Research articles
ScienceAsia 51 (2023): 1-11 |doi:
10.2306/scienceasia1513-1874.2023.029
LncRNA MALAT1 promoted PA-induced damage and reduced
insulin secretion in MIN6 cells through Phospho-p38 pathway
Yang Oua, Jiaxin Liub, Chao Liuc, Zhongxiong Zhenga, Heng Sua,*
ABSTRACT: This study aimed to investigate the role of LncRNA MALAT1 in pancreatic ?-cell dysfunction in type 2
diabetes mellitus (T2DM) and its mechanisms, particularly focusing on the Phospho-p38 signaling pathway. MIN6 cells
were treated with palmitic acid (PA) to induce ?-cell dysfunction. Transcriptome analysis revealed upregulation of
LncRNA MALAT1, which was further investigated for its effects on cell proliferation, apoptosis, ROS production, and
insulin secretion. The involvement of the Phospho-p38 signaling pathway was explored through rescue experiments
using DHC, an activator of Phospho-p38. In vivo validation was conducted using a T2DM rat model. PA treatment
reduced cell proliferation, increased apoptosis, elevated ROS, and decreased insulin secretion. Knockdown of
MALAT1 improved these dysfunctions and downregulated the Phospho-p38 pathway. In vivo studies confirmed the
upregulation of MALAT1 and Phospho-p38 alongside significant ?-cell dysfunction. This study demonstrated that
LncRNAMALAT1playedacrucialroleinpancreatic ?-cell dysfunction in T2DM by activating the Phospho-p38 signaling
pathway. Knockdown of MALAT1 mitigated PA-induced ?-cell damage by downregulating Phospho-p38, highlighting
the MALAT1/Phospho-p38 axis as a potential therapeutic target for preserving pancreatic ?-cell function in T2DM.
These findings provide new insights into the molecular mechanisms underlying T2DM and suggest novel avenues for
intervention.
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| a |
Department of Endocrinology and Metabolism, First People?s Hospital of Yunnan Province (The Affiliated Hospital
of Kunming University of Science and Technology), Kunming 650032 China |
| b |
School of Medicine, Kunming University of Science and Technology, Kunming 650500 China |
| c |
Department of General Affairs, First People?s Hospital of Yunnan Province (The Affiliated Hospital of Kunming
University of Science and Technology), Kunming 650032 China |
* Corresponding author, E-mail: su_hen@hotmail.com
Received 25 Jun 2024, Accepted 14 Nov 2024
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