CD41+/CD45+ Cells Without Acetylcholinesterase Activity Are Immature and a Major Megakaryocytic Population in Murine Bone Marrow
Murine megakaryocytes (MKs) are defined by CD41/CD61 expression and acetylcholinesterase (AChE) activity; however, their stages of differentiation in bone marrow (BM) have not been fully elucidated. In murine lineage‐negative (Lin−)/CD45+ BM cells, we found CD41+ MKs without AChE activity (AChE−) ex...
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description | Murine megakaryocytes (MKs) are defined by CD41/CD61 expression and acetylcholinesterase (AChE) activity; however, their stages of differentiation in bone marrow (BM) have not been fully elucidated. In murine lineage‐negative (Lin−)/CD45+ BM cells, we found CD41+ MKs without AChE activity (AChE−) except for CD41++ MKs with AChE activity (AChE+), in which CD61 expression was similar to their CD41 level. Lin−/CD41+/CD45+/AChE− MKs could differentiate into AChE+, with an accompanying increase in CD41/CD61 during in vitro culture. Both proplatelet formation (PPF) and platelet (PLT) production for Lin−/CD41+/CD45+/AChE− MKs were observed later than for Lin−/CD41++/CD45+/AChE+ MKs, whereas MK progenitors were scarcely detected in both subpopulations. GeneChip and semiquantitative polymerase chain reaction analyses revealed that the Lin−/CD41+/CD45+/AChE− MKs are assigned at the stage between the progenitor and PPF preparation phases in respect to the many MK/PLT‐specific gene expressions, including β1‐tubulin. In normal mice, the number of Lin−/CD41+/CD45+/AChE− MKs was 100 times higher than that of AChE+ MKs in BM. When MK destruction and consequent thrombocytopenia were caused by an antitumor agent, mitomycin‐C, Lin−/CD41+/CD45+/AChE− MKs led to an increase in AChE+ MKs and subsequent PLT recovery with interleukin‐11 administration. It was concluded that MKs in murine BM at least in part consist of immature Lin−/CD41+/CD45+/AChE− MKs and more differentiated Lin−/CD41++/CD45+/AChE+ MKs. Immature Lin−/CD41+/CD45+/AChE− MKs are a major MK population compared with AChE+ MKs in BM and play an important role in rapid PLT recovery in vivo.
Disclosure of potential conflicts of interest is found at the end of this article. |
doi_str_mv | 10.1634/stemcells.2006-0363 |
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Disclosure of potential conflicts of interest is found at the end of this article.</description><identifier>ISSN: 1066-5099</identifier><identifier>EISSN: 1549-4918</identifier><identifier>DOI: 10.1634/stemcells.2006-0363</identifier><identifier>PMID: 17420226</identifier><language>eng</language><publisher>Bristol: John Wiley & Sons, Ltd</publisher><subject>Acetylcholinesterase - analysis ; Animals ; Biomarkers - analysis ; Bone marrow ; Bone Marrow Cells - cytology ; Bone Marrow Cells - immunology ; Cell Culture Techniques ; Colony-Forming Units Assay ; Gene Expression Profiling ; Leukocyte Common Antigens - genetics ; Male ; Megakaryocytes ; Megakaryocytes - cytology ; Megakaryocytes - immunology ; Mice ; Mice, Inbred BALB C ; Microarray ; Mouse ; Platelet Membrane Glycoprotein IIb - genetics ; Polymerase Chain Reaction ; Thrombopoiesis</subject><ispartof>Stem cells (Dayton, Ohio), 2007-04, Vol.25 (4), p.862-870</ispartof><rights>Copyright © 2007 AlphaMed Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3962-4fcc05bf022bbc7ae41afe93f639ad4f807c74a015e6edb58d652fdc100fa9503</citedby><cites>FETCH-LOGICAL-c3962-4fcc05bf022bbc7ae41afe93f639ad4f807c74a015e6edb58d652fdc100fa9503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17420226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsumura‐Takeda, Kuniko</creatorcontrib><creatorcontrib>Sogo, Shinji</creatorcontrib><creatorcontrib>Isakari, Yoshimasa</creatorcontrib><creatorcontrib>Harada, Yasuo</creatorcontrib><creatorcontrib>Nishioka, Kinue</creatorcontrib><creatorcontrib>Kawakami, Takuma</creatorcontrib><creatorcontrib>Ono, Toshihide</creatorcontrib><creatorcontrib>Taki, Takao</creatorcontrib><title>CD41+/CD45+ Cells Without Acetylcholinesterase Activity Are Immature and a Major Megakaryocytic Population in Murine Bone Marrow</title><title>Stem cells (Dayton, Ohio)</title><addtitle>Stem