Figure 1.
Increased TPO plasma levels and platelet galactosylation in MPNs. (A) TPO plasma levels were measured in samples from patients with MPNs with different driver mutations and percentages of allelic burden. The percentage of allelic burden correlated with TPO concentration (n = 38, P < .0001, R2 = 0.6). (B) Platelets that expose galactose are recognized by the hepatic AMR to regulate hepatic TPO production (LacNAc; N-acetylglucosamine [GlcNAc]). (C) Flow cytometry analysis of expression of GpIbα and GpIIb in platelets from HCs and MPN patients. (D) HC and MPN platelets were lysed, and total lysates were subjected to SDS-PAGE and probed with ECL (i) and RCA (ii) in order to evaluate galactosylation status. GpIbα, GPIIIa, and β-actin have been used as loading controls. (E-F) Densitometric analysis of ECL and RCA signal in MPNs (n = 12) relative to HCs (n = 8). Data are presented as mean ± SD (*P < .05). FSC, forward scatter; SSC, side scatter.

Increased TPO plasma levels and platelet galactosylation in MPNs. (A) TPO plasma levels were measured in samples from patients with MPNs with different driver mutations and percentages of allelic burden. The percentage of allelic burden correlated with TPO concentration (n = 38, P < .0001, R2 = 0.6). (B) Platelets that expose galactose are recognized by the hepatic AMR to regulate hepatic TPO production (LacNAc; N-acetylglucosamine [GlcNAc]). (C) Flow cytometry analysis of expression of GpIbα and GpIIb in platelets from HCs and MPN patients. (D) HC and MPN platelets were lysed, and total lysates were subjected to SDS-PAGE and probed with ECL (i) and RCA (ii) in order to evaluate galactosylation status. GpIbα, GPIIIa, and β-actin have been used as loading controls. (E-F) Densitometric analysis of ECL and RCA signal in MPNs (n = 12) relative to HCs (n = 8). Data are presented as mean ± SD (*P < .05). FSC, forward scatter; SSC, side scatter.

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