |
|a 126547-89-5
|2 NLM
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| 700 |
1 |
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|a Peng, Fang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cui, Xudong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Jianfei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sun, Chaofeng
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 238(2022) vom: 01. Mai, Seite 109006
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:238
|g year:2022
|g day:01
|g month:05
|g pages:109006
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| 856 |
4 |
0 |
|u http://dx.doi.org/10.1016/j.clim.2022.109006
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 238
|j 2022
|b 01
|c 05
|h 109006
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