Beyond the t-test: statistical equivalence testing.
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Data Interpretation, Statistical↗
Biomedical subjects
Feng Ye
Publications and source records attributed to Feng Ye.
Novel cyclopentane dicarboxamide sodium channel blockers as a potential treatment for chronic pain.
A series of new voltage-gated sodium channel blockers were prepared based on the screening lead succinic diamide BPBTS. Replacement of the succinimide linker with the more rigid cyclic 1,2-trans-diamide linker was well tolerated. N-Methylation on the biphenylsulfonamide side of the amide moiety significantly reduced the clearance rate in rat pharmacokinetic studies.
Administration, Oral↗
Expression of ST13 in colorectal cancer and adjacent normal tissues.
AIM: To investigate the in situ expression of suppression of tumorigenecity 13 (ST13) mRNA in both colorectal cancer and adjacent normal tissues. METHODS: Colorectal cancer cell lines SW1116, SW620 and CoLo205 were enrolled to confirm the feasibility of the in situ hybridization procedure. Seven colorectal cancer and adjacent normal tissues were included for RNA-RNA in situ hybridization. RESULTS: The expression of ST13 in the seven normal colon tissues was positive and the positive signals appeared in mucosal cells. Only three of the seven colorectal cancer tissues had positive hybridization signals that appeared in adenocarcinoma cells. CONCLUSION: The expression of ST13 decreases in colorectal cancer tissue compared with that in adjacent normal tissue. ST13 is mostly expressed in colorectal epithelia and adenocarcinoma cells.
Adenocarcinoma↗
Interactions of sympathetic nerves with capsaicin-sensitive sensory nerves: neurogenic mechanisms for phenol-induced hypertension in the rat.
BACKGROUND: Previous investigations have shown that norepinephrine is capable of inhibiting neurotransmission in capsaicin-sensitive sensory nerves via a prejunctional mechanism. The alteration in the activity of sympathetic or capsaicin-sensitive sensory nerves in the development of phenol-induced hypertension was observed separately in rats. METHODS: In the present study, we examined interactions of adrenergic nerves with capsaicin-sensitive sensory nerves in phenol-induced hypertensive rats. Blood pressure, the synthesis and release of calcitonin gene-related peptide (CGRP) and the content of nerve growth factor in (NGF) arteries were determined. RESULTS: Intrarenal injection of phenol caused a permanent elevation of blood pressure concomitantly with a decrease in the concentration of CGRP in plasma, the content of CGRP in dorsal root ganglia and the density of CGRP-containing nerves in the mesenteric artery, and vascular NGF content. Chronic treatment with prazosin (an alpha1-adrenoreceptor antagonist, 3 mg/kg per day) failed to alter the synthesis and release of CGRP and vascular NGF content, even though it completely normalized blood pressure. However, treatment with yohimbine (an alpha2-adrenoreceptor antagonist, 5 mg/kg per day) significantly increased CGRP level and vascular NGF content. Combined administration of prazosin and yohimbine not only significantly elevated the synthesis and release of CGRP and arterial NGF content, but also completely normalized blood pressure. CONCLUSION: These results indicate that the decreased production and release of CGRP and reduced vascular NGF content are attributed to the activation of alpha2-adrenoreceptors in phenol-induced hypertensive rats.
Animals↗
[Effect of high salt diet on expression of osteopontin mRNA in Sprague-Dawley rat kidney].
OBJECTIVE: To investigate the effect of high-salt diet on the expression of osteopontin (OPN) mRNA and its protein in Sprague-Dawley rat kidney. METHODS: Forty-eight male SD rats aged 10 weeks receiving normal salt diet were enrolled in study, and were divided into two groups and fed with high salt diet (4%NaCl) or normal salt diet (0.6%NaCl) for 12 weeks respectively, with 24 rats in each group. Tail systolic blood pressure and bodyweight were measured in all rats every week. At the end of 4th, 8th and 12th week, 6 rats in each group were sacrificed for detection of the expression of OPN mRNA and its protein in the kidney with quantitatine real-time (QRT)-PCR and immunohistochemistry, respectively. RESULTS: No significant difference was found in blood pressure, bodyweight and kidney weight/bodyweight between high-salt diet group and normal salt diet group (P>0.05). The expression of OPN mRNA (0.27+/-0.16 vs 0.15+/-0.13, P<0.05) and its protein (0.78+/-0.15 vs 0.61+/-0.11, P<0.01) in SD rat kidney with high-salt diet were up-regulated at the end of 12th week compared with the rats with normal salt diet. CONCLUSIONS: High-salt diet increase the expression of OPN mRNA and its protein in SD rat kidney. Renal injury induced by high salt intake might be independent of blood pressure change.
