NFĸB Targeting in Bone Marrow Mesenchymal Stem Cell-Mediated Support of Age-Linked Hematological Malignancies
Mesenchymal stem cells (MSCs) can become dysfunctional in patients with hematological disorders. An unanswered question is whether age-linked disruption of the bone marrow (BM) microenvironment is secondary to hematological dysfunction or vice versa. We therefore studied MSC function in patients wit...
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| Veröffentlicht in: | Stem cell reviews and reports 2021-12, Vol.17 (6), p.2178-2192 |
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| creator | Sherman, Lauren S. Patel, Shyam A. Castillo, Marianne D. Unkovic, Rachel Taborga, Marcelo Gergues, Marina Patterson, Shaun Etchegaray, Jean-Pierre Jaloudi, Mohammed Hooda-Nehra, Anupama Kra, Joshua Rojas, Darling P. Chang, Victor T. Rameshwar, Pranela |
| description | Mesenchymal stem cells (MSCs) can become dysfunctional in patients with hematological disorders. An unanswered question is whether age-linked disruption of the bone marrow (BM) microenvironment is secondary to hematological dysfunction or vice versa. We therefore studied MSC function in patients with different hematological disorders and found decreased MHC-II except from one sample with acute myeloid leukemia (AML). The patients’ MSCs were able to exert veto properties except for AML MSCs. While the expression of MHC-II appeared to be irrelevant to the immune licensing of MSCs, AML MSCs lost their ability to differentiate upon contact and rather, continued to proliferate, forming foci-like structures. We performed a retrospective study that indicated a significant increase in MSCs, based on phenotype, for patients with BM fibrosis. This suggests a role for MSCs in patients transitioning to leukemia. NFĸB was important to MSC function and was shown to be a potential target to sensitize leukemic CD34+/CD38− cells to azacitidine. This correlated with their lack of allogeneic stimulation. This study identified NFĸB as a potential target for combination therapy to treat leukemia stem cells and showed that understanding MSC biology and immune response could be key in determining how the aging BM might support leukemia. More importantly, we show how MSCs might be involved in transitioning the high risk patient with hematological disorder to AML.
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| doi_str_mv | 10.1007/s12015-021-10235-6 |
| format | Article |
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Graphic abstract</description><identifier>ISSN: 2629-3269</identifier><identifier>EISSN: 2629-3277</identifier><identifier>DOI: 10.1007/s12015-021-10235-6</identifier><identifier>PMID: 34410592</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acute myeloid leukemia ; Aging ; Biomedical and Life Sciences ; Biomedical Engineering and Bioengineering ; Bone marrow ; CD34 antigen ; CD38 antigen ; Cell Biology ; Fibrosis ; Hematological diseases ; Hematology ; Immune response ; Leukemia ; Life Sciences ; Major histocompatibility complex ; Mesenchymal stem cells ; Microenvironments ; Myelodysplastic syndromes ; Myeloid leukemia ; Phenotypes ; Regenerative Medicine/Tissue Engineering ; Risk groups ; Stem Cells ; Targeted cancer therapy</subject><ispartof>Stem cell reviews and reports, 2021-12, Vol.17 (6), p.2178-2192</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3346-643a0f088336f7110d38a95b39ca0bd36952c069f33e44a7b2469fc80fc75a663</citedby><cites>FETCH-LOGICAL-c3346-643a0f088336f7110d38a95b39ca0bd36952c069f33e44a7b2469fc80fc75a663</cites><orcidid>0000-0003-0434-9034</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12015-021-10235-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12015-021-10235-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34410592$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sherman, Lauren S.</creatorcontrib><creatorcontrib>Patel, Shyam A.</creatorcontrib><creatorcontrib>Castillo, Marianne D.</creatorcontrib><creatorcontrib>Unkovic, Rachel</creatorcontrib><creatorcontrib>Taborga, Marcelo</creatorcontrib><creatorcontrib>Gergues, Marina</creatorcontrib><creatorcontrib>Patterson, Shaun</creatorcontrib><creatorcontrib>Etchegaray, Jean-Pierre</creatorcontrib><creatorcontrib>Jaloudi, Mohammed</creatorcontrib><creatorcontrib>Hooda-Nehra, Anupama</creatorcontrib><creatorcontrib>Kra, Joshua</creatorcontrib><creatorcontrib>Rojas, Darling P.</creatorcontrib><creatorcontrib>Chang, Victor T.</creatorcontrib><creatorcontrib>Rameshwar, Pranela</creatorcontrib><title>NFĸB Targeting in Bone Marrow Mesenchymal Stem Cell-Mediated Support of Age-Linked Hematological Malignancies</title><title>Stem cell reviews and reports</title><addtitle>Stem Cell Rev and Rep</addtitle><addtitle>Stem Cell Rev Rep</addtitle><description>Mesenchymal stem cells (MSCs) can become dysfunctional in patients with hematological disorders. An unanswered question is whether age-linked disruption of the bone marrow (BM) microenvironment is secondary to hematological dysfunction or vice versa. We therefore studied MSC function in patients with different hematological disorders and found decreased MHC-II except from one sample with acute myeloid leukemia (AML). The patients’ MSCs were able to exert veto properties except for AML MSCs. While the expression of MHC-II appeared to be irrelevant to the immune licensing of MSCs, AML MSCs lost their ability to differentiate upon contact and rather, continued to proliferate, forming foci-like structures. We performed a retrospective study that indicated a significant increase in MSCs, based on phenotype, for patients with BM fibrosis. This suggests a role for MSCs in patients transitioning to leukemia. NFĸB was important to MSC function and was shown to be a potential target to sensitize leukemic CD34+/CD38− cells to azacitidine. This correlated with their lack of allogeneic stimulation. This study identified NFĸB as a potential target for combination therapy to treat leukemia stem cells and showed that understanding MSC biology and immune response could be key in determining how the aging BM might support leukemia. More importantly, we show how MSCs might be involved in transitioning the high risk patient with hematological disorder to AML.
