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. Author manuscript; available in PMC: 2010 Nov 6.
Published in final edited form as: Circ Res. 2009 Sep 24;105(10):984–993. doi: 10.1161/CIRCRESAHA.109.199489

Figure 2. Targeted tissue-specific deletion of dystroglycan gene expression in cardiac and smooth muscle.

Figure 2

A) Immunostaining with an antibody against beta-dystroglycan Double arrows indicate smooth muscle in coronary vessels. Single arrows indicate cardiac myocytes expressing residual beta-DG. In MLC2vcre- L/L mice, the field shown was specifically chosen to show the residual positive cells while most fields were negative for dystroglycan expression. In SMMHCcre- L/L mice dystroglycan expression was not detected in smooth muscle. A very small portion of cardiac myocytes also showed gene targeting, most likely due to the transient expression of smooth muscle markers in cardiac myocytes during development, although most fields analyzed showed normal dystroglycan expression in all cardiac myocytes B) Analysis of dystroglycan, dystrophin (dystr), dysferlin (dysf), sarcoglycan (β-SG) and integrin (itg) protein expression in MLC2vcre-L/L ventricular myocardium compared to littermate L/L (WT) mice. Each lane represents ventricular muscle from a different animal. C) Immunofluorescence localization of dystrophin is retained at the plasma membrane of cardiac myocytes in MLC2vcre-L/L mice despite loss of dystroglycan expression, while alpha-sarcoglycan expression is reduced. Samples in A-C were from mice age 14-20 weeks.