Neutrophil Extracellular Traps Are Increased in Chronic Myeloid Leukemia and Are Differentially Affected by Tyrosine Kinase Inhibitors
Cardiovascular complications are increasingly reported with the use of certain tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML). We studied neutrophil extracellular trap (NET) formation in CML and evaluated the effect of TKIs on NET formation. Neutrophils isolated from treat...
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| Veröffentlicht in: | Cancers 2021-12, Vol.14 (1), p.119 |
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| creator | Telerman, Alona Granot, Galit Leibovitch, Chiya Yarchovsky-Dolberg, Osnat Shacham-Abulafia, Adi Partouche, Shirly Yeshurun, Moshe Ellis, Martin H Raanani, Pia Wolach, Ofir |
| description | Cardiovascular complications are increasingly reported with the use of certain tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML). We studied neutrophil extracellular trap (NET) formation in CML and evaluated the effect of TKIs on NET formation. Neutrophils isolated from treatment-naïve patients with CML showed a significant increase in NET formation compared to matched controls at baseline and after stimulation with ionomycin (IO) and phorbol 12-myristate 13-acetate (PMA). Expression of citrullinated histone H3 (H3cit), peptidyl arginine deiminase 4 (PAD4) and reactive oxygen species (ROS) was significantly higher in CML samples compared to controls. Pre-treatment of neutrophils with TKIs was associated with a differential effect on NET formation, and ponatinib significantly augmented NET-associated elastase and ROS levels as compared to controls and other TKIs.
retroviral transduced
-immortalized mouse hematopoietic progenitors, which differentiate into neutrophils in-vitro, demonstrated increased H3cit & myeloperoxidase (MPO) expression consistent with excess NET formation. This was inhibited by Cl-amidine, a PAD4 inhibitor, but not by the NADPH inhibitor diphenyleneiodonium (
). Ponatinib pre-exposure significantly increased H3cit expression in
cells after stimulation with IO. In summary, CML is associated with increased NET formation, which is augmented by ponatinib, suggesting a possible role for NETs in promoting vascular toxicity in CML. |
| doi_str_mv | 10.3390/cancers14010119 |
| format | Article |
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retroviral transduced
-immortalized mouse hematopoietic progenitors, which differentiate into neutrophils in-vitro, demonstrated increased H3cit & myeloperoxidase (MPO) expression consistent with excess NET formation. This was inhibited by Cl-amidine, a PAD4 inhibitor, but not by the NADPH inhibitor diphenyleneiodonium (
). Ponatinib pre-exposure significantly increased H3cit expression in
cells after stimulation with IO. In summary, CML is associated with increased NET formation, which is augmented by ponatinib, suggesting a possible role for NETs in promoting vascular toxicity in CML.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers14010119</identifier><identifier>PMID: 35008283</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acetic acid ; Arginine deiminase ; Chronic myeloid leukemia ; Citrulline ; Elastase ; Estrogens ; Gender ; Hemopoiesis ; Histone H3 ; Histones ; Ionomycin ; Leukemia ; Leukocytes (neutrophilic) ; Microscopy ; Morphology ; Myeloid leukemia ; Neutrophils ; Patients ; Peroxidase ; Phorbol 12-myristate 13-acetate ; Progenitor cells ; Protein-arginine deiminase ; Reactive oxygen species ; Thrombosis ; Toxicity ; Tyrosine kinase inhibitors</subject><ispartof>Cancers, 2021-12, Vol.14 (1), p.119</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-e9b88e61ab6617e433bc7e4f3db5f53a2e8e3c9e12b5b703e784078736d4f7533</citedby><cites>FETCH-LOGICAL-c421t-e9b88e61ab6617e433bc7e4f3db5f53a2e8e3c9e12b5b703e784078736d4f7533</cites><orcidid>0000-0002-8662-0707 ; 0000-0001-9973-639X</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/PMC8750902/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750902/$$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/35008283$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Telerman, Alona</creatorcontrib><creatorcontrib>Granot, Galit</creatorcontrib><creatorcontrib>Leibovitch, Chiya</creatorcontrib><creatorcontrib>Yarchovsky-Dolberg, Osnat</creatorcontrib><creatorcontrib>Shacham-Abulafia, Adi</creatorcontrib><creatorcontrib>Partouche, Shirly</creatorcontrib><creatorcontrib>Yeshurun, Moshe</creatorcontrib><creatorcontrib>Ellis, Martin H</creatorcontrib><creatorcontrib>Raanani, Pia</creatorcontrib><creatorcontrib>Wolach, Ofir</creatorcontrib><title>Neutrophil Extracellular Traps Are Increased in Chronic Myeloid Leukemia and Are Differentially Affected by Tyrosine Kinase Inhibitors</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Cardiovascular complications are increasingly reported with the use of certain tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML). We studied neutrophil extracellular trap (NET) formation in CML and evaluated the effect of TKIs on NET formation. Neutrophils isolated from treatment-naïve patients with CML showed a significant increase in NET formation compared to matched controls at baseline and after stimulation with ionomycin (IO) and phorbol 12-myristate 13-acetate (PMA). Expression of citrullinated histone H3 (H3cit), peptidyl arginine deiminase 4 (PAD4) and reactive oxygen species (ROS) was significantly higher in CML samples compared to controls. Pre-treatment of neutrophils with TKIs was associated with a differential effect on NET formation, and ponatinib significantly augmented NET-associated elastase and ROS levels as compared to controls and other TKIs.
