Images present the histological examination of the BM (femur) and spleen of 1 representative mouse per treatment group in the MF post-JAK2^V617F model (W37). (A and C) H&E coloration shows BM and spleen cellularity, respectively. (B and D) Silver reticulin coloration shows a dense network of reticulin fibers in the BM and spleens of untreated animals, whereas only scattered fibers are seen in the BM and spleens of mice treated with pioglitazone or mesalazine. (Original magnification, ×100.) (E–G) PPARγ agonists counteract the decrease of hemoglobin levels related to the development of BM fibrosis in the MF TPO^high model (E), MF post-JAK2^V617Fmodel (F), and MF post-CALRdel52 model (G). The black vertical dashed lines indicate initiation of treatment. (H–M) PPARγ agonists prevent BM hematopoietic cell depletion in the MF TPO^high model (H), MF post-JAK2^V617F model (J), and MF post-CALRdel52 model (L) and preserve the clonogenic potential of BM hematopoietic progenitors in the MF TPO^high model (I), MF post-JAK2^V617Fmodel (K), and MF post-CALRdel52 model (M). The black horizontal lines represent the mean. *Statistically significant difference (P < 0.05). BMT, bone marrow transplantation; CFC, colony-forming cell; d52, CALRdel52; Mes, mesalazine; Pio, pioglitazone; TBI, total-body irradiation; Un, untreated; W, week; WT, CALR-WT. (n = 10 mice per condition, except CALR-WT pioglitazone n = 5).