Animals↗
[Effects of high salt diet on blood pressure, renal morphology and osteopontin expression in Sprague-Dawley rat with Ang II-induced renal injury].
OBJECTIVE: To investigate the effect of high-salt diet on blood pressure, renal morphology and osteopontin (OPN) expression in Sprague-Dawley rat with Ang II-induced renal injury. METHODS: Thirty-six male SD rats aged 12 weeks receiving normal salt diet were rolled in the study, and received Ang II (100 ng.kg-1.min-1) for two weeks using subcutaneous minipump. Rats were then fed high sodium (n=18, 4% NaCl) or normal sodium (n=18, 0.6% NaCl) diet from third week respectively and lasted for 12 weeks. Eighteen rats in the control were sham-operated and fed normal sodium diet. Tail systolic blood pressure (SBP) was determined every two weeks. Expressions of TGF-beta1 OPN mRNA and its protein in SD rat kidney were measured with quantitative RT-PCR and immunohistochemistry respectively at the end of Ang II infusion and at the end of the experiment. Renal ultrastructure was observed by electronmicroscopy. RESULTS: SBP of the rats received Ang II increased significantly compared with controls (P?0.05). SBP returned to normal after Ang II infusion stopped. No significant difference existed in blood pressure between rats fed high salt diet and normal salt diet in the period of 12 weeks (P<0.05). Expressions of TGF-beta1, OPN mRNA and its protein in the kidney of the rats fed with high salt diet were up-regulated at the end of Ang II infusion (P>0.05) and at the end of the 12th week compared with the rats fed normal salt diet and controls (P<0.01). The kidney was damaged by Ang II, which was further aggravated by the infusion of high salt diet. CONCLUSIONS: High salt diet could aggravate the renal injury of the rats with Ang II-induced renal injury that may be independent of blood pressure change. Expressions of the TGF-beta1, OPN mRNA and its protein were up-regulated after renal injury.
Angiotensin II↗
Delayed preconditioning by cardiac ischemia involves endogenous calcitonin gene-related peptide via the nitric oxide pathway.
Previous investigations have shown separately that calcitonin gene-related peptide (CGRP) or nitric oxide (NO) is involved in mediation of ischemic preconditioning. In the present study, we tested interactions of CGRP with NO in mediation of delayed preconditioning. In Sprague-Dawley rats, ischemia-reperfusion injury was induced by 45-min occlusion followed by 3-h reperfusion of coronary artery, and preconditioning was induced by four cycles of 3-min ischemia and 5-min reperfusion. Infarct size, plasma creatine kinase activity, the plasma level of NO and CGRP, and the expression of CGRP mRNA in dorsal root ganglion were measured. Pretreatment with preconditioning significantly reduced infarct size and the release of creatine kinase during reperfusion, and caused a significant increase in the expression of CGRP mRNA, concomitantly with an elevation in the plasma level of CGRP and NO. The effects of preconditioning were completely abolished by administration of L-nitroarginine methyl ester (L-NAME, 10 mg/kg, i.p.), an inhibitor of NO synthase. Pretreatment with capsaicin (50 mg/kg, s.c.), which depletes transmitters in capsaicin-sensitive sensory nerves, also blocked the cardioprotection of preconditioning and reduced the synthesis and release of CGRP, but did not affect the concentration of NO. The present results suggest the delayed protection afforded by ischemic preconditioning is also mediated by endogenous CGRP via the NO pathway in rat heart.
Animals↗
Role of calcitonin gene-related peptide in the phenol-induced neurogenic hypertension in rats.