Cells</addtitle><description>Murine megakaryocytes (MKs) are defined by CD41/CD61 expression and acetylcholinesterase (AChE) activity; however, their stages of differentiation in bone marrow (BM) have not been fully elucidated. In murine lineage‐negative (Lin−)/CD45+ BM cells, we found CD41+ MKs without AChE activity (AChE−) except for CD41++ MKs with AChE activity (AChE+), in which CD61 expression was similar to their CD41 level. Lin−/CD41+/CD45+/AChE− MKs could differentiate into AChE+, with an accompanying increase in CD41/CD61 during in vitro culture. Both proplatelet formation (PPF) and platelet (PLT) production for Lin−/CD41+/CD45+/AChE− MKs were observed later than for Lin−/CD41++/CD45+/AChE+ MKs, whereas MK progenitors were scarcely detected in both subpopulations. GeneChip and semiquantitative polymerase chain reaction analyses revealed that the Lin−/CD41+/CD45+/AChE− MKs are assigned at the stage between the progenitor and PPF preparation phases in respect to the many MK/PLT‐specific gene expressions, including β1‐tubulin. In normal mice, the number of Lin−/CD41+/CD45+/AChE− MKs was 100 times higher than that of AChE+ MKs in BM. When MK destruction and consequent thrombocytopenia were caused by an antitumor agent, mitomycin‐C, Lin−/CD41+/CD45+/AChE− MKs led to an increase in AChE+ MKs and subsequent PLT recovery with interleukin‐11 administration. It was concluded that MKs in murine BM at least in part consist of immature Lin−/CD41+/CD45+/AChE− MKs and more differentiated Lin−/CD41++/CD45+/AChE+ MKs. Immature Lin−/CD41+/CD45+/AChE− MKs are a major MK population compared with AChE+ MKs in BM and play an important role in rapid PLT recovery in vivo.
Disclosure of potential conflicts of interest is found at the end of this article.</description><subject>Acetylcholinesterase - analysis</subject><subject>Animals</subject><subject>Biomarkers - analysis</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - immunology</subject><subject>Cell Culture Techniques</subject><subject>Colony-Forming Units Assay</subject><subject>Gene Expression Profiling</subject><subject>Leukocyte Common Antigens - genetics</subject><subject>Male</subject><subject>Megakaryocytes</subject><subject>Megakaryocytes - cytology</subject><subject>Megakaryocytes - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microarray</subject><subject>Mouse</subject><subject>Platelet Membrane Glycoprotein IIb - genetics</subject><subject>Polymerase Chain Reaction</subject><subject>Thrombopoiesis</subject><issn>1066-5099</issn><issn>1549-4918</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1v1DAQhi0EoqXwC5CQT1yqtOP4I4k4LdsClRqBRBFHy3Fs6pLEi-20yq0_HUe7gmsv45H1zmPPg9BbAmdEUHYekxm1GYZ4VgKIAqigz9Ax4awpWEPq57kHIQoOTXOEXsV4B0AYr-uX6IhUrISyFMfocXvByOl5rvwUb1ca_unSrZ8T3miTlkHf-sFNJj8WVDT5Mrl7lxa8CQZfjaNKc27U1GOFW3XnA27NL_VbhcXrJTmNv_ndPKjk_ITdhNs5ZBj-6HNpVQj-4TV6YdUQzZvDeYJ-fLq82X4prr9-vtpurgtNG1EWzGoNvLP5112nK2UYUdY01AraqJ7ZGipdMQWEG2H6jte94KXtNQGwquFAT9D7PXcX_J857yNHF1d9ajJ-jrICWlVCNDlI90EdfIzBWLkLbswLSQJyFS__iZereLmKz1PvDvi5G03_f-ZgOgc-7AMPbjDLU5jy-81lW3KoRUn_AkctlW0</recordid><startdate>200704</startdate><enddate>200704</enddate><creator>Matsumura‐Takeda, Kuniko</creator><creator>Sogo, Shinji</creator><creator>Isakari, Yoshimasa</creator><creator>Harada, Yasuo</creator><creator>Nishioka, Kinue</creator><creator>Kawakami, Takuma</creator><creator>Ono, Toshihide</creator><creator>Taki, Takao</creator><general>John Wiley & Sons, Ltd</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></search><sort><creationdate>200704</creationdate><title>CD41+/CD45+ Cells Without Acetylcholinesterase Activity Are Immature and a Major Megakaryocytic Population in Murine Bone Marrow</title><author>Matsumura‐Takeda, Kuniko ; Sogo, Shinji ; Isakari, Yoshimasa ; Harada, Yasuo ; Nishioka, Kinue ; Kawakami, Takuma ; Ono, Toshihide ; Taki, Takao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3962-4fcc05bf022bbc7ae41afe93f639ad4f807c74a015e6edb58d652fdc100fa9503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acetylcholinesterase - analysis</topic><topic>Animals</topic><topic>Biomarkers - analysis</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone Marrow Cells - immunology</topic><topic>Cell