Figure 6.
Hematopoietic knockout of CXCL4 leads to reduced expression of profibrotic pathways and reduced inflammation. (A) Schematic of cell populations analyzed. CD41+ MKs are either WT or CXCL4 knockout (GFP+) and transduced with either ThPO-inducing fibrosis or EV as a control. tdTom+ stromal cells were exposed to CXCL4 expressing or knockout hematopoietic cells/MKs in control or fibrosis. Heatmap representation of PROGENy analysis of sort-purified MKs and Gli1+ stromal cells from WT ThPO or Cxcl4−/− ThPO mice compared with EV control mice. (B) Heatmap representation of specific PROGENy pathways such as JAK-STAT, NF-κB, and TNF-α. (C) Heatmap representation of Discriminant Regulon Enrichment Analysis of transcription factors of sort-purified MKs and Gli1+ stromal cells from WT ThPO or Cxcl4−/− ThPO mice compared with EV controls.

Hematopoietic knockout of CXCL4 leads to reduced expression of profibrotic pathways and reduced inflammation. (A) Schematic of cell populations analyzed. CD41+ MKs are either WT or CXCL4 knockout (GFP+) and transduced with either ThPO-inducing fibrosis or EV as a control. tdTom+ stromal cells were exposed to CXCL4 expressing or knockout hematopoietic cells/MKs in control or fibrosis. Heatmap representation of PROGENy analysis of sort-purified MKs and Gli1+ stromal cells from WT ThPO or Cxcl4−/− ThPO mice compared with EV control mice. (B) Heatmap representation of specific PROGENy pathways such as JAK-STAT, NF-κB, and TNF-α. (C) Heatmap representation of Discriminant Regulon Enrichment Analysis of transcription factors of sort-purified MKs and Gli1+ stromal cells from WT ThPO or Cxcl4−/− ThPO mice compared with EV controls.

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