Journal: BioMed Research International

Article Title: PPAR δ Agonist GW501516 Inhibits PDGF-Stimulated Pulmonary Arterial Smooth Muscle Cell Function Related to Pathological Vascular Remodeling

doi: 10.1155/2013/903947

Figure Lengend Snippet: Expression patterns of PPAR isoforms in human pulmonary vascular cells. (a) Expression of PPAR δ or PPAR γ is higher in HPASMCs compared with HPAECs. Results were similar in three independent experiments. (b) PPAR α mRNA level in HPASMCs was set to 100.0. Other mRNA levels were expressed relative to this value. Experiments were performed in triplicate and repeated a minimum of three times. # P < 0.01, * P < 0.05 versus PPAR α .

Article Snippet: The human pulmonary arterial smooth muscle cells (HPASMCs) and human pulmonary arterial endothelial cells (HPAECs) were purchased from Lonza.

Techniques: Expressing

Journal: BioMed Research International

Article Title: PPAR δ Agonist GW501516 Inhibits PDGF-Stimulated Pulmonary Arterial Smooth Muscle Cell Function Related to Pathological Vascular Remodeling

doi: 10.1155/2013/903947

Figure Lengend Snippet: PDGF upregulates PPAR δ expression in a time- and dose-dependent manner. HPASMCs were made quiescent for 24 h and then treated with PDGF with increasing concentrations of PDGF for 24 h to study the effect of dose (a, b) or treated with PDGF (10 ng/mL) to study the effect of time, as indicated (c, d). The results were quantified by densitometry and normalized with respect to β -action; the control was set to 1.0. Results are expressed as the means ± SD of at least three independent experiments. * P < 0.01 versus control nontreated cells; † P < 0.05 versus control nontreated cells.

Article Snippet: The human pulmonary arterial smooth muscle cells (HPASMCs) and human pulmonary arterial endothelial cells (HPAECs) were purchased from Lonza.

Techniques: Expressing, Control

Journal: BioMed Research International

Article Title: PPAR δ Agonist GW501516 Inhibits PDGF-Stimulated Pulmonary Arterial Smooth Muscle Cell Function Related to Pathological Vascular Remodeling

doi: 10.1155/2013/903947

Figure Lengend Snippet: Effects of GW501516 on cell proliferation and expression of multiple cell cycle regulatory genes in HPASMCs. (a) HAPSMCs were pretreated with GW501516 (GW, 3 μ M) for 6 h prior to 36 h of PDGF-BB treatment (PDGF, 10 ng/mL). DNA synthesis was measured by BrdU incorporation assay. (b) mRNA levels of multiple cell cycle regulatory genes were determined in HPASMCs. Experiments were performed in triplicate and repeated a minimum of three times. # P < 0.01, † P < 0.05 versus control; * P < 0.05 versus PDGF-treated cells.

Article Snippet: The human pulmonary arterial smooth muscle cells (HPASMCs) and human pulmonary arterial endothelial cells (HPAECs) were purchased from Lonza.

Techniques: Expressing, DNA Synthesis, BrdU Incorporation Assay, Control

Journal: BioMed Research International

Article Title: PPAR δ Agonist GW501516 Inhibits PDGF-Stimulated Pulmonary Arterial Smooth Muscle Cell Function Related to Pathological Vascular Remodeling

doi: 10.1155/2013/903947

Figure Lengend Snippet: Regulation of migration, collagen synthesis, and MCP-1 expression in HPASMCs by GW501516. PDGF-stimulated (a) cell migration, (b) collagen synthesis, and (c) TNF-induced MCP-1 mRNA expression were significantly inhibited by GW501516. Experiments were performed in triplicate and repeated a minimum of three times. # P < 0.01, † P < 0.05 versus control; * P < 0.05 versus PDGF/TNF-treated cells.

Article Snippet: The human pulmonary arterial smooth muscle cells (HPASMCs) and human pulmonary arterial endothelial cells (HPAECs) were purchased from Lonza.