retroviral transduced
-immortalized mouse hematopoietic progenitors, which differentiate into neutrophils in-vitro, demonstrated increased H3cit & myeloperoxidase (MPO) expression consistent with excess NET formation. This was inhibited by Cl-amidine, a PAD4 inhibitor, but not by the NADPH inhibitor diphenyleneiodonium (
). Ponatinib pre-exposure significantly increased H3cit expression in
cells after stimulation with IO. In summary, CML is associated with increased NET formation, which is augmented by ponatinib, suggesting a possible role for NETs in promoting vascular toxicity in CML.</description><subject>Acetic acid</subject><subject>Arginine deiminase</subject><subject>Chronic myeloid leukemia</subject><subject>Citrulline</subject><subject>Elastase</subject><subject>Estrogens</subject><subject>Gender</subject><subject>Hemopoiesis</subject><subject>Histone H3</subject><subject>Histones</subject><subject>Ionomycin</subject><subject>Leukemia</subject><subject>Leukocytes (neutrophilic)</subject><subject>Microscopy</subject><subject>Morphology</subject><subject>Myeloid leukemia</subject><subject>Neutrophils</subject><subject>Patients</subject><subject>Peroxidase</subject><subject>Phorbol 12-myristate 13-acetate</subject><subject>Progenitor cells</subject><subject>Protein-arginine deiminase</subject><subject>Reactive oxygen species</subject><subject>Thrombosis</subject><subject>Toxicity</subject><subject>Tyrosine kinase inhibitors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkctuEzEUhi1E1VZp190hS2zYhPoyY3s2SFFaSkWATVhbHs8Z4uLYwZ5BzAvw3HXSUpV6c2z5O_-5_AhdUPKe84ZcWhMspEwrQgmlzSt0yohkcyGa6vWz-wk6z_mOlMM5lUIeoxNeE6KY4qfo71cYhxR3G-fx9Z8hGQvej94kvE5ml_EiAb4NNoHJ0GEX8HKTYnAWf5nAR9fhFYw_YesMNqE70Feu7yFBGJzxfsKL8rJDyW0nvJ5SzC4A_uxC0SvCG9e6IaZ8ho564zOcP8YZ-v7xer38NF99u7ldLlZzWzE6zKFplQJBTSsElVBx3toSet61dV9zw0ABtw1Q1tatJBykqohUkouu6mXN-Qx9eNDdje0WOlvaTMbrXXJbkyYdjdP__wS30T_ib61kTRrCisC7R4EUf42QB711eb8zEyCOWTNBVUMadqj19gV6F8cUyngHihGxt2SGLh8oW3aTE_RPzVCi9zbrFzaXjDfPZ3ji_5nK7wH-ZqaR</recordid><startdate>20211227</startdate><enddate>20211227</enddate><creator>Telerman, Alona</creator><creator>Granot, Galit</creator><creator>Leibovitch, Chiya</creator><creator>Yarchovsky-Dolberg, Osnat</creator><creator>Shacham-Abulafia, Adi</creator><creator>Partouche, Shirly</creator><creator>Yeshurun, Moshe</creator><creator>Ellis, Martin H</creator><creator>Raanani, Pia</creator><creator>Wolach, Ofir</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8662-0707</orcidid><orcidid>https://orcid.org/0000-0001-9973-639X</orcidid></search><sort><creationdate>20211227</creationdate><title>Neutrophil Extracellular Traps Are Increased in Chronic Myeloid Leukemia and Are Differentially Affected by Tyrosine Kinase Inhibitors</title><author>Telerman, Alona ; Granot, Galit ; Leibovitch, Chiya ; Yarchovsky-Dolberg, Osnat ; Shacham-Abulafia, Adi ; Partouche, Shirly ; Yeshurun, Moshe ; Ellis, Martin H ; Raanani, Pia ; Wolach, Ofir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-e9b88e61ab6617e433bc7e4f3db5f53a2e8e3c9e12b5b703e784078736d4f7533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acetic acid</topic><topic>Arginine deiminase</topic><topic>Chronic myeloid leukemia</topic><topic>Citrulline</topic><topic>Elastase</topic><topic>Estrogens</topic><topic>Gender</topic><topic>Hemopoiesis</topic><topic>Histone H3</topic><topic>Histones</topic><topic>Ionomycin</topic><topic>Leukemia</topic><topic>Leukocytes (neutrophilic)</topic><topic>Microscopy</topic><topic>Morphology</topic><topic>Myeloid leukemia</topic><topic>Neutrophils</topic><topic>Patients</topic><topic>Peroxidase</topic><topic>Phorbol 12-myristate 13-acetate</topic><topic>Progenitor