Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway
Acute pancreatitis (AP) is an inflammatory disease of the pancreas. A growing number of studies have shown that long noncoding RNAs (lncRNAs) play an important role in AP progression. Here, we aimed to elucidate the role of Small Nucleolar RNA Host Gene 11(SNHG11) and its underlying molecular mechan...
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MDPI AG
2022-12-01
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author | Tian-Jiao Song Jun Ke Feng Chen Jiu-Yun Zhang Chun Zhang Hong-Yi Chen |
author_facet | Tian-Jiao Song Jun Ke Feng Chen Jiu-Yun Zhang Chun Zhang Hong-Yi Chen |
author_sort | Tian-Jiao Song |
collection | DOAJ |
description | Acute pancreatitis (AP) is an inflammatory disease of the pancreas. A growing number of studies have shown that long noncoding RNAs (lncRNAs) play an important role in AP progression. Here, we aimed to elucidate the role of Small Nucleolar RNA Host Gene 11(SNHG11) and its underlying molecular mechanisms behind AP progression. The in vivo and in vitro AP cell models were established by retrograde injection of sodium taurocholate and caerulein stimulation into AR42J cells and HPDE6-C7 cells, respectively. A bioinformatics website predicted the relationship between SNHG11, miR-7-5p, and Phospholipase C Beta 1(PLCB1) and validated it with a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. AR42J cells and HPDE6-C7 cells were transfected with an overexpression of plasmids or shRNA to investigate the effects of the SNHG11/miR-7-5p/PLCB1 axis on cell proliferation and apoptosis, inflammatory cytokine secretion, and acute pancreatitis. Low expression of SNHG11 and PLCB1 and high expression of miR-7-5p were observed in AP pancreatic tissue and AP cell models. SNHG11 overexpression inhibited apoptosis and inflammatory responses induced by caerulein. Simultaneously, we discovered that SNHG11 regulates PLCB1 expression by sponging miR-7-5p. PLCB1 overexpression abrogated inflammatory damage exacerbated by miR-7-5p enrichment. In addition, the SNHG11/miR-7-5p/PLCB1 axis could be involved in caerulein-induced inflammatory injury by participating in the p38MAPK signaling pathway. The overexpressed SNHG11/miR-7-5p/PLCB1 axis can inhibit AP progression by participating in the p38MAPK signaling pathway, thereby providing a potential therapeutic target and therapeutic direction for AP therapy. |
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language | English |
last_indexed | 2024-03-11T10:06:01Z |
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spelling | doaj.art-92fed80962ff40f0a4059d591a2451692023-11-16T15:05:40ZengMDPI AGCells2073-44092022-12-011216510.3390/cells12010065Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK PathwayTian-Jiao Song0Jun Ke1Feng Chen2Jiu-Yun Zhang3Chun Zhang4Hong-Yi Chen5Shengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, ChinaShengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, ChinaShengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, ChinaShengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, ChinaDepartment of Hepatobiliary and Pancreatic Surgery, Mindong Hospital, Ningde, Fujian Medical University, No. 89, Heshan Road, Fuan 355000, ChinaShengli Clinical Medical College, Fujian Medical University, Fuzhou 350001, ChinaAcute pancreatitis (AP) is an inflammatory disease of the pancreas. A growing number of studies have shown that long noncoding RNAs (lncRNAs) play an important role in AP progression. Here, we aimed to elucidate the role of Small Nucleolar RNA Host Gene 11(SNHG11) and its underlying molecular mechanisms behind AP progression. The in vivo and in vitro AP cell models were established by retrograde injection of sodium taurocholate and caerulein stimulation into AR42J cells and HPDE6-C7 cells, respectively. A bioinformatics website predicted the relationship between SNHG11, miR-7-5p, and Phospholipase C Beta 1(PLCB1) and validated it with a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. AR42J cells and HPDE6-C7 cells were transfected with an overexpression of plasmids or shRNA to investigate the effects of the SNHG11/miR-7-5p/PLCB1 axis on cell proliferation and apoptosis, inflammatory cytokine secretion, and acute pancreatitis. Low expression of SNHG11 and PLCB1 and high expression of miR-7-5p were observed in AP pancreatic tissue and AP cell models. SNHG11 overexpression inhibited apoptosis and inflammatory responses induced by caerulein. Simultaneously, we discovered that SNHG11 regulates PLCB1 expression by sponging miR-7-5p. PLCB1 overexpression abrogated inflammatory damage exacerbated by miR-7-5p enrichment. In addition, the SNHG11/miR-7-5p/PLCB1 axis could be involved in caerulein-induced inflammatory injury by participating in the p38MAPK signaling pathway. The overexpressed SNHG11/miR-7-5p/PLCB1 axis can inhibit AP progression by participating in the p38MAPK signaling pathway, thereby providing a potential therapeutic target and therapeutic direction for AP therapy.https://www.mdpi.com/2073-4409/12/1/65acute pancreatitisLncRNA-SNHG11miR-7-5pPLCB1p38MAPK |
spellingShingle | Tian-Jiao Song Jun Ke Feng Chen Jiu-Yun Zhang Chun Zhang Hong-Yi Chen Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway Cells acute pancreatitis LncRNA-SNHG11 miR-7-5p PLCB1 p38MAPK |
title | Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway |
title_full | Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway |
title_fullStr | Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway |
title_full_unstemmed | Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway |
title_short | Effect of SNHG11/miR-7-5p/PLCB1 Axis on Acute Pancreatitis through Inhibiting p38MAPK Pathway |
title_sort | effect of snhg11 mir 7 5p plcb1 axis on acute pancreatitis through inhibiting p38mapk pathway |
topic | acute pancreatitis LncRNA-SNHG11 miR-7-5p PLCB1 p38MAPK |
url | https://www.mdpi.com/2073-4409/12/1/65 |
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