{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T07:09:44Z","timestamp":1791443384403,"version":"4.3.3"},"reference-count":60,"publisher":"American Society of Hematology","issue":"20","license":[{"start":{"date-parts":[[2021,12,27]],"date-time":"2021-12-27T00:00:00Z","timestamp":1640563200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/legalcode"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,5,19]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Impairment of normal hematopoiesis and leukemia progression are 2 well-linked processes during leukemia development and are controlled by the bone marrow (BM) niche. Extracellular matrix proteins, including laminin, are important BM niche components. However, their role in hematopoiesis regeneration and leukemia is unknown. Laminin \u03b14 (Lama4), a major receptor-binding chain of several laminins, is altered in BM niches in mice with acute myeloid leukemia (AML). So far, the impact of Lama4 on leukemia progression remains unknown. We here report that Lama4 deletion in mice resulted in impaired hematopoiesis regeneration following irradiation-induced stress, which is accompanied by altered BM niche composition and inflammation. Importantly, in a transplantation-induced MLL-AF9 AML mouse model, we demonstrate accelerated AML progression and relapse in Lama4\u2212\/\u2212 mice. Upon AML exposure, Lama4\u2212\/\u2212 mesenchymal stem cells (MSCs) exhibited dramatic molecular alterations, including upregulation of inflammatory cytokines that favor AML growth. Lama4\u2212\/\u2212 MSCs displayed increased antioxidant activities and promoted AML stem cell proliferation and chemoresistance to cytarabine, which was accompanied by increased mitochondrial transfer from the MSCs to AML cells and reduced reactive oxygen species in AML cells in\u00a0vitro. Similarly, we detected lower levels of reactive oxygen species in AML cells from Lama4\u2212\/\u2212 mice post\u2013cytarabine treatment. Notably, LAMA4 inhibition or knockdown in human MSCs promoted human AML cell proliferation and chemoprotection. Together, our study for the first time demonstrates the critical role of Lama4 in impeding AML progression and chemoresistance. Targeting Lama4 signaling pathways may offer potential new therapeutic options for AML.<\/jats:p>","DOI":"10.1182\/blood.2021011510","type":"journal-article","created":{"date-parts":[[2021,12,27]],"date-time":"2021-12-27T21:51:07Z","timestamp":1640641867000},"page":"3040-3057","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":41,"title":["Critical role of <i>Lama4<\/i> for hematopoiesis regeneration and acute myeloid leukemia progression"],"prefix":"10.1182","volume":"139","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2752-5598","authenticated-orcid":false,"given":"Huan","family":"Cai","sequence":"first","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5978-0043","authenticated-orcid":false,"given":"Makoto","family":"Kondo","sequence":"additional","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lakshmi","family":"Sandhow","sequence":"additional","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pingnan","family":"Xiao","sequence":"additional","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne-Sofie","family":"Johansson","sequence":"additional","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0514-9931","authenticated-orcid":false,"given":"Takako","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Department of Matrix Medicine, Faculty of Medicine, Oita University, Yufu, Oita, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna","family":"Zawacka-Pankau","sequence":"additional","affiliation":[{"name":"Center for Hematology and Regenerative Medicine (HERM), Department of Medicine Huddinge, Karolinska University Hospital, Karolinska Institute, Stockholm, 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