Fig. 7: Ezrin is required for FAK and AKT signaling in monocytes leading to cell adhesion to ECM and survival in response to LPS. | Cell Death & Disease

Fig. 7: Ezrin is required for FAK and AKT signaling in monocytes leading to cell adhesion to ECM and survival in response to LPS.

From: Ezrin drives adaptation of monocytes to the inflamed lung microenvironment

Fig. 7

A Schematic representation of ezrin signaling. Ezrin links plasma membrane (PM) and filamentous actin (F-actin) and adheres to the extracellular matrix (e.g., collagen) via integrin α/β. The activation of focal adhesion kinase leads to efficient cell spreading and adhesion, and PI3K/AKT signaling activation is required for cell survival. B Quantification of crystal violet absorbance emitted from adherent primary BM monocytes of murine WT and Ezr-KOm untreated or treated with LPS (6 h). Absorbance values are relative to WT Untr. C Representative WB of phospho-FAK (pFAK, tyrosine 397), total FAK, phospho-AKT (pAKT, serine 473) and total AKT and densitometric analysis of pFAK and pAKT in primary BM monocytes of murine WT and Ezr-KOm untreated or treated with LPS (6 h). Bar graphs represent pFAK/FAK and pAKT/AKT ratios. Protein fold increase was normalized to β-actin and relative to untreated cells. D Quantification of the percentage of dead cells in primary BM monocytes of murine WT and Ezr-KOm, post-exposure to LPS. See also Fig. S8C. E Relative fluorescence units measuring caspase3/7 activity in primary BM monocytes of murine WT and Ezr-KOm, untreated or treated with LPS at different time points. Data are represented as mean ± SEM from three independent experiments. Statistical analysis was performed using one-way ANOVA or Tukey’s test for multiple comparisons between the genotype and treatment conditions. *p < 0.05, **p < 0.01 and ****p < 0.001. See also Supplementary Fig. S9.

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