Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis
Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PD...
Gespeichert in:
| Veröffentlicht in: | BioMed research international 2021, Vol.2021 (1), p.8899863-8899863 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 8899863 |
|---|---|
| container_issue | 1 |
| container_start_page | 8899863 |
| container_title | BioMed research international |
| container_volume | 2021 |
| creator | Chen, Qinchao Cao, Meng Ge, Hanyi |
| description | Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment. |
| doi_str_mv | 10.1155/2021/8899863 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7870306</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A683531067</galeid><sourcerecordid>A683531067</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-ab6b17722e8c72967621ee69433703de9fc6bafcfa2c6aa16775b8e3074dbdc33</originalsourceid><addsrcrecordid>eNqFks1v0zAchi0EYtPYjTOyxAUJQv2R-OOCFFWMVRQxoXK2HMdJPFK7s9ON_fdzaSkfB_DFlvzo-em1XwCeY_QW46qaEUTwTAgpBaOPwCmhuCwYLvHj45nSE3Ce0jXKS2CGJHsKTihlqKRCnAL30QfzrQ13HoYOfqqX9QrDhR9c46YEp8HCqxj6aFNy4QcyH2LwzsArG11og5_c5BK8dRqudOzt5HwP1-5LwZksqs3scnFBa1h_d-kZeNLpMdnzw34Gvl68X80vi-XnD4t5vSxMhcqp0A1rMOeEWGE4kYwzgq1lsqSUI9pa2RnW6M50mhimNWacV42wFPGybVpD6Rl4t_duts3atsb6KepRbaJb63ivgnbqzxvvBtWHW8VFHoBYFrw6CGK42do0qbVLxo6j9jZskyKlxLLEFREZffkXeh220ed4mRIyf5Eg8hfV69Eq57uQ55qdVNVMMlnllP-hBK0oRoxn6s2eMjGkFG13DIaR2lVC7SqhDpXI-IvfH-MI_yxABl7vgcH5Vt-5f-seALXNuk4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2489115829</pqid></control><display><type>article</type><title>Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Chen, Qinchao ; Cao, Meng ; Ge, Hanyi</creator><contributor>Xu, Yanming</contributor><creatorcontrib>Chen, Qinchao ; Cao, Meng ; Ge, Hanyi ; Xu, Yanming</creatorcontrib><description>Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2021/8899863</identifier><identifier>PMID: 33604388</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Adenocarcinoma ; Adult ; Analysis ; Apoptosis ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Arthritis ; Assaying ; BAX protein ; Bcl-2 protein ; Binding sites ; Care and treatment ; Caspase-3 ; Cell Survival - genetics ; Cell viability ; Cells, Cultured ; Chronic Periodontitis - genetics ; Chronic Periodontitis - metabolism ; Chronic Periodontitis - pathology ; Cytokines ; Development and progression ; Disease ; Enzyme-linked immunosorbent assay ; Female ; Gene amplification ; Gene expression ; Gene Knockdown Techniques ; Genetic regulation ; Gingiva - chemistry ; Gingiva - metabolism ; Gum disease ; Humans ; Hypoxia ; Hypoxia-inducible factors ; Inflammation - genetics ; Inflammatory diseases ; Ligaments ; Lipopolysaccharides ; Lung cancer ; Male ; Medical research ; Medicine, Experimental ; Metastases ; Methods ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Patient outcomes ; Periodontal ligament ; Periodontal Ligament - cytology ; Periodontitis ; Polymerase chain reaction ; Regulatory mechanisms (biology) ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Software ; Transcription ; Tumor necrosis factor-TNF</subject><ispartof>BioMed research international, 2021, Vol.2021 (1), p.8899863-8899863</ispartof><rights>Copyright © 2021 Qinchao Chen et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Qinchao Chen et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Qinchao Chen et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-ab6b17722e8c72967621ee69433703de9fc6bafcfa2c6aa16775b8e3074dbdc33</citedby><cites>FETCH-LOGICAL-c504t-ab6b17722e8c72967621ee69433703de9fc6bafcfa2c6aa16775b8e3074dbdc33</cites><orcidid>0000-0002-1173-3387</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7870306/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7870306/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33604388$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Xu, Yanming</contributor><creatorcontrib>Chen, Qinchao</creatorcontrib><creatorcontrib>Cao, Meng</creatorcontrib><creatorcontrib>Ge, Hanyi</creatorcontrib><title>Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.</description><subject>Adenocarcinoma</subject><subject>Adult</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Arthritis</subject><subject>Assaying</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Binding sites</subject><subject>Care and treatment</subject><subject>Caspase-3</subject><subject>Cell Survival - genetics</subject><subject>Cell viability</subject><subject>Cells, Cultured</subject><subject>Chronic Periodontitis - genetics</subject><subject>Chronic Periodontitis - metabolism</subject><subject>Chronic Periodontitis - pathology</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Gene amplification</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Genetic regulation</subject><subject>Gingiva - chemistry</subject><subject>Gingiva - metabolism</subject><subject>Gum disease</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factors</subject><subject>Inflammation - genetics</subject><subject>Inflammatory diseases</subject><subject>Ligaments</subject><subject>Lipopolysaccharides</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Metastases</subject><subject>Methods</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Patient outcomes</subject><subject>Periodontal ligament</subject><subject>Periodontal Ligament - cytology</subject><subject>Periodontitis</subject><subject>Polymerase chain reaction</subject><subject>Regulatory