To migrate or to degranulate, that is the question
To avoid loss of their munitions before reaching their final destination
at inflamed sites, mature MCs need to be regulated to migrate, but not
yet degranulate (Figure 3). This is a challenging requirement as some of
the MC chemokines induce degranulation of basophils 77and synergize with secretagogues to potentiate MC degranulation78,79. Thus, it was proposed that chemokines may
either elicit distinct signals in MCs, as opposed to basophils, or that
MC SGs are linked to the cell cytoskeleton differently from the basophil
granules 77. Marked differences observed between the
actin skeleton in migrating versus secreting MCs support the
latter possibility 80. Analysis of actin
rearrangements following chemokine stimulation of MCs revealed an
accumulation of pericentral actin clusters that prevent cell flattening
and converge the SGs in the cell center 80. By
contrast, reduction in the actin mesh density characterizes the
secretory actin phenotype. Thus, the migratory actin phenotype
immobilizes the secretory granules by trapping them in the cell center,
whereas the secretory actin phenotype supports mobility and exocytosis.
Diaphanous-related formin, mDia1, appears to be key player in these
actin rearrangements 80 (Figure 3).