Evidence map›Paper›PMID 33042438›Full record

ArticleAmerican journal of translational research2020

LncRNA-NEF regulated the hyperoxia-induced injury of lung epithelial cells by FOXA2.

Mei Mei, Jing Nie, Huawei Sun, He Wang, Li Rong

Abstract read
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Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Mei MeiThe First Affiliated Hospital of Jms University Jiamusi 154000, Heilongjiang Province, China.
Jing NieThe First Affiliated Hospital of Jms University Jiamusi 154000, Heilongjiang Province, China.
Huawei SunThe First Affiliated Hospital of Jms University Jiamusi 154000, Heilongjiang Province, China.
He WangThe First Affiliated Hospital of Jms University Jiamusi 154000, Heilongjiang Province, China.
Li RongThe First Hospital of Qiqihar, Affiliated Qiqihar Hospital of Southern Medical Qiqihar 161000, Heilongjiang Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHyperoxia-induced injury is a common form of damage in lung tissues, which could lead to bronchopulmonary dysplasia (BPD) in newborns. Recent studies have discovered that FOXA2 played a substantial role in protecting lung tissues from various injuries and lncRNA-NEF could activate the expression of FOXA2. However, it is unclear whether lncRNA-NEF could alleviate hyperoxia-caused damage of lung tissues by activating FOXA2. MATERIAL AND

methodsIn this study, we used the lentivirus to establish the lncRNA-NEF overexpression RLE-6TN and MLE-12 cells. After that, the lentivirus was also used to knockdown the expression of FOXA2 in the two lncRNA-NEF overexpression cells. ELISA was performed to detect the levels of TNF-α, IL-1β and IL-6. The production of ROS, SOD, MDA and LDH was determined with the commercial kits. The apoptosis rates of these cells were measured with the flow cytometry.

resultsThe secretion of TNF-α, IL-1β and IL-6 was inhibited in RLE-6TN and MLE-12 cells after the overexpression of lncRNA-NEF. Furthermore, the production of ROS, MDA and LDH was also suppressed after the upregulation of lncRNA-NEF. The promotion of lncRNA-NEF also restricted the hyperoxia-induced apoptosis. However, the knockdown of FOXA2 abolished all the inhibitory effects exerted by lncRNA-NEF.

conclusionLncRNA-NEF regulated hyperoxia-caused inflammatory response, oxidative damage and apoptosis of RLE-6TN and MLE-12 cells by affecting the expression of FOXA2.

Indexed as

Bronchopulmonary dysplasiaFOXA2Hyperoxia-induced lung injuryinflammationLncRNA-NEF

Identifiers

PMID33042438
PMCPMC7540126

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