mechanisms (biology)</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Software</subject><subject>Transcription</subject><subject>Tumor necrosis factor-TNF</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFks1v0zAchi0EYtPYjTOyxAUJQv2R-OOCFFWMVRQxoXK2HMdJPFK7s9ON_fdzaSkfB_DFlvzo-em1XwCeY_QW46qaEUTwTAgpBaOPwCmhuCwYLvHj45nSE3Ce0jXKS2CGJHsKTihlqKRCnAL30QfzrQ13HoYOfqqX9QrDhR9c46YEp8HCqxj6aFNy4QcyH2LwzsArG11og5_c5BK8dRqudOzt5HwP1-5LwZksqs3scnFBa1h_d-kZeNLpMdnzw34Gvl68X80vi-XnD4t5vSxMhcqp0A1rMOeEWGE4kYwzgq1lsqSUI9pa2RnW6M50mhimNWacV42wFPGybVpD6Rl4t_duts3atsb6KepRbaJb63ivgnbqzxvvBtWHW8VFHoBYFrw6CGK42do0qbVLxo6j9jZskyKlxLLEFREZffkXeh220ed4mRIyf5Eg8hfV69Eq57uQ55qdVNVMMlnllP-hBK0oRoxn6s2eMjGkFG13DIaR2lVC7SqhDpXI-IvfH-MI_yxABl7vgcH5Vt-5f-seALXNuk4</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Chen, Qinchao</creator><creator>Cao, Meng</creator><creator>Ge, Hanyi</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1173-3387</orcidid></search><sort><creationdate>2021</creationdate><title>Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis</title><author>Chen, Qinchao ; Cao, Meng ; Ge, Hanyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-ab6b17722e8c72967621ee69433703de9fc6bafcfa2c6aa16775b8e3074dbdc33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenocarcinoma</topic><topic>Adult</topic><topic>Analysis</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Arthritis</topic><topic>Assaying</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Binding sites</topic><topic>Care and treatment</topic><topic>Caspase-3</topic><topic>Cell Survival - genetics</topic><topic>Cell viability</topic><topic>Cells, Cultured</topic><topic>Chronic Periodontitis - genetics</topic><topic>Chronic Periodontitis - metabolism</topic><topic>Chronic Periodontitis - pathology</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Disease</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Gene amplification</topic><topic>Gene expression</topic><topic>Gene Knockdown Techniques</topic><topic>Genetic regulation</topic><topic>Gingiva - chemistry</topic><topic>Gingiva - metabolism</topic><topic>Gum disease</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factors</topic><topic>Inflammation - genetics</topic><topic>Inflammatory diseases</topic><topic>Ligaments</topic><topic>Lipopolysaccharides</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Metastases</topic><topic>Methods</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Patient outcomes</topic><topic>Periodontal ligament</topic><topic>Periodontal Ligament - cytology</topic><topic>Periodontitis</topic><topic>Polymerase chain reaction</topic><topic>Regulatory mechanisms (biology)</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Software</topic><topic>Transcription</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Qinchao</creatorcontrib><creatorcontrib>Cao, Meng</creatorcontrib><creatorcontrib>Ge, Hanyi</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Qinchao</au><au>Cao, Meng</au><au>Ge, Hanyi</au><au>Xu, Yanming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><issue>1</issue><spage>8899863</spage><epage>8899863</epage><pages>8899863-8899863</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>33604388</pmid><doi>10.1155/2021/8899863</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-1173-3387</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2314-6133 |
| ispartof | BioMed research international, 2021, Vol.2021 (1), p.8899863-8899863 |
| issn | 2314-6133 2314-6141 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7870306 |
| source | MEDLINE; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Adenocarcinoma Adult Analysis Apoptosis Apoptosis - genetics Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Arthritis Assaying BAX protein Bcl-2 protein Binding sites Care and treatment Caspase-3 Cell Survival - genetics Cell viability Cells, Cultured Chronic Periodontitis - genetics Chronic Periodontitis - metabolism Chronic Periodontitis - pathology Cytokines Development and progression Disease Enzyme-linked immunosorbent assay Female Gene amplification Gene expression Gene Knockdown Techniques Genetic regulation Gingiva - chemistry Gingiva - metabolism Gum disease Humans Hypoxia Hypoxia-inducible factors Inflammation - genetics Inflammatory diseases Ligaments Lipopolysaccharides Lung cancer Male Medical research Medicine, Experimental Metastases Methods MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Middle Aged Patient outcomes Periodontal ligament Periodontal Ligament - cytology Periodontitis Polymerase chain reaction Regulatory mechanisms (biology) Repressor Proteins - genetics Repressor Proteins - metabolism RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Software Transcription Tumor necrosis factor-TNF |
| title | Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T01%3A43%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Knockdown%20of%20MALAT1%20Inhibits%20the%20Progression%20of%20Chronic%20Periodontitis%20via%20Targeting%20miR-769-5p/HIF3A%20Axis&rft.jtitle=BioMed%20research%20international&rft.au=Chen,%20Qinchao&rft.date=2021&rft.volume=2021&rft.issue=1&rft.spage=8899863&rft.epage=8899863&rft.pages=8899863-8899863&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2021/8899863&rft_dat=%3Cgale_pubme%3EA683531067%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2489115829&rft_id=info:pmid/33604388&rft_galeid=A683531067&rfr_iscdi=true |