Figure 6
Figure 6. Distinct regulation of CXCL4 and CXCL4L1 secretion by PKC activation in T cells and HCoSMCs. (A) Effect of PKC inhibitors on PMA-induced CXCL4 secretion by T cells (CD3+). Cells were cultured for 6 hours in serum-free medium at a concentration of 1 × 106 cells/mL medium in the presence or absence of 50 ng/mL PMA, and in the presence or absence of different PKC inhibitors. Data represent mean ± SEM of 3 independent experiments performed in duplicates. *P < .05 versus PMA-treated cells. (B) Constitutive secretion of CXCL4L1 by HCoSMCs is not further modulated by PMA or PKC inhibitors. Cells were cultured for 6 hours in serum-free medium at a concentration of 1 × 106 cells/mL medium in the presence or absence of 50 ng/mL PMA and in the presence or absence of different PKC inhibitors. Data represent mean ± SEM of 3 independent experiments performed in duplicate.

Distinct regulation of CXCL4 and CXCL4L1 secretion by PKC activation in T cells and HCoSMCs. (A) Effect of PKC inhibitors on PMA-induced CXCL4 secretion by T cells (CD3+). Cells were cultured for 6 hours in serum-free medium at a concentration of 1 × 106 cells/mL medium in the presence or absence of 50 ng/mL PMA, and in the presence or absence of different PKC inhibitors. Data represent mean ± SEM of 3 independent experiments performed in duplicates. *P < .05 versus PMA-treated cells. (B) Constitutive secretion of CXCL4L1 by HCoSMCs is not further modulated by PMA or PKC inhibitors. Cells were cultured for 6 hours in serum-free medium at a concentration of 1 × 106 cells/mL medium in the presence or absence of 50 ng/mL PMA and in the presence or absence of different PKC inhibitors. Data represent mean ± SEM of 3 independent experiments performed in duplicate.

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