SM22α Loss Contributes to Apoptosis of Vascular Smooth Muscle Cells via Macrophage-Derived circRasGEF1B

Figure 2

SM22α loss contributes to interaction of VSMCs with macrophages via expression of VCAM-1. (a) Relative quantification for RAW264.7 cell migration induced by the CM from WT and Sm22α^-/- VSMCs treated with (+) or without (-) Ang II. (b) The fluorescent intensity quantification of calcein-AM-labeled RAW264.7 cell adhesion to WT or Sm22α^-/- VSMCs. (c) qRT-PCR of the mRNA of TNF-α, MCP-1, IL-6, and IL-1β in RAW264.7 cells stimulated by CM from WT or Sm22α^-/- VSMCs. (d) The relative number of RAW264.7 cell adhesion to Ad-vector- or Ad-SM22α-infected Sm22α^-/- VSMCs. (e) Relative quantification for RAW264.7 cell migration induced by the CM from Ad-vector- or Ad-SM22α-infected Sm22α^-/- VSMCs. (f) qRT-PCR of the mRNA of TNF-α, MCP-1, IL-6, and IL-1β in RAW264.7 cells stimulated by CM from Ad-vector- or Ad-SM22α-infected Sm22α^-/- VSMCs. (g) Western blot analysis of differentially expressed adhesion molecules in CM from WT or Sm22α^-/- VSMCs. (h, i) The fluorescent intensity quantification of calcein-AM-labeled RAW264.7 cell adhesion to Sm22α^-/- VSMCs transfected with si-VCAM-1 (h) or preincubated with IgG or VCAM-1 neutralizing antibody (i). Data are presented as of three independent experiments. , , and .

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