Previous investigations have demonstrated that capsaicin-sensitive sensory nerves are involved in the development of hypertension in some rat models of hypertension. To determine the role played by calcitonin gene-related peptide (CGRP; the predominant neurotransmitter in capsaicin-sensitive sensory nerves) in a rat model of neurogenic hypertension, in which hypertension was induced by injecting 50 microl of 10% phenol in the lower pole of the left kidney, systolic blood pressure (SBP) was monitored by the tail-cuff method throughout the experiment. Fifteen days after injection of phenol, mean arterial pressure (MAP), concentrations of CGRP in the plasma, the expression of CGRP mRNA in dorsal root ganglia (DRG) and CGRP content in laminae I and II of the spinal cord were measured. SBP was significantly increased 5 days after the intrarenal injection of phenol (164+/-7 mm Hg, p<0.01). At the end of experiment, blood pressure (BP) was significantly elevated in the phenol-injected rats compared with the controls (SBP: 187+/-6 vs. 122+/-4 mm Hg, p<0.01; MAP: 157.56+/-3.02 vs. 103.80+/-2.04 mm Hg, p<0.01). Treatment with capsaicin, which selectively depletes neurotransmitters from the capsaicin-sensitive nerves, failed to enhance the development of hypertensive responses to the intrarenal injection of phenol. Intravenous administration of CGRP(8-37), the specific CGRP receptor antagonist, also failed to increase the already elevated MAP. The expression of CGRP mRNA (both alpha- and beta-CGRP isoforms), the content of CGRP in laminae I and II of the dorsal horn of the spinal cord and the concentration of CGRP in the plasma was decreased in the rats treated with phenol. These results suggest that CGRP does not play a counterregulatory role in the phenol-induced hypertensive rats, and support the hypothesis that reduction of CGRP (alpha and beta isoforms) could contribute to a blood pressure elevation in this setting.
Animals↗
Effect of calcitonin gene-related peptide on angiotensin II-induced proliferation of rat vascular smooth muscle cells.
The present study was designed to examine the effect of calcitonin gene-related peptide (CGRP) on angiotensin II-induced proliferation of cultured rat vascular smooth muscle cells. Vascular smooth muscle cells were grown from explants of Sprague-Dawley rat aorta. Vascular smooth muscle cells (between passages 5 and 10) were incubated with 0.1% neonatal calf serum for 48 h, and then treated with angiotensin II (100 nM) in the absence or presence of CGRP for 24 h. The viability, DNA synthesis and cell cycle of vascular smooth muscle cells were measured. Western blotting was used to determine the activity of intracellular extracellular regulated kinase (ERK1/2). Angiotensin II significantly decreased the viability and proliferation of vascular smooth muscle cells, decreased the proliferation index, and increased the activity of ERK1/2; the effects of angiotensin II were inhibited by CGRP (1-100 nM) in a concentration-dependent manner. In conclusion, CGRP significantly inhibits angiotensin II-induced proliferation of vascular smooth muscle cells, an effect related to a decrease in the activation of mitogen-activated protein kinase pathway.
Angiotensin II↗
Self-diffusion in liquid interfaces.
For studying self-diffusion in liquid interfaces, 59Fe tracer diffusion was measured on ultrafine-grained Nd2Fe14B which undergoes an intergranular melting transition for low Nd excess. The diffusion coefficient in the intergranular liquid layers is found to be lower than in bulk melts indicating a hampered atomic mobility due to confinement. Well above the intergranular melting transition, the diffusivity in the liquid interfaces approaches a value characteristic for bulk melts.
Journal Article↗
Vascular endothelial growth factor (VEGF) and ovarian carcinoma cell supernatant activate signal transducers and activators of transcription (STATs) via VEGF receptor-2 (KDR) in human hemopoietic progenitor cells.
OBJECTIVE: To investigate the STATs signaling pathway activated by VEGF in human hemopoietic progenitor cells. METHODS: CD34(+) hemopoietic progenitor cells, which isolated from umbilical cord blood, were treated with VEGF or culture supernatant of ovarian carcinoma cell line which could secrete large amount of VEGF, phosphorylation and nuclear translocation of STAT3 and STAT5 were then detected by Western Blot and immunocytochemistry. Expression of VEGFR2/KDR on CD34(+) cells was studied by immunocytochemistry. The specific VEGFR2/KDR heptapeptide antagonist ATWLPPR was used to identify whether the activation of STATs signaling pathway was specifically mediated by VEGFR2/KDR. RESULTS: The concentration of VEGF in SKOV3-supernatant was 4024.84+/- 505.59 pg/ml. CD34(+) progenitor cells could express VEGFR2/KDR. When CD34(+) cells were stimulated by VEGF and SKOV3-supernatant, STAT3 appeared tyrosine-phosphorylation and nuclear translocation, but STAT5 was only phosphorylated, and not translocated. When ATWLPPR was used to block the binding of VEGF to KDR, VEGF and the SKOV3-supernatant failed to activate the phosphorylation of STAT3 and STAT5. CONCLUSIONS: STAT3 may participate in the signal transduction pathways activated by VEGF specifically mediated by VEGFR2/KDR in human hemopoietic progenitor cells, and the aforementioned signaling pathway participated in the interaction of ovarian carcinoma cells and progenitor cells.
