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Small G‐protein Rho is involved in the maintenance of cardiac myocyte morphology
Author(s) -
Grounds Haslett R.,
Ng Dominic C.H.,
Bogoyevitch Marie A.
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20441
Subject(s) - myocyte , rhoa , cardiac myocyte , microbiology and biotechnology , biology , medicine , cell , gq alpha subunit , endocrinology , signal transduction , g protein , biochemistry
The use of small membrane‐permeable sequences or protein transduction domains (PTDs) can facilitate the transport of proteins into many cell types. In preliminary studies with the application of three PTDs (penetratin, modified penetratin, and the HIV TAT transduction domains) to cardiac myocytes, we found that the TAT and penetratin sequences showed high efficiency of uptake and low toxicity. Rho has been previously shown to be an important regulator of cytoskeletal organization and morphology in other non‐cardiac cell types. To evaluate a role for Rho in cardiac myocyte morphology, we used the TAT‐PTD to deliver a RhoA‐specific inhibitor, the C3 exoenzyme, to cultured cardiac myocytes. We showed that this incubation with TAT‐C3 abolished the basal levels of RhoA activity, demonstrating the efficacy of this treatment. Incubation with TAT‐C3 also altered cardiac myocyte morphology so that TAT‐C3‐treated cells produced multiple projections from the major cell body. This was accompanied by a statistically significant increase in cell size, albeit to a lesser extent than the changes accompanying exposure to the hypertrophic agent, endothelin‐1. Furthermore, the change in size of TAT‐C3‐treated cells was not accompanied by the induction of atrial natriuretic factor (ANF) expression that accompanies the hypertrophy of cardiac myocytes. These results reveal a role for RhoA in the maintenance of normal myocyte morphology. © 2005 Wiley‐Liss, Inc.