Premium
Endothelin‐induced cytoskeletal actin re‐organization in cultured astrocytes: Inhibition by C 3 ADP‐ribosyltransferase
Author(s) -
Koyama Yutaka,
Baba Akemichi
Publication year - 1996
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199604)16:4<342::aid-glia6>3.0.co;2-1
Subject(s) - cytoskeleton , biology , stress fiber , cytoplasm , actin , microbiology and biotechnology , pertussis toxin , cytochalasin d , astrocyte , cytochalasin , signal transduction , g protein , biochemistry , endocrinology , cell , central nervous system
We investigated signal transduction mechanisms of endothelin (ET) receptor‐mediated actin re‐organization of rat cultured astrocytes. Staining of filamentous actin (F‐actin) showed that stress fibers were a prominent cytoskeletal actin structure in protoplasmic astrocytes. A treatment with 0.5 mM dibutyryl cAMP (DBcAMP) caused cytoplasmic retraction and disappearance of stress fibers of astrocytes. A subsequent addition of 1 nM ET‐3 after the DBcAMP treatment expanded the cytoplasm and stimulated stress fiber formation. ET‐1, sarafotoxin S6b, and [Ala 1,3,11,15 ]‐ET‐1 had similar effects. Pre‐treatment with 0.1 μg/ml pertussis toxin (PTX) and chelation of cytosolic Ca 2+ did not affect astrocytic stress fiber formation by ET‐3. ET‐3 stimulated stress fiber formation in stellate astrocytes induced by 50 μM ML‐9, 20 μM W‐7, and 5 μM cytochalasin B (CB). Cytoplasmic microinjection of C 3 ADP‐ribosyltransferase of C. botulinum (C 3 enzyme), which impairs the interaction between rho proteins and the effectors, prevented ET‐3‐induced stress fiber formation and cytoplasmic expansion in DBcAMP‐ and CB‐treated cells. Effects of ET‐1 and sarafotoxin on stress fiber formation were also prevented by C 3 enzyme. On the other hand, injection of C 3 enzyme did not affect increase in cytoplasmic Ca 2+ levels induced by ET‐3. These results suggest that rho proteins are involved in the ET receptor‐mediated actin re‐organization of astrocytes. © 1996 Wiley‐Liss, Inc.