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1.
Figure 2

Figure 2. Endothelin-1 induced cell constriction in normal CONTROL-1 and IPAH-3 PASMC. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

Cellular constriction was determined as change in cell size measured by impedance as described in Material and Methods. CONTROL-1 and IPAH-3 PASMC were chosen for the assay. RED = no ET-1 added, GREEN = 10 nM ET-1 stimulated, BLUE = 10 nM ET-1 + 1 uM BQ123 added.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
2.
Figure 4

Figure 4. ETA and ETB receptor sites per cell in control and PAH PASMC. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

The receptor sites per cell were determined as described in the Material and Methods. The ratio of ETA/ETB is presented as a line graph. * p < 0.05 compared with the ETA sites per cell in CONTROL-1 PASMC. # p < 0.05 compared with the ETB sites per cell in CONTROL-1 PASMC.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
3.
Figure 6

Figure 6. Effect of BQ123 on ERK activation in CHO cells stably transfected with ETA or ETB or both receptors. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

The CHO cells expressing either ETA or ETB receptors were treated with 10 nM ET-1 with or without 1 mM BQ123 or 0.5 mM BQ788 for 5 minutes. After incubation the cell lysates were isolated and analyzed by western blot. GAPDH was used as a loading control.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
4.
Figure 3

Figure 3. mRNA levels of endothelin receptor type A (ETA) and type B (ETB) in the normal control and PAH PASMC. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

Results are presented as relative expression normalized to GAPDH and were calculated using the ΔΔCt method. The mRNA level from CONTROL-1 samples was set as 1. * p < 0.05 compared with the ETA expression level of CONTROL-1. # p < 0.05 compared with ETB expression level from CONTROL-1 PASMC.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
5.
Figure 5

Figure 5. Effect of BQ123 and BQ788 on calcium influx in CHO cells transfected with ETA or ETB receptors. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

Calcium ion mobilization was measured as described in Materials and Methods. The ET1 induced calcium influx was normalized as 100. The effect of the BQ123 or BQ788 was represented as the percent of ET-1 induced calcium influx. Three separate experiments showed similar results. * p < 0.05 compared with ET-1 stimulated calcium influx.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
6.

Figure 1. ET-1 induced Ca2+ mobilization in the PASMC from normal control, hPAH and iPAH subjects. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

A) The dose-response curves of ET-1 induced calcium mobilization were measured in the normal control, hPAH and iPAH PASMC as described in Materials and Methods. B) The maximal response of ET-1 induced Ca2+ influx was calculated with SigmaPlot 11 software. * The maximal Ca2+ response was significantly stronger in all the PASMC from hPAH or iPAH subjects compared with normal control cells (p < 0.05). There are no significant differences in maximal Ca2+ response among PASMC from hPAH and iPAH patients.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
7.

Figure 8. ERK and Akt activation in the human PASMC. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

A. Human PASMC from control and PAH subjects were incubated with or without 10 nM ET-1 for 5 minutes with or without 1 uM BQ123. After incubation, the cytosolic extracts were isolated and analyzed by Western blot. GAPDH was used as a loading control. B. The quantitation of the p-Akt is illustrated as a bar graph which shows fold change in spot intensity of the bands normalized with GAPDH with basal level as 1. * p< 0.05 compared with WT. C. The quantitation of the p-ERK is illustrated as a bar graph using the same procedure as previously described.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.
8.

Figure 7. ET-1 mediated phosphorylation events in CONTROL-1 and HPAH-1 PASMC. From: Altered Expression and Signal Transduction of Endothelin-1 Receptors in Heritable and Idiopathic Pulmonary Arterial Hypertension.

The human phospho-antibody array detected phosphorylated proteins in untreated and treated cell lysates from donor control CONTROL-1 (A) and BMPR2 deletion HPAH-1 PASMC (B). The cells were either left untreated or treated with 10 nM ET-1 for 5 minutes with or without 1 uM BQ123. Profiles were created by quantifying the mean spot pixel densities normalized by positive control dots. Array signals from scanned X-ray film images were analyzed using image analysis software NIH ImageJ. The effect of ET-1 or ET1 + BQ123 was presented as fold change compared with the basal level of untreated sample. Only the targets with the fold change greater than 1.5 or less than 0.67 upon ET-1 stimulation were presented. The statistical analysis was performed using t-test. * p < 0.05 compared with untreated basal.

Jun Yu, et al. J Cell Physiol. 2013 February;228(2):322-329.

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