Figure 8.

Impact of hyaluronidase activity on pulmonary artery smooth muscle cell proliferation. (A) Effect of a competitive pan-hyaluronidase inhibitor, poly-(4-styrenesulfonate)[PSS], on hypoxanthine/xanthine oxidase-induced HPASMC proliferation. (B) Dose-dependent effect of PSS on normoxic and hypoxic (1% O₂) HPASMC proliferation. (C) Zymographic degradation assay for hyaluronidase activity in HPASMCs supplemented with bovine erythrocyte SOD, cultured in normoxia vs 1% O₂ for 72 hours. (D) Effect of low-dose hyaluronidase (4 × 10⁻⁶ units) on HPASMC proliferation. (E) Proliferation of HPASMCs in response to three molecular weight species of HA in the high (average MW 1500 kD), intermediate (150 kD), and low (10 kD) mass ranges. (F) Proliferation of HPASMCs in response to replacement of growth medium with three progressive gradations (25%/50%, 50%/50%, and 75%/25%) of high vs intermediate-low molecular weight HA. All experiments were conducted with 3–5 unique primary cell lines. Data are normalized within each individual cell line and represented as mean ± SEM *p < 0.05 **p < 0.01 by 2-way ANOVA (multiple comparisons) or 2-sided paired t-test (D).