FcεRI cross‐linking‐induced actin assembly mediates calcium signalling in RBL‐2H3 mast cells
To determine the role of actin assembly in the Ca2+ signalling of mast cells activated by
cross‐linking of FcεRI, we examined the effects of cytochalasin D, an inhibitor of actin
polymerization. In the RBL‐2H3 cells, F‐actin content was increased by sensitization with
anti‐dinitrophenol (DNP) IgE. In these cells, cytochalasin D induced oscillatory increases in
cytosolic Ca2+ ([Ca2+] i); these increase were inhibited by jasplakinolide, a stabilizer of
actin filaments. In the IgE‐sensitized RBL‐2H3 cells, DNP‐human serum albumin (DNP …
cross‐linking of FcεRI, we examined the effects of cytochalasin D, an inhibitor of actin
polymerization. In the RBL‐2H3 cells, F‐actin content was increased by sensitization with
anti‐dinitrophenol (DNP) IgE. In these cells, cytochalasin D induced oscillatory increases in
cytosolic Ca2+ ([Ca2+] i); these increase were inhibited by jasplakinolide, a stabilizer of
actin filaments. In the IgE‐sensitized RBL‐2H3 cells, DNP‐human serum albumin (DNP …
- To determine the role of actin assembly in the Ca2+ signalling of mast cells activated by cross‐linking of FcεRI, we examined the effects of cytochalasin D, an inhibitor of actin polymerization.
- In the RBL‐2H3 cells, F‐actin content was increased by sensitization with anti‐dinitrophenol (DNP) IgE. In these cells, cytochalasin D induced oscillatory increases in cytosolic Ca2+ ([Ca2+]i); these increase were inhibited by jasplakinolide, a stabilizer of actin filaments.
- In the IgE‐sensitized RBL‐2H3 cells, DNP‐human serum albumin (DNP‐HSA) augmented actin assembly. DNP‐HSA also increased the production of IP3, [Ca2+]i and degranulation. Cytochalasin D enhanced all of these DNP‐HSA‐induced effects.
- In a Ca2+‐free solution, DNP‐HSA induced a transient increase in [Ca2+]i, and this increase was accelerated by cytochalasin D. After cessation of the DNP‐HSA‐induced Ca2+ release, the re‐addition of Ca2+ induced a sustained increase in [Ca2+]i through capacitative Ca2+ entry (CCE), and this increase was enhanced by cytochalasin D.
- The effect of cytochalasin D in enhancing the CCE activity was prevented by xestospongin C.
- In contrast, neither the Ca2+ release nor the CCE activation that was induced by thapsigargin was affected by cytochalasin D.
- These results suggest that actin de‐polymerization stimulates the FcεRI‐mediated signalling to augment the release of Ca2+ from the endoplasmic reticulum in RBL‐2H3 cells.
British Journal of Pharmacology (2002) 136, 837–846. doi:10.1038/sj.bjp.0704788
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