Skip to main content
. 2021 Jan 1;11(6):2706–2721. doi: 10.7150/thno.48679

Figure 5.

Figure 5

Pharmacological and genetic inhibition of JMJD3 upregulates TGFβ1 and Smad3 and downregulates Smad7 in the kidney following SNx. (A) The kidney tissue lysates from non-surgical (Sham) and remnant kidneys after surgery (SNx) with and without administration of GSKJ4 were subjected to immunoblot analysis with specific antibodies to TGFβ1, p-Smad3, Smad3, Smad7, DNMT1 or β-actin. Expression levels of TGFβ1 (B), p-Smad3 (C), Smad3 (D), Smad7 (E), and DNMT1 (F) were quantified by densitometry analysis and then normalized with β-actin. (G) Foxd1-cre-:JMJD3fl/fl (JMJD3-WT) and Foxd1-cre+:JMJD3fl/fl (JMJD3-KO) mice were left to shamed operation or subjected to SNx and sacrificed 8 weeks after operations; the whole kidney tissue lysates were subjected to immunoblot analysis with specific antibodies against TGFβ1, p-Smad3, Smad3, Smad7, DNMT1 or β-actin. Expression levels of TGFβ1, p-Smad3, Smad3, Smad7, DNMT1 or β-actin were quantified by densitometry analysis. p-Smad3 was normalized with Smad3 (I); TGFβ1 (H), Smad3 (J), Smad7 (K), DNMT1 (L) was normalized with β-actin. Values are the means ± sem of 6 samples. *P < 0.05; **P < 0.01.