cells</topic><topic>Protein-arginine deiminase</topic><topic>Reactive oxygen species</topic><topic>Thrombosis</topic><topic>Toxicity</topic><topic>Tyrosine kinase inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Telerman, Alona</creatorcontrib><creatorcontrib>Granot, Galit</creatorcontrib><creatorcontrib>Leibovitch, Chiya</creatorcontrib><creatorcontrib>Yarchovsky-Dolberg, Osnat</creatorcontrib><creatorcontrib>Shacham-Abulafia, Adi</creatorcontrib><creatorcontrib>Partouche, Shirly</creatorcontrib><creatorcontrib>Yeshurun, Moshe</creatorcontrib><creatorcontrib>Ellis, Martin H</creatorcontrib><creatorcontrib>Raanani, Pia</creatorcontrib><creatorcontrib>Wolach, Ofir</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Telerman, Alona</au><au>Granot, Galit</au><au>Leibovitch, Chiya</au><au>Yarchovsky-Dolberg, Osnat</au><au>Shacham-Abulafia, Adi</au><au>Partouche, Shirly</au><au>Yeshurun, Moshe</au><au>Ellis, Martin H</au><au>Raanani, Pia</au><au>Wolach, Ofir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophil Extracellular Traps Are Increased in Chronic Myeloid Leukemia and Are Differentially Affected by Tyrosine Kinase Inhibitors</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2021-12-27</date><risdate>2021</risdate><volume>14</volume><issue>1</issue><spage>119</spage><pages>119-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Cardiovascular complications are increasingly reported with the use of certain tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML). We studied neutrophil extracellular trap (NET) formation in CML and evaluated the effect of TKIs on NET formation. Neutrophils isolated from treatment-naïve patients with CML showed a significant increase in NET formation compared to matched controls at baseline and after stimulation with ionomycin (IO) and phorbol 12-myristate 13-acetate (PMA). Expression of citrullinated histone H3 (H3cit), peptidyl arginine deiminase 4 (PAD4) and reactive oxygen species (ROS) was significantly higher in CML samples compared to controls. Pre-treatment of neutrophils with TKIs was associated with a differential effect on NET formation, and ponatinib significantly augmented NET-associated elastase and ROS levels as compared to controls and other TKIs.
retroviral transduced
-immortalized mouse hematopoietic progenitors, which differentiate into neutrophils in-vitro, demonstrated increased H3cit & myeloperoxidase (MPO) expression consistent with excess NET formation. This was inhibited by Cl-amidine, a PAD4 inhibitor, but not by the NADPH inhibitor diphenyleneiodonium (
). Ponatinib pre-exposure significantly increased H3cit expression in
cells after stimulation with IO. In summary, CML is associated with increased NET formation, which is augmented by ponatinib, suggesting a possible role for NETs in promoting vascular toxicity in CML.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35008283</pmid><doi>10.3390/cancers14010119</doi><orcidid>https://orcid.org/0000-0002-8662-0707</orcidid><orcidid>https://orcid.org/0000-0001-9973-639X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acetic acid Arginine deiminase Chronic myeloid leukemia Citrulline Elastase Estrogens Gender Hemopoiesis Histone H3 Histones Ionomycin Leukemia Leukocytes (neutrophilic) Microscopy Morphology Myeloid leukemia Neutrophils Patients Peroxidase Phorbol 12-myristate 13-acetate Progenitor cells Protein-arginine deiminase Reactive oxygen species Thrombosis Toxicity Tyrosine kinase inhibitors |
| title | Neutrophil Extracellular Traps Are Increased in Chronic Myeloid Leukemia and Are Differentially Affected by Tyrosine Kinase Inhibitors |
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