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. 2016 Apr 21;1(5):e85923. doi: 10.1172/jci.insight.85923

Figure 8. GSK3β knockdown prevents loss of junctional signal of ID proteins in ACM neonatal rat ventricular myocytes.

Figure 8

(A) GSK3β knockdown was confirmed via Western immunoblots in GSK3β shRNA–transfected neonatal rat ventricular myocytes (NRVMs) compared with untransfected controls. Cotransfected NRVM lysates probed for changes in plakoglobin (PLK), connexin43 (Cx43), and GSK3α/β, normalized to GAPDH. Immunoblots are representative of n = 3/cohort. (B) Representative images of untransfected controls and GSK3β shRNA–transfected NRVMs. Note that GSK3β shRNA–transfected NRVMs display control-like PLK and Cx43 distribution. Images are representative of n = 3/cohort. (C) Mutant ACM expressing NRVMs displayed increased nuclear PLK localization and near absent Cx43 signal. Cotransfected NRVMs (ACM expressing construct and GSK3β shRNA transgene) immunostained for changes in PLK and Cx43 distribution. Note that abnormal PLK and Cx43 localization was prevented in cotransfected NRVMs, and Cx43 signal was increased compared with ACM myocytes without GSK3β shRNA construct (white arrows, junctional signal; yellow arrowheads, nuclear localization). Scale bar: 50 μm. Images are representative of n = 3/cohort.