ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of tumor necrosis factor-alpha(TNF-alpha) on syndecan-4 protein expression and proliferation of cultured human umbilical vein endothelial-like cells (HUVECs) in vitro.</p><p><b>METHODS</b>HUVECs exposed to different concentrations of TNF-alpha(100, 20, 10, and 1 ng/ml) were cultured for 24 h and 36 h to observe their proliferation in comparison with the control group. The cell proliferation rate was determined by non-radioactive MTS/PES assay. The expression of syndecan-4 protein was evaluated by immunoblotting technique using anti-syndecan-4 antibody. Results The proliferation rate of the endothelial-like cells was 1.956-/+0.214 in the control group, and 2.154-/+0.250, 2.260-/+0.151, 2.118-/+0.205 and 2.106-/+0.136 in TNF-alpha-treated groups corresponding to TNF-alpha concentrations of 100, 20, 10 and 1 ng/ml at 24 h, respectively. It was shown that TNF-alpha significantly stimulated cell proliferation at the concentration above 1 ng/ml (P<0.05) as compared with the control group (P<0.05). The proliferation rate of the endothelial-like cell was 1.915-/+0.236 in the control group, and 2.067-/+0.328, 2.207-/+0.150, 2.052-/+0.126 and 2.051-/+0.180 in TNF-alpha-treated groups corresponding to TNF-alphaconcentrations of 100, 20, 10 and 1 ng/ml at 36 h, respectively. The expression of syndecan-4 protein was significantly enhanced by TNF-alpha.</p><p><b>CONCLUSIONS</b>TNF-alpha can stimulate HUVEC proliferation, and expression of syndean-4 may represent an additional component of the pro-inflammatory, growth-stimulating pathways that are activated in response to changes in the vascular wall.</p>
Subject(s)
Humans , Cell Proliferation , Cells, Cultured , Endothelial Cells , Metabolism , Syndecan-4 , Metabolism , Tumor Necrosis Factor-alpha , Pharmacology , Umbilical Veins , Cell BiologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes and the effects of captopril on the renal blood flow and microvascular perfusion in dogs with acute cardiac insufficiency.</p><p><b>METHODS</b>Acute cardial insufficiency was induced by combining occlusion of the left anterior descending artery with right ventricular pacing in 12 mongrel dogs. The ascending aorta and left kidney were dissected and ultrasonic flow probes were placed on ascending aorta and renal artery to monitor cardiac output (CO) and renal blood flow (RBF). Contrast-enhanced ultrasound of the kidney was performed as CO was reduced to 25% (LCO25%) and 50% (LCO50%) from the basic measurement and microvascular flow velocity (beta), microvascular volume (A) and microvascular blood flow (renal cortex) were observed. After CO reduced to 50%, captopril 1 mg/kg and 2 mg/kg were injected successively and contrast-enhanced ultrasound of the kidney were performed again before and after injection.</p><p><b>RESULTS</b>At baseline, CO, RBF, CXbeta (beta of renal cortex), A and A x beta were (1.46 +/- 0.16) ml/min, (107.5 +/- 35.7) ml/min, 1.39 +/- 0.14, 120.3 +/- 14.8 and 167.4 +/- 25.0, respectively. After the LCO25% was reached, RAF, CXbeta, A and A x beta decreased to (72.50 +/- 32.4) ml/min, 0.87 +/- 0.082, 117.6 +/- 13.1, and 102.6 +/- 15.5, respectively. The corresponding values after the LCO50% was reached were (44.1 +/- 17.2) ml/min, 0.61 +/- 0.039, 106.9 +/- 12.0, and 64.7 +/- 8.83, respectively. It is suggested that the volume of the renal microvasculature remained stable until the LCO50% was reached. When captopril 1 mg/kg and 2 mg/kg were injected successively at LCO50%, MAP decreased from (85.4 +/- 7.8) mm Hg to (78.7 +/- 7.3) mm Hg and to (69.1 +/- 6.3) mm Hg (P < 0.05), respectively, while CO increased from 0.73 +/- 0.084 to 0.83 +/- 0.065 and to 0.9 +/- 0.054 (P < 0.05), respectively. RBF increased from (44.1 +/- 17.2) ml/min to 60.3 +/- 17.8 and to 79.4 +/- 17.8 (P < 0.05), respectively. After captopril 1 mg/kg and 2 mg/kg were injected, the increased flow ratios with CO were 0.15 +/- 0.084 and 0.31 +/- 0.011, respectively, and with RBF were 0.29 +/- 089 and 0.522 +/- 0.040, respectively. The increased renal blood flow ratio was higher than that of CO after captopril was used. The corresponding increases were from 0.61 +/- 0.039 to 0.75 +/- 0.020 and to 0.86 +/- 0.027 for CX beta, from 106.9 +/- 11.9 to 115.4 +/- 11.1 and to 116.6 +/- 8.9 for A, from 64.7 +/- 8.83 to 87.0 +/- 8.6 and to 100.6 +/- 8.9 for A x beta, respectively.</p><p><b>CONCLUSION</b>The renal microvasculature plays a role by keeping its volume stable in the protection against renal ischemia when acute cardiac output decreases slightly. The role of captopril to improve renal microvascular perfusion is independent of increased total cardiac output or increased systemic blood pressure.</p>