Figure 6
Figure 6. In mouse primary hepatocytes, deficiency of both ActR2a and BMPR2 markedly decreased basal hepcidin mRNA levels and blocked the ability of BMP6 to induce hepcidin gene expression. Hepatocytes were isolated from livers of ActR2a+/+;Bmpr2fl/fl, ActR2a+/+;Bmpr2fl/fl;Alb-Cre, ActR2a−/−;Bmpr2fl/fl, and ActR2a−/−;Bmpr2fl/fl;Alb-Cre mice. Two days later, cells were incubated without or with BMP6 (10 ng/ml) for 4 hours. RNA was extracted to measure the expression of the genes encoding ActR2a (A), BMPR2 (B), and hepcidin (C, with a logarithmic y-axis). ANOVAs P < .002; *P < .03 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl mice, not stimulated with BMP6; §P < .003 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl;Alb-Cre mice, not stimulated with BMP6; #P < .03 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl mice, stimulated with BMP6; †P < .001 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl;Alb-Cre mice, stimulated with BMP6.

In mouse primary hepatocytes, deficiency of both ActR2a and BMPR2 markedly decreased basal hepcidin mRNA levels and blocked the ability of BMP6 to induce hepcidin gene expression. Hepatocytes were isolated from livers of ActR2a+/+;Bmpr2fl/fl, ActR2a+/+;Bmpr2fl/fl;Alb-Cre, ActR2a−/−;Bmpr2fl/fl, and ActR2a−/−;Bmpr2fl/fl;Alb-Cre mice. Two days later, cells were incubated without or with BMP6 (10 ng/ml) for 4 hours. RNA was extracted to measure the expression of the genes encoding ActR2a (A), BMPR2 (B), and hepcidin (C, with a logarithmic y-axis). ANOVAs P < .002; *P < .03 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl mice, not stimulated with BMP6; §P < .003 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl;Alb-Cre mice, not stimulated with BMP6; #P < .03 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl mice, stimulated with BMP6; P < .001 vs hepatocytes from ActR2a+/+;Bmpr2fl/fl;Alb-Cre mice, stimulated with BMP6.

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