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. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2010 Jan 7;30(4):694–701. doi: 10.1161/ATVBAHA.109.200741

Figure 4. Smooth muscle lacking CRP1 expresses markers indicative of normal smooth muscle differentiation.

Figure 4

(A) Western blot to detect protein expression in smooth muscle tissues of wild-type, Csrp1-null and Csrp2-null mice. An equivalent amount of each tissue extract was added per lane. Protein levels were examined by immunoblotting with antibodies against smooth muscle α-actin (α-actin), smooth muscle myosin heavy chain (MHC), vinculin, and tubulin (as a loading control). Blots were also probed with antibodies specific for CRP1, CRP2, and CRP3 to confirm genotypes and demonstrate lack of upregulation other family members in the null mice. (B) Csrp2−/− VSMCs do not upregulate a SMA-luciferase reporter in response to TGF-beta. Values are mean ± SEM of 3 experiments. *p<0.05, compared to no TGF-beta control. (C) Quantitative RT-PCR analysis of SM α-actin in WT, Csrp1−/− or Csrp2−/− VSMCs in response to TFG-beta stimulation. *p<0.05, compared to no TGF-beta control.