MALAT1 participates in ultraviolet B-induced photo-aging via regulation of the ERK/MAPK signaling pathway.


:Long non-coding RNA (lncRNA), transcripts of >200 bp in length that do not appear to exhibit any coding capacity, are important in the occurrence and development of cancer, cardiovascular and neurological diseases. However, effects of lncRNAs on photo‑aging remain to be elucidated. To explore the potential effects of the lncRNA metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) on photo‑aging in fibroblasts, MALAT1 expression was silenced in fibroblasts using small interference RNA. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to examine MALAT1 expression in normal and silenced fibroblasts following irradiation with 60 mJ/cm2 ultraviolet B (UVB) and an ELISA assay was used to identify matrix metalloproteinase‑1 (MMP‑1) content in the cellular supernatant. A β-galactosidase kit was applied to measure the number of senescent cells and a western blot assay was used to detect extracellular signal‑regulated kinase (ERK), c‑Jun N‑terminal kinase (JNK) and p38 phosphorylation levels. RT‑qPCR was additionally used to detect changes in MALAT1 expression following suppression of UVB‑induced reactive oxygen species (ROS) generation with N‑acetyl‑L‑cysteine (NAC). Fibroblasts irradiated with 60 mJ/cm2 UVB demonstrated increased MALAT1 expression, MMP‑1 secretory volume and number of senescent cells, and greater levels of ERK, p38 and JNK phosphorylation. Following silencing of MALAT1 expression in photo‑aged fibroblasts, decreases were observed in MMP‑1 secretory volume, number of senescent cells and phosphorylation levels of ERK. NAC reduced ROS content, however, it did not affect MALAT1 expression. Therefore, it was concluded that MALAT1 may participate in UVB‑induced photo‑aging via regulation of the ERK/mitogen‑activated protein kinase signaling pathway and UVB‑induced MALAT1 expression is independent of ROS generation.


Mol Med Rep


Lei L,Zeng Q,Lu J,Ding S,Xia F,Kang J,Tan L,Gao L,Kang L,Cao K,Zhou J,Xiao R,Chen J,Huang J




Has Abstract


2017-06-01 00:00:00












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