Active Transport, Cell Nucleus↗
Protective effects of evodiamine on myocardial ischemia-reperfusion injury in rats.
Previous investigations have indicated that the pharmacological activities of evodiamine, a major alkaloidal component of the dried, unripe fruit of Evodia rutaecarpa Bentham (Rutaceae), are associated with the stimulation of calcitonin gene-related peptide (CGRP) release and that CGRP protects the myocardium against ischemia-reperfusion injury. In the present study, we have examined whether evodiamine protects against myocardial ischemia-reperfusion injury in rats and whether the protective effects of evodiamine are related to the activation of capsaicin-sensitive sensory nerves. Rats were pretreated with evodiamine 10 min before the experiment, and then the left main coronary artery of rat hearts was subjected to 60 min occlusion followed by 180 min reperfusion. Infarct size, the activity of serum creatine kinase, serum concentrations of TNF-alpha and plasma concentrations of CGRP were measured. Pretreatment with evodiamine (30 or 60 microg/kg, i.v.) markedly increased the content of CGRP in plasma concomitantly with a significant reduction in infarct size, the activity of serum creatine kinase, and TNF-alpha level, and the effects of evodiamine were completely abolished by capsazepine (5.0 mg/kg, s.c.), a competitive vanilloid receptor antagonist. These results suggest that evodiamine exerts a protection against myocardial ischemia-reperfusion injury in rats and that the protective effects of evodiamine are related to stimulation of CGRP release via activation of vanilloid receptors.
Animals↗
Stimulation of calcitonin gene-related peptide synthesis and release: mechanisms for a novel antihypertensive drug, rutaecarpine.
BACKGROUND: Previous investigations have demonstrated that capsaicin-sensitive primary sensory nerves play an important role in modulation of the peripheral resistance of the circulation system. The vanilloid receptor subtype 1 (VR1) is expressed almost exclusively in the primary sensory nerves and cell bodies of these sensory neurons. Rutaecarpine (Rut) can relax vascular smooth muscle via stimulation of calcitonin gene-related peptide (CGRP) release by activation of VR1. METHODS: In the present study, we examined the depressor effect of Rut and the possible mechanisms in the phenol-induced hypertensive rats, in which hypertension was induced by injecting 50 microl of 10% phenol in the lower pole of the left kidney. RESULTS: Acute administration of Rut (30, 100 or 300 microg/kg, i.v.) caused a depressor effect concomitantly with an increase in the plasma concentration of CGRP in a dose-dependent manner, which was blocked by capsaicin (used to deplete the CGRP from sensory nerves) or capsazepine (a competitive VR1 antagonist), causing an approximately 85% and approximately 80% change in mean arterial pressure, respectively, and by either of them, causing an approximately 90% elevation of plasma CGRP. In the chronic study, Rut at a dose of 3 or 6 mg/kg per day significantly lowered tail-cuff systolic blood pressure to 159 +/- 8 and 136 +/- 10 mmHg, respectively, compared with hypertensive rats (179 +/- 8 mmHg), and caused a sustained hypotensive effect from day 6 on. Pretreatment with capsaicin blocked the depressor effect of Rut by approximately 65%. Treatment with Rut significantly increased the synthesis and release of CGRP, as shown by the increase in the levels of CGRP mRNA and peptide in the dorsal root ganglia, the density of CGRP immunoreactive nerve fibers in the mesenteric artery, the CGRP content in the spinal cord and the plasma concentration of CGRP, which was markedly attenuated by pretreatment with capsaicin. CONCLUSION: These results suggest, for the first time, that the hypotensive effect of Rut is mediated by stimulation of CGRP synthesis and release via activation of VR1 in the phenol-induced hypertensive rat.
Alkaloids↗
[Minilaparotomy approach for curative resection of colorectal cancer].
