PPARγ agonists promote the resolution of myelofibrosis in preclinical models

Juliette Lambert; Joseph Saliba; Carolina Calderon; Karine Sii-Felice; Mohammad Salma; Valérie Edmond; Jean Claude Alvarez; Marc Delord; Caroline Marty; Isabelle Plo; Jean Jacques Kiladjian; Eric Soler; William Vainchenker; Jean Luc Villeval; Philippe Rousselot; Stéphane Prost

doi:10.1172/JCI136713

PPARγ agonists promote the resolution of myelofibrosis in preclinical models

Juliette Lambert, Joseph Saliba, Carolina Calderon, Karine Sii-Felice, Mohammad Salma, Valérie Edmond, Jean Claude Alvarez, Marc Delord, Caroline Marty, Isabelle Plo, Jean Jacques Kiladjian, Eric Soler, William Vainchenker, Jean Luc Villeval, Philippe Rousselot, Stéphane Prost

Résultats de recherche: Contribution à un journal › Article › Revue par des pairs

5 Citations (Scopus)

Résumé

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 PPARγ agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARγ constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.

langue originale	Anglais
Numéro d'article	e136713
journal	Journal of Clinical Investigation
Volume	131
Numéro de publication	11
Les DOIs	https://doi.org/10.1172/JCI136713
état	Publié - 1 juin 2021

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10.1172/JCI136713

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Lambert, J., Saliba, J., Calderon, C., Sii-Felice, K., Salma, M., Edmond, V., Alvarez, J. C., Delord, M., Marty, C., Plo, I., Kiladjian, J. J., Soler, E., Vainchenker, W., Villeval, J. L., Rousselot, P., & Prost, S. (2021). PPARγ agonists promote the resolution of myelofibrosis in preclinical models. Journal of Clinical Investigation, 131(11), Article e136713. https://doi.org/10.1172/JCI136713

@article{04c8066c75914b729c12fc3f98883ebe,

title = "PPARγ agonists promote the resolution of myelofibrosis in preclinical models",

abstract = "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 PPARγ agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARγ constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.",

author = "Juliette Lambert and Joseph Saliba and Carolina Calderon and Karine Sii-Felice and Mohammad Salma and Val{\'e}rie Edmond and Alvarez, {Jean Claude} and Marc Delord and Caroline Marty and Isabelle Plo and Kiladjian, {Jean Jacques} and Eric Soler and William Vainchenker and Villeval, {Jean Luc} and Philippe Rousselot and St{\'e}phane Prost",

note = "Publisher Copyright: {\textcopyright} 2021, American Society for Clinical Investigation.",

year = "2021",

month = jun,

day = "1",

doi = "10.1172/JCI136713",

language = "English",

volume = "131",

journal = "Journal of Clinical Investigation",

issn = "0021-9738",

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}

Lambert, J, Saliba, J, Calderon, C, Sii-Felice, K, Salma, M, Edmond, V, Alvarez, JC, Delord, M, Marty, C, Plo, I, Kiladjian, JJ, Soler, E, Vainchenker, W, Villeval, JL, Rousselot, P & Prost, S 2021, 'PPARγ agonists promote the resolution of myelofibrosis in preclinical models', Journal of Clinical Investigation, VOL. 131, Numéro 11, e136713. https://doi.org/10.1172/JCI136713

TY - JOUR

T1 - PPARγ agonists promote the resolution of myelofibrosis in preclinical models

AU - Lambert, Juliette

AU - Saliba, Joseph

AU - Calderon, Carolina

AU - Sii-Felice, Karine

AU - Salma, Mohammad

AU - Edmond, Valérie

AU - Alvarez, Jean Claude

AU - Delord, Marc

AU - Marty, Caroline

AU - Plo, Isabelle

AU - Kiladjian, Jean Jacques

AU - Soler, Eric

AU - Vainchenker, William

AU - Villeval, Jean Luc

AU - Rousselot, Philippe

AU - Prost, Stéphane

PY - 2021/6/1

Y1 - 2021/6/1

N2 - 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 PPARγ agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARγ constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.

AB - 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 PPARγ agonists reduce myeloproliferation, modulate inflammation, and protect the BM stroma in vitro and ex vivo. Activation of PPARγ constitutes a relevant therapeutic target in MF, and our data support the possibility of using PPARγ agonists in clinical practice.

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U2 - 10.1172/JCI136713

DO - 10.1172/JCI136713

M3 - Article

C2 - 33914703

AN - SCOPUS:85107177008

SN - 0021-9738

VL - 131

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

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