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. 2022 Oct 17;31(6):1688–1704. doi: 10.1016/j.ymthe.2022.10.005

Figure 3.

Figure 3

The cA-circSlc8a1-transgenic mice developed cardiogenic hepatic steatosis

(A) Representative photographs of gross appearance, H&E staining and Oil Red O staining of livers from cA-circSlc8a1 mice at different ages, detecting hepatic steatosis in cA-circSlc8a1(+) mice. (B) The expression levels of cA-circSlc8a1 precursor in the heart and liver of cA-circSlc8a1-transgenic mice, confirming specificity of the heart promoter. n = 8; ∗∗p < 0.01 versus negative heart. (C) A schematic illustration of the interaction of circSlc8a1 probes to circSlc8a1 with or without the presence of cA-circSlc8a1. (D) circSlc8a1 was pulled down significantly less by the circSlc8a1 probe in the heart (left) of cA-circSlc8a1(+) mice (∗∗p < 0.01 versus negative), whereas no difference was observed in the liver (right) of cA-circSlc8a1(+) mice compared with the litter-matched negative mice. n = 16–20.