OBJECTIVE: To evaluate the feasibility and safety of a minilaparotomy approach for curative resection of colorectal cancer in comparison with the conventional laparotomy. METHODS: Seventy-eight patients underwent radical resection for rectal cancer with minilaparotomy during April 2001 to December 2002. The minilaparotomy involved complete resection and a skin incision 2 cm above the link line of left anterior superior iliac spine to pubic symphysis and was about 7-10 cm in length. Another 86 patients who served as control group underwent a similar resection with a conventional laparotomy during the same period. RESULT: The minilaparotomy approach was successful in all 78 patients. The general status of patients, operative types and histopathological features of tumor were similar in the two groups (P>0.05). Operative blood loss in control group was greater (P<0.001), whereas incision length in minilaparotomy group was significantly shorter than that in conventional laparotomy (9.38 cm compared with 17.32 cm). The operative time, analgesia requirement, first passing flatus,first oral fluids and postoperative hospital stay were significantly shorter in the minilaparotomy group (P<0. 001). In an average 25.4-month follow-up, there were no tumor recurrences in the minilaparotomy group. CONCLUSION: A minilaparotomy approach for curative resection of rectal cancer may be an ideal alternative approach to conventional laparotomy.
Adult↗
[Activation of signal transducers and activators of transcription induced by vascular endothelial growth factor in CD34+ hematopoietic progenitor cells in vitro].
OBJECTIVE: To investigate the activation pattern of signal transducers and activators of transcription (STAT) induced by vascular endothelial growth factor (VEGF) in CD34+ hematopoietic progenitor cells, and gain an insight into the molecular mechanism and signal transduction pathway of VEGF that has an effect on CD34+ hematopoietic progenitor cells. METHODS: After isolated from umbilical cord blood by using a high-gradient magnetically activated cell sorting system (MACS), CD34+ cells were stimulated by VEGF (50 ng/ml) for different time (0, 15, 30, 45, 60, 90 min) to detect the tyrosine phosphorylation and nuclear translocation of STAT-3 and STAT-5 with Western blot and immunocytochemistry methods. The expression of VEGF receptor-2 (VEGFR2) on the membrane of CD34+ progenitor cells was examined by immunocytochemistry. ATWLPPR, an effective peptide screened from phage epitope library by affinity for membrane-expressed VEGFR2 and blocking the binding of VEGF to VEGFR2, was used to determine whether the activation of STAT pathway induced by VEGF was blocked. RESULTS: Tyrosine phosphorylation of STAT-3 and STAT-5 was undetectable in unstimulated CD34+ cells, but was evident at 15 min in response to VEGF stimulation. VEGF resulted in a rapid and transient tyrosine phosphorylation of STAT-3 and STAT-5. The maximal tyrosine phosphorylation was catched at 30 and 45 min, respectively (P = 0.0001), and returned to basal levels at 90 min. Immunocytochemistry confirmed that increased phosphorylated STAT-3 was translocated into the nuclei at 30 min (P = 0.0001), and mainly in cytoplasms again at 90 min after stimulation with VEGF. However, compared with unstimulated CD34+ cells, there was only increased phosphorylation of STAT-5 appeared mainly in cytoplasms, but no significant nuclear translocation was found after stimulation with VEGF (P > 0.05). The presence of VEGFR2 was confirmed using anti-VEGFR2 antibody staining by immunocytochemistry, moreover, the phosphorylation of STAT-3 and STAT-5 failed to be activated by the co-culture with ATWLPPR and VEGF, suggesting that activation of the STAT pathway be specifically mediated by VEGFR2 in CD34+ progenitor cells. CONCLUSIONS: STAT signaling pathway participates in the signal transduction of VEGF via VEGFR2 in CD34+ hemopoietic progenitor cells.
Adult↗
[Phosphorylation of signal transducer and activators of transcription 3 induced by vascular endothelial growth factor in ovarian carcinoma cell line in vitro].
