We investigated the structural proteins in the compensatory hypertrophied myocardium (remodeling) after myocardial infarction. We made myocardial infarction (M) by ligating the left coronary artery in SD rats and sham operated rats (C). We kept them for 3 weeks and 6 weeks. We analyzed noninfarcted left ventricular myocardium qualitatively and quantitatively by two-dimensional electrophoresis. The contents of desmin and actin increased in M compared with C after 6 week. Particularly, we measured the dephosphorylated desmin. Dephosphorylated desmin increased in M after 3 week and, more over, dephosphorylated desmin increased in M after 6 week. Desmin, one of the intermediate filaments, connects actin filaments and contacts myofibrils to nuclear and cell membrane. Dephosphorylation of desmin forms desmin filaments. We thought desmin initially changed qualitatively and, thereafter, increased quantitatively. Therefore, desmin plays a role as maintaining cell structure against volume overload. In conclusion, desmin participated in LV remodeling.
View full abstract