Graphic abstract</description><subject>Acute myeloid leukemia</subject><subject>Aging</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Bone marrow</subject><subject>CD34 antigen</subject><subject>CD38 antigen</subject><subject>Cell Biology</subject><subject>Fibrosis</subject><subject>Hematological diseases</subject><subject>Hematology</subject><subject>Immune response</subject><subject>Leukemia</subject><subject>Life Sciences</subject><subject>Major histocompatibility complex</subject><subject>Mesenchymal stem cells</subject><subject>Microenvironments</subject><subject>Myelodysplastic syndromes</subject><subject>Myeloid leukemia</subject><subject>Phenotypes</subject><subject>Regenerative Medicine/Tissue Engineering</subject><subject>Risk groups</subject><subject>Stem Cells</subject><subject>Targeted cancer 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Age-Linked Hematological Malignancies</title><author>Sherman, Lauren S. ; Patel, Shyam A. ; Castillo, Marianne D. ; Unkovic, Rachel ; Taborga, Marcelo ; Gergues, Marina ; Patterson, Shaun ; Etchegaray, Jean-Pierre ; Jaloudi, Mohammed ; Hooda-Nehra, Anupama ; Kra, Joshua ; Rojas, Darling P. ; Chang, Victor T. ; Rameshwar, Pranela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3346-643a0f088336f7110d38a95b39ca0bd36952c069f33e44a7b2469fc80fc75a663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acute myeloid leukemia</topic><topic>Aging</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Bone marrow</topic><topic>CD34 antigen</topic><topic>CD38 antigen</topic><topic>Cell Biology</topic><topic>Fibrosis</topic><topic>Hematological diseases</topic><topic>Hematology</topic><topic>Immune 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Pranela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NFĸB Targeting in Bone Marrow Mesenchymal Stem Cell-Mediated Support of Age-Linked Hematological Malignancies</atitle><jtitle>Stem cell reviews and reports</jtitle><stitle>Stem Cell Rev and Rep</stitle><addtitle>Stem Cell Rev Rep</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>17</volume><issue>6</issue><spage>2178</spage><epage>2192</epage><pages>2178-2192</pages><issn>2629-3269</issn><eissn>2629-3277</eissn><abstract>Mesenchymal stem cells (MSCs) can become dysfunctional in patients with hematological disorders. An unanswered question is whether age-linked disruption of the bone marrow (BM) microenvironment is secondary to hematological dysfunction or vice versa. We therefore studied MSC function in patients with different hematological disorders and found decreased MHC-II except from one sample with acute myeloid leukemia (AML). The patients’ MSCs were able to exert veto properties except for AML MSCs. While the expression of MHC-II appeared to be irrelevant to the immune licensing of MSCs, AML MSCs lost their ability to differentiate upon contact and rather, continued to proliferate, forming foci-like structures. We performed a retrospective study that indicated a significant increase in MSCs, based on phenotype, for patients with BM fibrosis. This suggests a role for MSCs in patients transitioning to leukemia. NFĸB was important to MSC function and was shown to be a potential target to sensitize leukemic CD34+/CD38− cells to azacitidine. This correlated with their lack of allogeneic stimulation. This study identified NFĸB as a potential target for combination therapy to treat leukemia stem cells and showed that understanding MSC biology and immune response could be key in determining how the aging BM might support leukemia. More importantly, we show how MSCs might be involved in transitioning the high risk patient with hematological disorder to AML.
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| subjects | Acute myeloid leukemia Aging Biomedical and Life Sciences Biomedical Engineering and Bioengineering Bone marrow CD34 antigen CD38 antigen Cell Biology Fibrosis Hematological diseases Hematology Immune response Leukemia Life Sciences Major histocompatibility complex Mesenchymal stem cells Microenvironments Myelodysplastic syndromes Myeloid leukemia Phenotypes Regenerative Medicine/Tissue Engineering Risk groups Stem Cells Targeted cancer therapy |
| title | NFĸB Targeting in Bone Marrow Mesenchymal Stem Cell-Mediated Support of Age-Linked Hematological Malignancies |
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