Culture Techniques</topic><topic>Colony-Forming Units Assay</topic><topic>Gene Expression Profiling</topic><topic>Leukocyte Common Antigens - genetics</topic><topic>Male</topic><topic>Megakaryocytes</topic><topic>Megakaryocytes - cytology</topic><topic>Megakaryocytes - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Microarray</topic><topic>Mouse</topic><topic>Platelet Membrane Glycoprotein IIb - genetics</topic><topic>Polymerase Chain Reaction</topic><topic>Thrombopoiesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumura‐Takeda, Kuniko</creatorcontrib><creatorcontrib>Sogo, Shinji</creatorcontrib><creatorcontrib>Isakari, Yoshimasa</creatorcontrib><creatorcontrib>Harada, Yasuo</creatorcontrib><creatorcontrib>Nishioka, Kinue</creatorcontrib><creatorcontrib>Kawakami, Takuma</creatorcontrib><creatorcontrib>Ono, Toshihide</creatorcontrib><creatorcontrib>Taki, Takao</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><jtitle>Stem cells (Dayton, Ohio)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsumura‐Takeda, Kuniko</au><au>Sogo, Shinji</au><au>Isakari, Yoshimasa</au><au>Harada, Yasuo</au><au>Nishioka, Kinue</au><au>Kawakami, Takuma</au><au>Ono, Toshihide</au><au>Taki, Takao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD41+/CD45+ Cells Without Acetylcholinesterase Activity Are Immature and a Major Megakaryocytic Population in Murine Bone Marrow</atitle><jtitle>Stem cells (Dayton, Ohio)</jtitle><addtitle>Stem Cells</addtitle><date>2007-04</date><risdate>2007</risdate><volume>25</volume><issue>4</issue><spage>862</spage><epage>870</epage><pages>862-870</pages><issn>1066-5099</issn><eissn>1549-4918</eissn><abstract>Murine megakaryocytes (MKs) are defined by CD41/CD61 expression and acetylcholinesterase (AChE) activity; however, their stages of differentiation in bone marrow (BM) have not been fully elucidated. In murine lineage‐negative (Lin−)/CD45+ BM cells, we found CD41+ MKs without AChE activity (AChE−) except for CD41++ MKs with AChE activity (AChE+), in which CD61 expression was similar to their CD41 level. Lin−/CD41+/CD45+/AChE− MKs could differentiate into AChE+, with an accompanying increase in CD41/CD61 during in vitro culture. Both proplatelet formation (PPF) and platelet (PLT) production for Lin−/CD41+/CD45+/AChE− MKs were observed later than for Lin−/CD41++/CD45+/AChE+ MKs, whereas MK progenitors were scarcely detected in both subpopulations. GeneChip and semiquantitative polymerase chain reaction analyses revealed that the Lin−/CD41+/CD45+/AChE− MKs are assigned at the stage between the progenitor and PPF preparation phases in respect to the many MK/PLT‐specific gene expressions, including β1‐tubulin. In normal mice, the number of Lin−/CD41+/CD45+/AChE− MKs was 100 times higher than that of AChE+ MKs in BM. When MK destruction and consequent thrombocytopenia were caused by an antitumor agent, mitomycin‐C, Lin−/CD41+/CD45+/AChE− MKs led to an increase in AChE+ MKs and subsequent PLT recovery with interleukin‐11 administration. It was concluded that MKs in murine BM at least in part consist of immature Lin−/CD41+/CD45+/AChE− MKs and more differentiated Lin−/CD41++/CD45+/AChE+ MKs. Immature Lin−/CD41+/CD45+/AChE− MKs are a major MK population compared with AChE+ MKs in BM and play an important role in rapid PLT recovery in vivo.
Disclosure of potential conflicts of interest is found at the end of this article.</abstract><cop>Bristol</cop><pub>John Wiley & Sons, Ltd</pub><pmid>17420226</pmid><doi>10.1634/stemcells.2006-0363</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acetylcholinesterase - analysis Animals Biomarkers - analysis Bone marrow Bone Marrow Cells - cytology Bone Marrow Cells - immunology Cell Culture Techniques Colony-Forming Units Assay Gene Expression Profiling Leukocyte Common Antigens - genetics Male Megakaryocytes Megakaryocytes - cytology Megakaryocytes - immunology Mice Mice, Inbred BALB C Microarray Mouse Platelet Membrane Glycoprotein IIb - genetics Polymerase Chain Reaction Thrombopoiesis |
title | CD41+/CD45+ Cells Without Acetylcholinesterase Activity Are Immature and a Major Megakaryocytic Population in Murine Bone Marrow |
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