PPARγ agonists promote the resolution of myelofibrosis in preclinical models
I Myelofibrosis (MF) is a non-BCR-ABL myeloproliferative neoplasm associated with poor outcomes. Current treatment has little effect on the natural history of the disease. MF results from complex interactions between (a) the malignant clone, (b) an inflammatory context, and (c) remodeling of the bon...
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| Veröffentlicht in: | The Journal of clinical investigation 2021-06, Vol.131 (11), p.1-16 |
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| creator | Lambert, Juliette Saliba, Joseph Calderon, Carolina Sii-Felice, Karine Salma, Mohammad Edmond, Valérie Alvarez, Jean-Claude Delord, Marc Marty, Caroline Plo, Isabelle Kiladjian, Jean-Jacques Soler, Eric Vainchenker, William Villeval, Jean-Luc Rousselot, Philippe Prost, Stéphane |
| description | I Myelofibrosis (MF) is a non-BCR-ABL myeloproliferative neoplasm associated with poor outcomes. Current treatment has little effect on the natural history of the disease. MF results from complex interactions between (a) the malignant clone, (b) an inflammatory context, and (c) remodeling of the bone marrow (BM) microenvironment. Each of these points is a potential target of PPARγ activation. Here, we demonstrated the therapeutic potential of PPARγ agonists in resolving MF in 3 mouse models. We showed that PPARy agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARy constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice. |
| doi_str_mv | 10.1172/JCI136713. |
| format | Article |
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Current treatment has little effect on the natural history of the disease. MF results from complex interactions between (a) the malignant clone, (b) an inflammatory context, and (c) remodeling of the bone marrow (BM) microenvironment. Each of these points is a potential target of PPARγ activation. Here, we demonstrated the therapeutic potential of PPARγ agonists in resolving MF in 3 mouse models. We showed that PPARy agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARy constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/JCI136713.</identifier><language>eng</language><publisher>Ann Arbor: American Society for Clinical Investigation</publisher><subject>Agonists ; Anemia ; Animal models ; BCR-ABL protein ; Biomedical research ; Bone marrow ; Bone remodeling ; Cell growth ; Cloning ; Disease ; Fusion protein ; Hemoglobin ; Hyperplasia ; Inflammation ; Leukemia ; Medical prognosis ; Microenvironments ; Myelofibrosis ; Myeloproliferation ; Pathogenesis ; Spleen ; Stem cells ; Stroma ; Therapeutic targets</subject><ispartof>The Journal of clinical investigation, 2021-06, Vol.131 (11), p.1-16</ispartof><rights>Copyright American Society for Clinical Investigation Jun 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>Lambert, Juliette</creatorcontrib><creatorcontrib>Saliba, Joseph</creatorcontrib><creatorcontrib>Calderon, Carolina</creatorcontrib><creatorcontrib>Sii-Felice, Karine</creatorcontrib><creatorcontrib>Salma, Mohammad</creatorcontrib><creatorcontrib>Edmond, Valérie</creatorcontrib><creatorcontrib>Alvarez, Jean-Claude</creatorcontrib><creatorcontrib>Delord, Marc</creatorcontrib><creatorcontrib>Marty, Caroline</creatorcontrib><creatorcontrib>Plo, Isabelle</creatorcontrib><creatorcontrib>Kiladjian, Jean-Jacques</creatorcontrib><creatorcontrib>Soler, Eric</creatorcontrib><creatorcontrib>Vainchenker, William</creatorcontrib><creatorcontrib>Villeval, Jean-Luc</creatorcontrib><creatorcontrib>Rousselot, Philippe</creatorcontrib><creatorcontrib>Prost, Stéphane</creatorcontrib><title>PPARγ agonists promote the resolution of myelofibrosis in preclinical models</title><title>The Journal of clinical investigation</title><description>I Myelofibrosis (MF) is a non-BCR-ABL myeloproliferative neoplasm associated with poor outcomes. Current treatment has little effect on the natural history of the disease. MF results from complex interactions between (a) the malignant clone, (b) an inflammatory context, and (c) remodeling of the bone marrow (BM) microenvironment. Each of these points is a potential target of PPARγ activation. Here, we demonstrated the therapeutic potential of PPARγ agonists in resolving MF in 3 mouse models. We showed that PPARy agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARy constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.</description><subject>Agonists</subject><subject>Anemia</subject><subject>Animal models</subject><subject>BCR-ABL protein</subject><subject>Biomedical research</subject><subject>Bone marrow</subject><subject>Bone remodeling</subject><subject>Cell growth</subject><subject>Cloning</subject><subject>Disease</subject><subject>Fusion protein</subject><subject>Hemoglobin</subject><subject>Hyperplasia</subject><subject>Inflammation</subject><subject>Leukemia</subject><subject>Medical prognosis</subject><subject>Microenvironments</subject><subject>Myelofibrosis</subject><subject>Myeloproliferation</subject><subject>Pathogenesis</subject><subject>Spleen</subject><subject>Stem cells</subject><subject>Stroma</subject><subject>Therapeutic 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| subjects | Agonists Anemia Animal models BCR-ABL protein Biomedical research Bone marrow Bone remodeling Cell growth Cloning Disease Fusion protein Hemoglobin Hyperplasia Inflammation Leukemia Medical prognosis Microenvironments Myelofibrosis Myeloproliferation Pathogenesis Spleen Stem cells Stroma Therapeutic targets |
| title | PPARγ agonists promote the resolution of myelofibrosis in preclinical models |
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