Figure 6

Albumin stimulates an increase in the release of tissue inhibitor of metalloproteinase (TIMP)-1 in the conditioned media by astrocytes. (a) Astrocytes exposed to BSA had a time-dependent increase in TIMP-1. (b) Levels of TIMP-1 in astrocytes treated with albumin in the presence (+) or absence (−) of the TGF-β receptor I inhibitor SB431542. (c) Levels in astrocytes treated with albumin in the presence of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 (SB), the extracellular signal regulated protein kinase (ERK) pathway inhibitor PD98059 (PD), and the c-Jun N-terminal kinase (JNK) inhibitor SP600125 (SP). (d) Levels in astrocytes treated with albumin in the presence (+) or absence (−) of SIS3, the Smad pathway inhibitor. (e) Levels of TIMP-1 in astrocytes treated with albumin in the presence (+) or absence (−) of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) or (f) the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI). Data are representative of mean ± SEM of 3–4 independent experiments, and are expressed (B-F) as a percentage of the value of the BSA-treated group. **P < 0.01 compared with control-treated group. *P < 0.05 compared with BSA-treated group.