Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-κB signaling pathway

Publication: Biochemistry and Cell Biology
5 June 2020


The study investigated the expression of long noncoding RNA (lncRNA) MALAT1 in high glucose (HG)-induced human vascular endothelial cells (HUVECs) and the role of MALAT1 in the apoptosis of HG-induced HUVECs. The HUVECs were cultured and induced with 25 mmol/L HG. After that, the HUVECs were transfected with MALAT1 siRNA. The expression levels of MALAT1 were detected with qPCR, whereas the expression levels of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65, and p-p65 were detected using Western blot. The roles of MALAT1 in cell activities, including apoptosis, were evaluated using the CCK-8 assay, TUNEL staining, and flow cytometry. The expression levels of inflammatory factors (TNF-α and IL-6) were measured using ELISA. The expression levels of MALAT1, TNF-α, and IL-6 in HUVECs were increased in the HG environment; however, when MALAT1 was silenced in the HUVECs, cell proliferation increased significantly, the expression levels of TNF-α, IL-6, Bax, cleaved-caspase-3, and cleaved-caspase-9 decreased, and the rate of apoptosis also decreased. Silencing MALAT1 inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 is upregulated in HG-induced HUVECs, and inhibition of MALAT1 inhibits HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-κB signaling pathway.


Cette étude visait à examiner l’expression du long ARN non codant (ARNnc) MALAT1 dans les cellules vasculaires endothéliales humaines (HUVEC) exposées à une haute teneur en glucose (HG) et le rôle de MALAT1 dans l’apoptose des HUVEC induite par une HG. Les HUVEC ont été cultivées et stimulées avec 25 mmol/L de glucose. Ensuite, les HUVEC ont été transfectées avec un ARN interférent de MALAT1. L’expression de MALAT1 a été détectée par qPCR alors que l’expression de Bax, de Bcl-2, de la caspase-3 clivée, de la caspase-9 clivée, de p65 et de p-p65 a été détectée par buvardage Western. En parallèle, le rôle régulateur de MALAT1 dans l’activité cellulaire et l’apoptose a été détecté par un dosage avec le CCK-8, la coloration TUNEL et la cytométrie en flux. Par ailleurs, l’expression de facteurs inflammatoires (TNF-α, IL-6) a été détectée par ELISA. L’expression de MALAT1, du TNF-α et d’IL-6 dans les HUVEC était accrue dans un environnement à HG. Après que les HUVEC stimulées par une HG aient été soumises au silençage de MALAT1, il s’est avéré que la prolifération cellulaire augmentait significativement, que l’expression du TNF-α, d’IL-6, de Bax, de la caspase-3 clivée, de la caspase-9 clivée diminuait, et que l’apoptose diminuait. Le silençage de MALAT1 inhibait l’expression de p-p65 dans les HUVEC soumises à une HG. En conclusion, l’étude des auteurs a démontré que MALAT1 était régulé à la hausse dans les HUVEC stimulées par une HG, et l’inhibition de MALAT1 pouvait inhiber l’apoptose et l’inflammation induite par une HG dans les HUVEC par la suppression de la voie de signalisation du NF-κB. [Traduit par la Rédaction]

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Published In

cover image Biochemistry and Cell Biology
Biochemistry and Cell Biology
Volume 98Number 6December 2020
Pages: 669 - 675


Received: 28 October 2019
Accepted: 7 April 2020
Published online: 5 June 2020


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Key Words

  1. long noncoding RNA
  2. MALAT1
  3. human umbilical vein endothelial cells
  4. high glucose
  5. NF-κB signaling pathway
  6. apoptosis
  7. inflammation


  1. long ARN non codant
  2. MALAT1
  3. cellules endothéliales de cordon ombilical
  4. forte teneur en glucose
  5. voie de signalisation du NF-κB
  6. apoptose
  7. inflammation



Department of Endocrinology, Pingxiang People’s Hospital, Pingxiang 337000, P.R. China.
Ya-Wei Zhang
Department of Endocrinology, Pingxiang People’s Hospital, Pingxiang 337000, P.R. China.
Xiao-Qing Su
Department of Endocrinology, Pingxiang People’s Hospital, Pingxiang 337000, P.R. China.
Hai-Bo Gao
Department of Endocrinology, Pingxiang People’s Hospital, Pingxiang 337000, P.R. China.


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