Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells
To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22. One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the a...
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creator | Fu, Qiang Liu, Chuan-Jiang Zhang, Xu Zhai, Zhen-Sheng Wang, Yu-Zhu Hu, Ming-Xing Xu, Xian-Ling Zhang, Hong-Wei Qin, Tao |
description | To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22.
One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) 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 ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3.
After inducing apoptosis of AR42J cells
, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15
18.07 ± 0.89,
= 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells.
GR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway. |
doi_str_mv | 10.3748/wjg.v24.i45.5120 |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6288647</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2159325549</sourcerecordid><originalsourceid>FETCH-LOGICAL-c396t-1a2c0e0e4fca2f6b159cb88a39f4df958e21e0e1b6073e1224cd790b066039fe3</originalsourceid><addsrcrecordid>eNpVkUFv1DAQhS0EotvCnRPykUsWe-wk9gWpqqBFqkBCcLYcZ5K6SuxgJ11654fjVUsFpxlp3nsz9kfIG872opXq_eF23N-B3HtZ72sO7BnZAXBdgZLsOdlxxtpKC2hPyGnOt4yBEDW8JCeC1Y0SSu_I78tpc9HFtHoXfU8TOlzWmEozbpNdMVP8tSTM2cdA40Bn71L89uW8AqA29LSPh5DXhHam2Y_BTj6MdLHrzcHeUx-oXWLJyz4fzYsNrkjLLmqdDzZRh9OUX5EXg50yvn6sZ-THp4_fL66q66-Xny_OrysndLNW3IJjyFAOzsLQdLzWrlPKCj3IftC1QuBlzLuGtQI5gHR9q1nHmoYVDYoz8uEhd9m6GXuHYU12Mkvys033Jlpv_p8Ef2PGeGcaUKqRbQl49xiQ4s8N82pmn49PsAHjlg2UkwTUtdRFyh6k5btyTjg8reHMHOGZAs8UeKbAM0d4xfL23_OeDH9piT-r55tJ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2159325549</pqid></control><display><type>article</type><title>Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells</title><source>MEDLINE</source><source>Baishideng "World Journal of" online journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Fu, Qiang ; Liu, Chuan-Jiang ; Zhang, Xu ; Zhai, Zhen-Sheng ; Wang, Yu-Zhu ; Hu, Ming-Xing ; Xu, Xian-Ling ; Zhang, Hong-Wei ; Qin, Tao</creator><creatorcontrib>Fu, Qiang ; Liu, Chuan-Jiang ; Zhang, Xu ; Zhai, Zhen-Sheng ; Wang, Yu-Zhu ; Hu, Ming-Xing ; Xu, Xian-Ling ; Zhang, Hong-Wei ; Qin, Tao</creatorcontrib><description>To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22.
One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) 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 ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3.
After inducing apoptosis of AR42J cells
, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15
18.07 ± 0.89,
= 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells.
GR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.v24.i45.5120</identifier><identifier>PMID: 30568389</identifier><language>eng</language><publisher>United States: Baishideng Publishing Group Inc</publisher><subject>Acinar Cells - physiology ; Animals ; Apoptosis - drug effects ; Apoptosis - genetics ; Basic Study ; Cell Line ; Ceruletide - pharmacology ; Down-Regulation ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Pancreas - cytology ; Rats ; Receptors, Glucocorticoid - genetics ; Receptors, Glucocorticoid - metabolism ; RNA, Small Interfering - metabolism ; Signal Transduction - genetics ; Transcription Initiation Site ; Up-Regulation</subject><ispartof>World journal of gastroenterology : WJG, 2018-12, Vol.24 (45), p.5120-5130</ispartof><rights>The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-1a2c0e0e4fca2f6b159cb88a39f4df958e21e0e1b6073e1224cd790b066039fe3</citedby><cites>FETCH-LOGICAL-c396t-1a2c0e0e4fca2f6b159cb88a39f4df958e21e0e1b6073e1224cd790b066039fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288647/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288647/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30568389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fu, Qiang</creatorcontrib><creatorcontrib>Liu, Chuan-Jiang</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhai, Zhen-Sheng</creatorcontrib><creatorcontrib>Wang, Yu-Zhu</creatorcontrib><creatorcontrib>Hu, Ming-Xing</creatorcontrib><creatorcontrib>Xu, Xian-Ling</creatorcontrib><creatorcontrib>Zhang, Hong-Wei</creatorcontrib><creatorcontrib>Qin, Tao</creatorcontrib><title>Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells</title><title>World journal of gastroenterology : WJG</title><addtitle>World J Gastroenterol</addtitle><description>To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22.