Techniques: Migration, Expressing, Control

Journal: Circulation

Article Title: Aberrant Chloride Intracellular Channel 4 Expression Contributes to Endothelial Dysfunction in Pulmonary Arterial Hypertension

doi: 10.1161/CIRCULATIONAHA.113.006797

Figure Lengend Snippet: Effects of CLIC4 expression on HPAEC metabolic activity, cell survival and angiogenesis. (A) Cell metabolic activity under normoxic and hypoxic conditions and following overexpression of CLIC4, scrambled shRNA (shRNA control) or CLIC4 shRNA, as indicated; MTS reduction assay. (B) HPAEC viability in cells cultured in full media, treated with apoptosis-inducer, menadione (6 hr, 10 μM) or serum-starved for 48 hr. The cells were overexpressing CLIC4 or CLIC4 and CLIC4 shRNA, as indicated. (C) Changes in total endothelial tube length (expressed as % of normoxic control) in cells treated, as indicated. (D) Representative images showing the effects AdCLIC4 and AdCLIC4 shRNA on tube formation in normoxic and hypoxic HPAECs. Bar=500 μm. In (A–C) each bar represents mean±SEM; (n=4–5). *P<0.05, **P<0.01, ***P<0.001, compared with normoxic control (A–C) or non-starved control (B); ###P<0.001, compared with hypoxic AdControl (A, C). Comparisons between AdCLIC4 and AdCLIC4 + CLIC4 shRNA groups are also indicated.

Article Snippet: Human pulmonary arterial endothelial cell (HPAEC) and smooth muscle cell (HPASMC) culture HPAECs were cultured in endothelial growth medium-2 (Promocell) while HPASMCs were cultured in smooth muscle cell growth medium-2 (Promocell).

Techniques: Expressing, Activity Assay, Over Expression, shRNA, Cell Culture

Journal: Circulation

Article Title: Aberrant Chloride Intracellular Channel 4 Expression Contributes to Endothelial Dysfunction in Pulmonary Arterial Hypertension

doi: 10.1161/CIRCULATIONAHA.113.006797

Figure Lengend Snippet: The effect of CLIC4 on HIF-dependent protein expression and tube formation in HPAECs. Production of (A) ET-1 and (B) VEGF in normoxic and hypoxic HPAECs overexpressing CLIC4 or CLIC4 shRNA (n=3–5). (C) HPAEC tube formation following siRNA-mediated HIF-1α knockdown in cells treated, as indicated (n=5). Each bar represents mean±SEM. *P<0.05; **P<0.01, ***P<0.001 compared with normoxic AdControl; ##P<0.01, ###P<0.001 compared with hypoxic AdControl. Comparisons between AdCLIC4 and CLIC4 shRNA or between scrambled siRNA and HIF-1α siRNA groups are also indicated.

Article Snippet: Human pulmonary arterial endothelial cell (HPAEC) and smooth muscle cell (HPASMC) culture HPAECs were cultured in endothelial growth medium-2 (Promocell) while HPASMCs were cultured in smooth muscle cell growth medium-2 (Promocell).

Techniques: Expressing, shRNA

Journal: BioMed Research International

Article Title: PPAR δ Agonist GW501516 Inhibits PDGF-Stimulated Pulmonary Arterial Smooth Muscle Cell Function Related to Pathological Vascular Remodeling

doi: 10.1155/2013/903947

Figure Lengend Snippet: Expression patterns of PPAR isoforms in human pulmonary vascular cells. (a) Expression of PPAR δ or PPAR γ is higher in HPASMCs compared with HPAECs. Results were similar in three independent experiments. (b) PPAR α mRNA level in HPASMCs was set to 100.0. Other mRNA levels were expressed relative to this value. Experiments were performed in triplicate and repeated a minimum of three times. # P < 0.01, * P < 0.05 versus PPAR α .

Article Snippet: The human pulmonary arterial smooth muscle cells (HPASMCs) and human pulmonary arterial endothelial cells (HPAECs) were purchased from Lonza.

Techniques: Expressing