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. 2016 Jun 29;7:12120. doi: 10.1038/ncomms12120

Figure 4. DCM in MLP knockout mice is prevented in the absence of CARP1 or CARP2.

Figure 4

(a) Expression levels of CARP1, MLP and GAPDH as control in total heart extracts of WT, MLP knockout, CARP1 knockout and CARP1-MLP double knockout (CMP1) mice. (b) Cardiac morphology of WT, MLP, CARP1, CARP2 or CARP3 knockouts, as well as CARP1-MLP (CMP1), CARP2-MLP (CMP2) and CARP3-MLP (CMP3) double knockouts. Hematoxylin-eosin stained frozen heart sections are shown. Scale bar=2 mm. (c) Analysis of cardiac function using M-mode transthoracic echocardiography and representative M-mode images of hearts from WT, MLP, CARP1, CMP1, CARP2, CMP2, CARP3 and CMP3 animals. (d) Immunofluorescence staining of frozen heart sections from adult WT, MLP knockout and CMP1 double knockout animals stained with antibodies against CARP1 (green in overlay, top two panels) and CARP2 (green in overlay, bottom two panels). Arrowheads indicate ID and arrows show Z-disc localization, respectively. (e) Frozen sections of adult WT, CARP1, MLP knockout and CMP1 hearts stained with antibodies against PLCβ1 and PKCα (all green; see Supplementary Fig. 2h,i for quantification of PKCα localization at ID). (d,e) Plakoglobin and α-actinin were used as counterstains (red and blue in overlay, respectively). Scale bars=10 μm. (f) Immunoblot for PLCβ1, phospho-PKCα/βII (T638/641), and PKCα in WT, CARP1 knockout, MLP knockout and CMP1 double knockout total heart extracts. GAPDH was used as a loading control.