SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells
Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent...
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| description | Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major. |
| doi_str_mv | 10.1155/2017/9496058 |
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Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2017/9496058</identifier><identifier>PMID: 29333458</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Anemia ; Anemia, Sickle Cell - blood ; Anemia, Sickle Cell - genetics ; Anemia, Sickle Cell - pathology ; beta-Thalassemia - blood ; beta-Thalassemia - genetics ; beta-Thalassemia - pathology ; Binding sites ; Cell culture ; Cooperation ; Erythroblasts ; Erythroblasts - metabolism ; Erythrocytes ; Erythrocytes - metabolism ; Erythrocytes - pathology ; Erythroid cells ; Erythroid Cells - metabolism ; Erythroid Cells - pathology ; Erythropoiesis ; Fetal Hemoglobin - genetics ; Fetuses ; gamma-Globins - genetics ; Gene expression ; Hematology ; Hemoglobin ; Humans ; Lentivirus - genetics ; Leukocytes (mononuclear) ; Life sciences ; Proteins ; Regulatory sequences ; Ribonucleic acid ; RNA ; RNA-mediated interference ; Sickle cell disease ; SOXD Transcription Factors - antagonists & inhibitors ; SOXD Transcription Factors - genetics ; Thalassemia ; Transcription factors</subject><ispartof>BioMed research international, 2017-01, Vol.2017 (2017), p.1-6</ispartof><rights>Copyright © 2017 Jing Li et al.</rights><rights>Copyright © 2017 Jing Li et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Jing Li et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-2b3397a2854252cf7fe33df32bc5008ece2882bcd237829832a2d8d3751f5a443</citedby><cites>FETCH-LOGICAL-c471t-2b3397a2854252cf7fe33df32bc5008ece2882bcd237829832a2d8d3751f5a443</cites><orcidid>0000-0002-8306-1954 ; 0000-0002-2182-029X ; 0000-0003-1355-4945 ; 0000-0003-4146-5202</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/PMC5733236/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733236/$$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/29333458$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lee, Wen-Hwa</contributor><creatorcontrib>Zhao, Weihua</creatorcontrib><creatorcontrib>Liu, Rongrong</creatorcontrib><creatorcontrib>Luo, Lin</creatorcontrib><creatorcontrib>Luo, Jun</creatorcontrib><creatorcontrib>Lai, Yongrong</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Liu, Zhenfang</creatorcontrib><title>SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major.</description><subject>Anemia</subject><subject>Anemia, Sickle Cell - blood</subject><subject>Anemia, Sickle Cell - genetics</subject><subject>Anemia, Sickle Cell - pathology</subject><subject>beta-Thalassemia - blood</subject><subject>beta-Thalassemia - genetics</subject><subject>beta-Thalassemia - pathology</subject><subject>Binding sites</subject><subject>Cell culture</subject><subject>Cooperation</subject><subject>Erythroblasts</subject><subject>Erythroblasts - metabolism</subject><subject>Erythrocytes</subject><subject>Erythrocytes - metabolism</subject><subject>Erythrocytes - pathology</subject><subject>Erythroid cells</subject><subject>Erythroid Cells - metabolism</subject><subject>Erythroid Cells - pathology</subject><subject>Erythropoiesis</subject><subject>Fetal Hemoglobin - genetics</subject><subject>Fetuses</subject><subject>gamma-Globins - genetics</subject><subject>Gene expression</subject><subject>Hematology</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Lentivirus - genetics</subject><subject>Leukocytes (mononuclear)</subject><subject>Life sciences</subject><subject>Proteins</subject><subject>Regulatory sequences</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA-mediated interference</subject><subject>Sickle cell disease</subject><subject>SOXD Transcription Factors - antagonists & inhibitors</subject><subject>SOXD Transcription Factors - genetics</subject><subject>Thalassemia</subject><subject>Transcription