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Updated: Jul 22, 2025
Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Long non-coding RNA MM2P suppresses M1-polarized macrophages-mediated excessive inflammation to prevent sodium
Kang Peng1, Chen Biao1, Yin Yong Zhao1
1General Surgery Department, The First People's Hospital of Urumqi, Urumqi, 830011, China.
Abstract:
M1 macrophage-mediated excessive inflammatory response plays a key role in the onset and progression of acute pancreatitis (AP), and this study aimed to investigate the role and underlying mechanisms by which the macrophage polarization-related long noncoding RNA (lncRNA) MM2P participated in the regulation of AP progression. By performing quantitative reverse-transcription PCR (qRT-PCR) assay, lncRNA MM2P was found to be downregulated in both sodium taurocholate-induced AP model mice tissues and lipopolysaccharide (LPS)-stimulated RAW264.7 cells, and gain-of-function experiments confirmed that overexpression of lncRNA MM2P counteracted inflammatory responses, reduced macrophage infiltration and facilitated M1-to-M2 transformation of macrophages to ameliorate AP development in vitro and in vivo. Further mechanical experiments revealed that lncRNA MM2P inhibited Src homology 2 containing protein tyrosine phosphatase 2 (SHP2)-mediated signal transducer and activator of transcription 3 (STAT3) dephosphorylation to activate the STAT3 signaling, and silencing of SHP2 suppressed M1 type skewing in LPS-induced RAW264.7 cells. Interestingly, our rescuing experiments verified that lncRNA MM2P-induced suppressing effects on M1-polarization of LPS-treated RAW264.7 cells were abrogated by co-treating cells with STAT3 inhibitor stattic. Collectively, our data for the first time revealed that lncRNA MM2P suppressed M1-polarized macrophages to attenuate the progression of sodium taurocholate-induced AP, and lncRNA MM2P might be an ideal biomarker for AP diagnosis and treatment.
Insights
Long noncoding RNA MM2P suppresses M1 macrophage polarization, reducing inflammation and ameliorating acute pancreatitis (AP) progression. Overexpression of MM2P offers a potential therapeutic strategy for AP treatment.
Area of Science:
- Molecular Biology
- Immunology
- Gastroenterology
Background:
- Excessive M1 macrophage inflammation drives acute pancreatitis (AP) onset and progression.
- Understanding macrophage polarization's role is crucial for AP therapeutic development.
Purpose of the Study:
- Investigate the role of the long noncoding RNA (lncRNA) MM2P in regulating AP.
- Elucidate the underlying mechanisms of MM2P in macrophage polarization and AP progression.
Main Methods:
- Quantitative reverse-transcription PCR (qRT-PCR) to assess lncRNA MM2P levels.
- Gain-of-function experiments in AP models (in vitro and in vivo).
- Mechanistic studies involving SHP2, STAT3 signaling, and STAT3 inhibition.
Main Results:
- lncRNA MM2P was downregulated in AP models and LPS-stimulated cells.
- Overexpression of MM2P counteracted inflammation, reduced macrophage infiltration, and promoted M1-to-M2 transformation.
- MM2P inhibited SHP2-mediated STAT3 dephosphorylation, activating STAT3 signaling and suppressing M1 polarization.
Conclusions:
- lncRNA MM2P suppresses M1-polarized macrophages, attenuating sodium taurocholate-induced AP progression.
- MM2P may serve as a valuable biomarker for AP diagnosis and a therapeutic target.
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