Figure 4.
ITGA2B is upregulated in human and murine platelets during clinical and experimental sepsis. (A) Integrated Genomics Viewer (IGV) image showing the expression of ITGA2B exonal reads in purified platelets from a healthy donor (top) vs a septic patient (bottom). The thicker bars on the bottom represent coding regions of ITGA2B with 5′ and 3′ ends indicated. The y-axis represents the expression of ITGA2B, with higher peaks indicating increased mRNA expression. Images representative of n = 5 subjects per group. (B) qRT-PCR of ITGA2B expression in platelets from septic patients (n = 94) assessed upon ICU admission (study day 1) and matched healthy donors (n = 37). Data show the fold change of ITGA2B expression in septic patients vs healthy donors. (C) Serial qRT-PCR measurements of ITGA2B in platelets from an independent cohort of septic patients assessed upon admission to the ICU (day 1, septic n = 19) and again in the same patients ∼90 days following hospital discharge (day 90, n = 19). For comparison, ITGA2B expression was also measured in an independent cohort of matched healthy donors (Healthy, n = 10). (D) IGV image showing Itga2b exonal reads in platelets from untreated control mice (top) and mice subject to CLP (bottom). The thicker bars on the bottom represent coding regions of Itga2b with 5′ and 3′ ends indicated. The y-axis represents the expression of Itga2b, with higher peaks indicating increased RNA expression. Images are representative of CLP (n = 3 biological replicates) and control (n = 4 biological replicates). (E) Serial measurements by qRT-PCR of Itga2b in primary bone marrow–derived megakaryocytes from control or CLP mice on days 1 and 3 (n = 4-13/ group). (F) Serial measurements by qRT-PCR of Itga2b in isolated platelets from untreated (control) or post-CLP mice on days 1, 2, 3, and 7. Day 7 post-CLP was considered a recovery time point (n = 6-10/group).

ITGA2B is upregulated in human and murine platelets during clinical and experimental sepsis. (A) Integrated Genomics Viewer (IGV) image showing the expression of ITGA2B exonal reads in purified platelets from a healthy donor (top) vs a septic patient (bottom). The thicker bars on the bottom represent coding regions of ITGA2B with 5′ and 3′ ends indicated. The y-axis represents the expression of ITGA2B, with higher peaks indicating increased mRNA expression. Images representative of n = 5 subjects per group. (B) qRT-PCR of ITGA2B expression in platelets from septic patients (n = 94) assessed upon ICU admission (study day 1) and matched healthy donors (n = 37). Data show the fold change of ITGA2B expression in septic patients vs healthy donors. (C) Serial qRT-PCR measurements of ITGA2B in platelets from an independent cohort of septic patients assessed upon admission to the ICU (day 1, septic n = 19) and again in the same patients ∼90 days following hospital discharge (day 90, n = 19). For comparison, ITGA2B expression was also measured in an independent cohort of matched healthy donors (Healthy, n = 10). (D) IGV image showing Itga2b exonal reads in platelets from untreated control mice (top) and mice subject to CLP (bottom). The thicker bars on the bottom represent coding regions of Itga2b with 5′ and 3′ ends indicated. The y-axis represents the expression of Itga2b, with higher peaks indicating increased RNA expression. Images are representative of CLP (n = 3 biological replicates) and control (n = 4 biological replicates). (E) Serial measurements by qRT-PCR of Itga2b in primary bone marrow–derived megakaryocytes from control or CLP mice on days 1 and 3 (n = 4-13/ group). (F) Serial measurements by qRT-PCR of Itga2b in isolated platelets from untreated (control) or post-CLP mice on days 1, 2, 3, and 7. Day 7 post-CLP was considered a recovery time point (n = 6-10/group).

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