factors</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkdFKHDEUhkOpVLHe9boM9KZgp07OmUySm4KsVgXFCxW8C9mZjJtlJrHJjIuv1b6Hz2Rk17V6ZTiQc8jHz_nzE_KFFj8pZWwPCsr3ZCmrgokPZAuQlnlFS_px3SNukp0Y50U6glaFrD6RTZCIWDKxRS4uzq-r7MAvXDA3Y6cH61124pqxNjF7-JcfdX5qXZbqeOy1yx7-5pcz3ekYTW91dqbnPmSH4X6YBW-bbGK6Ln4mG63uotlZ3dvk6vfh5eQ4Pz0_Opnsn-Z1yemQwxRRcg2ClcCgbnlrEJsWYVqztKupDQiRhgaQC5ACQUMjGuSMtkyXJW6TX0vd23Ham6Y2bgi6U7fB9jrcK6-tev3i7Ezd-DvFOCJglQS-rwSC_zOaOKjexjpZ0M74MSoqhWQS0icn9NsbdO7H4JK9RPGqgAI4JOrHkqqDjzGYdr0MLdRTYOopMLUKLOFf_zewhp_jScDuEphZ1-iFfaecSYxp9QtNUbKK4SP0Xqc3</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Zhao, Weihua</creator><creator>Liu, Rongrong</creator><creator>Luo, Lin</creator><creator>Luo, Jun</creator><creator>Lai, Yongrong</creator><creator>Li, Jing</creator><creator>Liu, Zhenfang</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><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/0000-0002-8306-1954</orcidid><orcidid>https://orcid.org/0000-0002-2182-029X</orcidid><orcidid>https://orcid.org/0000-0003-1355-4945</orcidid><orcidid>https://orcid.org/0000-0003-4146-5202</orcidid></search><sort><creationdate>20170101</creationdate><title>SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells</title><author>Zhao, Weihua ; Liu, Rongrong ; Luo, Lin ; Luo, Jun ; Lai, Yongrong ; Li, Jing ; Liu, Zhenfang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-2b3397a2854252cf7fe33df32bc5008ece2882bcd237829832a2d8d3751f5a443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Anemia</topic><topic>Anemia, Sickle Cell - blood</topic><topic>Anemia, Sickle Cell - genetics</topic><topic>Anemia, Sickle Cell - pathology</topic><topic>beta-Thalassemia - blood</topic><topic>beta-Thalassemia - genetics</topic><topic>beta-Thalassemia - pathology</topic><topic>Binding sites</topic><topic>Cell culture</topic><topic>Cooperation</topic><topic>Erythroblasts</topic><topic>Erythroblasts - metabolism</topic><topic>Erythrocytes</topic><topic>Erythrocytes - metabolism</topic><topic>Erythrocytes - pathology</topic><topic>Erythroid cells</topic><topic>Erythroid Cells - metabolism</topic><topic>Erythroid Cells - pathology</topic><topic>Erythropoiesis</topic><topic>Fetal Hemoglobin - genetics</topic><topic>Fetuses</topic><topic>gamma-Globins - genetics</topic><topic>Gene expression</topic><topic>Hematology</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Lentivirus - genetics</topic><topic>Leukocytes (mononuclear)</topic><topic>Life sciences</topic><topic>Proteins</topic><topic>Regulatory sequences</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA-mediated interference</topic><topic>Sickle cell disease</topic><topic>SOXD Transcription Factors - antagonists & inhibitors</topic><topic>SOXD Transcription Factors - genetics</topic><topic>Thalassemia</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Weihua</creatorcontrib><creatorcontrib>Liu, Rongrong</creatorcontrib><creatorcontrib>Luo, Lin</creatorcontrib><creatorcontrib>Luo, Jun</creatorcontrib><creatorcontrib>Lai, Yongrong</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Liu, Zhenfang</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</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>Access via ProQuest (Open Access)</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>Zhao, Weihua</au><au>Liu, Rongrong</au><au>Luo, Lin</au><au>Luo, Jun</au><au>Lai, Yongrong</au><au>Li, Jing</au><au>Liu, Zhenfang</au><au>Lee, Wen-Hwa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>6</epage><pages>1-6</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29333458</pmid><doi>10.1155/2017/9496058</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-8306-1954</orcidid><orcidid>https://orcid.org/0000-0002-2182-029X</orcidid><orcidid>https://orcid.org/0000-0003-1355-4945</orcidid><orcidid>https://orcid.org/0000-0003-4146-5202</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Anemia Anemia, Sickle Cell - blood Anemia, Sickle Cell - genetics Anemia, Sickle Cell - pathology beta-Thalassemia - blood beta-Thalassemia - genetics beta-Thalassemia - pathology Binding sites Cell culture Cooperation Erythroblasts Erythroblasts - metabolism Erythrocytes Erythrocytes - metabolism Erythrocytes - pathology Erythroid cells Erythroid Cells - metabolism Erythroid Cells - pathology Erythropoiesis Fetal Hemoglobin - genetics Fetuses gamma-Globins - genetics Gene expression Hematology Hemoglobin Humans Lentivirus - genetics Leukocytes (mononuclear) Life sciences Proteins Regulatory sequences Ribonucleic acid RNA RNA-mediated interference Sickle cell disease SOXD Transcription Factors - antagonists & inhibitors SOXD Transcription Factors - genetics Thalassemia Transcription factors |
| title | SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells |
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