Figure 6.
Selective impairment of STAT signaling through the OSM/OSMRβ axis in primary fibroblasts. (A) Schematic illustrating the OSM/OSMRβ axis. (B) Immunoblot in primary fibroblasts from P1, P2, and P3 (unable to obtain fibroblasts from P4 though P10) and three HCs for pSTAT1, pSTAT3, and pSTAT5 before and after treatment with OSM (100 ng/ml for 15 min); n = 3. (C–E) Quantification of the immunoblot in B for (C) pSTAT1, (D) pSTAT3, and (E) pSTAT5. Patients are in red and healthy controls are in blue. Statistical comparisons based on unpaired t test. Asterisks denote P values: **P < 0.01; ****P < 0.0001. (F) Immunoblot in primary fibroblasts from P1, P2, and P3 and three HCs for pSTAT1 and pSTAT3 before and after treatment with LIF (100 ng/ml for 15 min); n = 3. (G and H) Quantification of the immunoblot in F for (G) pSTAT1 and (H) pSTAT3. Patients are in red, and healthy controls are in blue. Source data are available for this figure: SourceData F6. Refer to the image caption for details. Panel A: A schematic diagram illustrates the OSM/OSMR axis, showing the interaction of LIF and OSM with their respective receptors and the subsequent signaling pathways involving JAK and STAT proteins. Panel B: Immunoblots show the levels of phosphorylated STAT1, STAT3, and STAT5 in primary fibroblasts from three patients and three healthy controls before and after treatment with OSM. Beta-actin is used as a loading control. Panel C: A paired scatter plot quantifies the relative STAT1 phosphorylation over beta-actin in patients (red) and healthy controls (blue) before and after OSM treatment. Panel D: A paired scatter plot quantifies the relative STAT3 phosphorylation over beta-actin in patients (red) and healthy controls (blue) before and after OSM treatment. Panel E: A paired scatter plot quantifies the relative STAT5 phosphorylation over beta-actin in patients (red) and healthy controls (blue) before and after OSM treatment. Panel F: Immunoblots show the levels of phosphorylated STAT1 and STAT3 in primary fibroblasts from three patients and three healthy controls before and after treatment with LIF. Beta-actin is used as a loading control. Panel G: A paired scatter plot quantifies the relative STAT1 phosphorylation over beta-actin in patients (red) and healthy controls (blue) before and after LIF treatment. Panel H: A paired scatter plot quantifies the relative STAT3 phosphorylation over beta-actin in patients (red) and healthy controls (blue) before and after LIF treatment.

Selective impairment of STAT signaling through the OSM/OSMRβ axis in primary fibroblasts. (A) Schematic illustrating the OSM/OSMRβ axis. (B) Immunoblot in primary fibroblasts from P1, P2, and P3 (unable to obtain fibroblasts from P4 though P10) and three HCs for pSTAT1, pSTAT3, and pSTAT5 before and after treatment with OSM (100 ng/ml for 15 min); n = 3. (C–E) Quantification of the immunoblot in B for (C) pSTAT1, (D) pSTAT3, and (E) pSTAT5. Patients are in red and healthy controls are in blue. Statistical comparisons based on unpaired t test. Asterisks denote P values: **P < 0.01; ****P < 0.0001. (F) Immunoblot in primary fibroblasts from P1, P2, and P3 and three HCs for pSTAT1 and pSTAT3 before and after treatment with LIF (100 ng/ml for 15 min); n = 3. (G and H) Quantification of the immunoblot in F for (G) pSTAT1 and (H) pSTAT3. Patients are in red, and healthy controls are in blue. Source data are available for this figure: SourceData F6.

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