OBJECTIVE: To observe phosphorylation of signal transducer and activators of transcription 3 (STAT3) in Caov-3 induced by vascular endothelial growth factor (VEGF), and to investigate molecular mechanisms of the effect of VEGF on ovarian carcinoma cells. METHODS: The expressions of phosphorylated STAT3 in Caov-3 induced by VEGF were detected by immunocytochemistry and Western blot methods. Furthermore, the relationship between STAT3 phosphorylation and VEGF stimulation in ovarian carcinoma cells was investigated using a peptide which could specifically bind VEGFR2 and thus block the binding of VEGF to its receptors. RESULTS: With VEGF stimulation, the expressions of phosphorylated STAT3 were significantly higher than those without VEGF stimulation in Caov-3. And 50 ng/ml was the effective dose resulting in a significant increase of phosphorylated STAT3 (2.20 +/- 0.28/1.37 +/- 0.17) compared to 0 ng/ml (0.56 +/- 0.15/0.47 +/- 0.19) (P < 0.001). Translocation into nuclei of activated STAT3 occurred after 30 min, while STAT3 phosphorylation decreased after 60 min of stimulation (0.95 +/- 0.18/0.66 +/- 0.20). A small peptide specific for VEGFR2, blocked the increase of STAT3 phosphorylation induced by VEGF in a dose dependent manner and 80 micro mol/L was the effective dose (P < 0.001). CONCLUSIONS: VEGF could induce STAT3 phosphorylation and translocation into nuclei of activated STAT3 in Caov-3, and the small peptide could effectively inhibit these effects of VEGF. It suggests that STAT3 participates in the VEGF signal transduction mediated by VEGFR2 in ovarian carcinoma cells.
Acute-Phase Proteins↗
Aspirin protected against endothelial damage induced by LDL: role of endogenous NO synthase inhibitors in rats.
AIM: To study the protective effect of aspirin on damages of the endothelium induced by low-density lipoprotein (LDL), and whether the protective effect of aspirin is related to reduction of nitric oxide synthase inhibitor level. METHODS: Vascular endothelial injury was induced by a single injection of native LDL (4 mg/kg) in rats. Vasodilator responses to acetylcholine (ACh) in the isolated aortic rings were determined, and serum concentrations of asymmetric dimethylarginine (ADMA), malondialdehyde (MDA), tumour necrosis factor-alpha (TNF-alpha), and the activity of dimethylaminohydrolase (DDAH) were measured. RESULTS: A single injection of LDL (4 mg/kg) significantly decreased vasodilator responses to ACh, increased the serum level of ADMA, MDA, and TNF-alpha, and decreased DDAH activity. Aspirin (30 or 100 mg/kg) markedly reduced the inhibition of vasodilator responses to ACh by LDL, and the protective effect of aspirin at the lower dose was greater compared with high-dose aspirin group. Aspirin inhibited the increased level of MDA and TNF-alpha induced by LDL. Aspirin at the dose of 30 mg/kg, but not at higher dose (100 mg/kg), significantly reduced the concentration of ADMA and increased the activity of DDAH. CONCLUSION: Aspirin at the lower dose (30 mg/kg) protects the endothelium against damages elicited by LDL in vivo, and the protective effect of aspirin on endothelium is related to reduction of ADMA concentration by increasing DDAH activity.
Amidohydrolases↗
[Effects of vascular endothelial growth factor on differentiation and function of dendritic cells generated from CD34+ hematopoietic progenitor cells in vitro].
OBJECTIVE: To investigate the effects of vascular endothelial growth factor (VEGF) on differentiation and function of dendritic cells derived from CD34+ hematopoietic progenitor cells. METHODS: After isolation from umbilical cord blood with a high-gradient magnetic cell sorting system (MACS), the CD34+ cells were cultured with a cocktail cytokines for differentiating into dendritic cells (DC). The cells were stimulated by VEGF (25 ng/ml) either at the beginning or at day 9 of culture. Kinetics analysis of cell proliferation was performed during the process of cell culture, and the expression of DC differentiation antigens including CD1alpha, CD83, CD80, CD54 and HLA-DR was examined by flow cytometry. DC function was evaluated by the ability to induce proliferation of allogeneic T cells in mixed lymphocyte reaction (MLR) assay, and the production of IL-12 by ELISA. RESULTS: VEGF added at day 1 of culture induced an increase of total cell numbers by (1.51 +/- 0.23)-folds (P = 0.001). VEGF added at the initial but not the late stage of culture could dramatically down-regulate the expression of CD1a [(33.00 +/- 2.12)% vs (81.20 +/- 6.93)%], CD83 [(42.23 +/- 1.15)% vs (87.98 +/- 7.97)%], CD80 (42.93 +/- 1.32)% vs (94.53 +/- 0.87)%], and HLA-DR [(37.93 +/- 5.30)% vs (74.15 +/- 3.74)%], while obviously up-regulate the expression of CD14. Moreover, the inhibitory effect of VEGF on DC function was confirmed by a reduced ability to induce proliferation of allogeneic T cells and production of IL-12 (P < 0.01). CONCLUSIONS: VEGF could induce the expansion of hematopoietic progenitor cells and inhibit at the early stage their differentiation into mature DC.
Antigens, CD↗