KIS protects against adverse vascular remodeling by opposing stathmin-mediated VSMC migration in mice
J. Clin. Invest. 118:12 doi:10.1172/JCI33206 [Go to this article.]

Figure 7
Increased stathmin expression in KIS^–/– VSMCs.

(A) Quantitative analysis of 4 independent Western blots demonstrated increased cytoplasmic stathmin protein concentrations normalized to GAPDH in KIS^–/– VSMCs serum starved and released for the indicated times. n = 4. (B) Representative Western blot of stathmin expression in KIS^+/+ and KIS^–/– VSMCs corresponding to quantitative data in A. GAPDH served as loading control. (C and D) Stathmin (C) and p27^Kip1 (D) immunohistochemistry demonstrated a higher abundance of stathmin and p27^Kip1 7 and 14 days after vascular injury in vessels of KIS^–/– mice than in KIS^+/+ mice. Arrows denote internal elastica. (E) Movat pentachrome staining revealed increased accumulation of glycosaminoglycans 14 days after injury in the neointima of KIS^–/– mice compared with KIS^+/+ mice (arrow indicates green staining), whereas there was no difference in extracellular matrix accumulation or composition between the genotypes 7 days after injury. Original magnification, ×400. *P < 0.05 vs. KIS^+/+.