One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) 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 ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3.
After inducing apoptosis of AR42J cells
, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15
18.07 ± 0.89,
= 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells.
GR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway.</description><subject>Acinar Cells - physiology</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Basic Study</subject><subject>Cell Line</subject><subject>Ceruletide - pharmacology</subject><subject>Down-Regulation</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Pancreas - cytology</subject><subject>Rats</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction - genetics</subject><subject>Transcription Initiation Site</subject><subject>Up-Regulation</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUFv1DAQhS0EotvCnRPykUsWe-wk9gWpqqBFqkBCcLYcZ5K6SuxgJ11654fjVUsFpxlp3nsz9kfIG872opXq_eF23N-B3HtZ72sO7BnZAXBdgZLsOdlxxtpKC2hPyGnOt4yBEDW8JCeC1Y0SSu_I78tpc9HFtHoXfU8TOlzWmEozbpNdMVP8tSTM2cdA40Bn71L89uW8AqA29LSPh5DXhHam2Y_BTj6MdLHrzcHeUx-oXWLJyz4fzYsNrkjLLmqdDzZRh9OUX5EXg50yvn6sZ-THp4_fL66q66-Xny_OrysndLNW3IJjyFAOzsLQdLzWrlPKCj3IftC1QuBlzLuGtQI5gHR9q1nHmoYVDYoz8uEhd9m6GXuHYU12Mkvys033Jlpv_p8Ef2PGeGcaUKqRbQl49xiQ4s8N82pmn49PsAHjlg2UkwTUtdRFyh6k5btyTjg8reHMHOGZAs8UeKbAM0d4xfL23_OeDH9piT-r55tJ</recordid><startdate>20181207</startdate><enddate>20181207</enddate><creator>Fu, Qiang</creator><creator>Liu, Chuan-Jiang</creator><creator>Zhang, Xu</creator><creator>Zhai, Zhen-Sheng</creator><creator>Wang, Yu-Zhu</creator><creator>Hu, Ming-Xing</creator><creator>Xu, Xian-Ling</creator><creator>Zhang, Hong-Wei</creator><creator>Qin, Tao</creator><general>Baishideng Publishing Group Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20181207</creationdate><title>Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells</title><author>Fu, Qiang ; Liu, Chuan-Jiang ; Zhang, Xu ; Zhai, Zhen-Sheng ; Wang, Yu-Zhu ; Hu, Ming-Xing ; Xu, Xian-Ling ; Zhang, Hong-Wei ; Qin, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-1a2c0e0e4fca2f6b159cb88a39f4df958e21e0e1b6073e1224cd790b066039fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acinar Cells - physiology</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Basic Study</topic><topic>Cell Line</topic><topic>Ceruletide - pharmacology</topic><topic>Down-Regulation</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Pancreas - cytology</topic><topic>Rats</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>Transcription Initiation Site</topic><topic>Up-Regulation</topic><toplevel>online_resources</toplevel><creatorcontrib>Fu, Qiang</creatorcontrib><creatorcontrib>Liu, Chuan-Jiang</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhai, Zhen-Sheng</creatorcontrib><creatorcontrib>Wang, Yu-Zhu</creatorcontrib><creatorcontrib>Hu, Ming-Xing</creatorcontrib><creatorcontrib>Xu, Xian-Ling</creatorcontrib><creatorcontrib>Zhang, Hong-Wei</creatorcontrib><creatorcontrib>Qin, Tao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of gastroenterology : WJG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fu, Qiang</au><au>Liu, Chuan-Jiang</au><au>Zhang, Xu</au><au>Zhai, Zhen-Sheng</au><au>Wang, Yu-Zhu</au><au>Hu, Ming-Xing</au><au>Xu, Xian-Ling</au><au>Zhang, Hong-Wei</au><au>Qin, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells</atitle><jtitle>World journal of gastroenterology : WJG</jtitle><addtitle>World J Gastroenterol</addtitle><date>2018-12-07</date><risdate>2018</risdate><volume>24</volume><issue>45</issue><spage>5120</spage><epage>5130</epage><pages>5120-5130</pages><issn>1007-9327</issn><eissn>2219-2840</eissn><abstract>To elucidate the underlying mechanism that microRNA-22 (miR-22) promotes the apoptosis of rat pancreatic acinar cells (AR42J) and the elements that regulate the expression of miR-22.
