ArticleWorld journal of gastroenterology2016
miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene.
Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Clinical and Genetic Interplay Between Chronic Pancreatitis, Cystic Fibrosis and CFTR-Related Disorders.International journal of molecular sciences · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- A New Strategy to Inhibit Scar Formation by Accelerating Normal Healing Using Silicate Bioactive Materials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- miR-9 alleviated the inflammatory response and apoptosis in caerulein-induced acute pancreatitis by regulating FGF10 and the NF-κB signaling pathway.Experimental and therapeutic medicine · 2021Article
- Mining prognostic markers of Asian hepatocellular carcinoma patients based on the apoptosis-related genes.BMC cancer · 2021Article
- LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-κB Pathway.Inflammation · 2021Article
- Overexpression of miR-29a-3p Suppresses Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells in Atherosclerosis via Targeting TNFRSF1A.BioMed research international · 2020Article
- miR-135a deficiency inhibits the AR42J cells damage in cerulein-induced acute pancreatitis through targeting FAM129A.Pflugers Archiv : European journal of physiology · 2019Article
- miR-352 participates in the regulation of trypsinogen activation in pancreatic acinar cells by influencing the function of autophagic lysosomes.Oncotarget · 2018Article
- miR-148a-3p exhaustion inhibits necrosis by regulating PTEN in acute pancreatitis.International journal of clinical and experimental pathology · 2018Article
- Targeting MicroRNA Function in Acute Pancreatitis.Frontiers in physiology · 2017Review
- Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms.Frontiers in pharmacology · 2017Review
- Yin-Chen-Hao Tang Attenuates Severe Acute Pancreatitis in Rat: An Experimental Verification ofFrontiers in pharmacology · 2016Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the expression of miR-29a in rat acute pancreatitis and its functional role in AR42J cell apoptosis.
methodsTwelve SD rats were divided into a control group and an acute edematous pancreatitis (AEP) group randomly. AEP was induced by intraperitoneal injection of L-arginine (150 mg/kg) in the AEP group and equal volume of 0.9% NaCl was injected in the control group. The apoptosis of acinar cells in pancreatic tissue was determined by TUNEL assay. miRNA chip assay was performed to examine the expression of miRNAs in two groups. Besides, to further explore the role of miR-29a in apoptosis in vitro, recombinant rat TNF-α (50 ng/mL) was administered to treat the rat pancreatic acinar cell line AR42J for inducing AR42J cell apoptosis. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-29a expression. Then, miRNA mimic, miRNA antisense oligonucleotide (AMO) and control vector were used to transfect AR42J cells. The expression of miR-29a was confirmed by qRT-PCR and the apoptosis rate of AR42J cells was detected by flow cytometry analysis. Western blot was used to detect the expression of activated caspase3. Moreover, we used bioinformatics software and luciferase assay to test whether TNFRSF1A was the target gene of miR-29a. After transfection, qRT-PCR and Western blot was used to detect the expression of TNFRSF1A in AR42J cells after transfection.
resultsThe expression of miR-29a was much higher in the AEP group compared with the control group as displayed by the miRNA chip assay. After inducing apoptosis of AR42J cells in vitro, the expression of miR-29a was significantly increased by 1.49 ± 0.04 times in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-29a was 2.68 ± 0.56 times higher in the miR-29a mimic group relative to the control vector group, accompanied with an obviously increased acinar cell apoptosis rate (42.83 ± 1.25 vs 24.97 ± 0.15, P < 0.05). Moreover, the expression of miR-29a in the miRNA AMO group was 0.46 ± 0.05 times lower than the control vector group, and the cell apoptosis rate was much lower accordingly (17.27 ± 1.36 vs 24.97 ± 0.15, P < 0.05). The results of bioinformatics software and luciferase assay showed that TNFRSF1A might be a target gene of miR-29a. TNFRSF1A expression was up-regulated in the miR-29a mimic group, while the miR-29a AMO group showed the reverse trend.
conclusionmiR-29a might promote the apoptosis of AR42J cells via up-regulating the expression of its target gene TNFRSF1A.
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