One hundred nanomoles per liter of caerulein (Cae) was administrated to induce the apoptosis of AR42J cells and the apoptosis rate was detected by flow cytometry analysis. An amylase assay kit was used to measure the amylase expression level in the supernatant. Quantitative real-time PCR (qRT-PCR) was adopted to measure miR-22 expression. We used online tools to predict the potential transcription promoter of miR-22 and the binding sites, which was further identified by using luciferase reporter analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR assays. Then, a mimic of miR-22, Nr3c1 plasmid encoding the glucocorticoid receptor (GR), and si-Nr3c1 were used to transfect AR42J cells, respectively. The mRNA expression of miR-22, Nr3c1, and Erb-b2 receptor tyrosine kinase 3 (ErbB3) 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 ErbB3, GR, PI3k, PI3k-p85α, Akt, p-Akt, Bad, Bax, Bcl-xl, Bcl-2, and cleaved caspase3.
After inducing apoptosis of AR42J cells
, the expression of miR-22 was significantly increased by 2.20 ± 0.26 and 4.19 ± 0.54 times, respectively, at 3 h and 6 h in comparison with the control group. As revealed by qRT-PCR assay, the expression of miR-22 was 78.25 ± 6.61 times higher in the miR-22 mimic group relative to the miRNA control group, accompanied with an obviously increased acinar cell apoptosis rate (32.53 ± 1.15
18.07 ± 0.89,
= 0.0006). The upregulation of miR-22 could suppress its target gene, ErbB3, and the phosphorylation of PI3k and Akt. Furthermore, we predicted the potential transcription promoter of miR-22 and the binding sites using online tools. Luciferase reporter analysis and site-directed mutagenesis indicated that the binding site (GACAGCCATGTACA) of the GR, which is encoded by the Nr3c1 gene. Downregulation of the expression of GR could upregulate the expression of miR-22, which further promoted the apoptosis of AR42J cells.
GR transcriptionally represses the expression of miR-22, which further promotes the apoptosis of pancreatic acinar cells by downregulating the downstream signaling pathway.</abstract><cop>United States</cop><pub>Baishideng Publishing Group Inc</pub><pmid>30568389</pmid><doi>10.3748/wjg.v24.i45.5120</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acinar Cells - physiology Animals Apoptosis - drug effects Apoptosis - genetics Basic Study Cell Line Ceruletide - pharmacology Down-Regulation MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism Pancreas - cytology Rats Receptors, Glucocorticoid - genetics Receptors, Glucocorticoid - metabolism RNA, Small Interfering - metabolism Signal Transduction - genetics Transcription Initiation Site Up-Regulation |
title | Glucocorticoid receptor regulates expression of microRNA-22 and downstream signaling pathway in apoptosis of pancreatic acinar cells |
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