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Donghua Xie

Publications and source records attributed to Donghua Xie.

4 recordsLinked to original sources

An engineered vascular endothelial growth factor-activating transcription factor induces therapeutic angiogenesis in ApoE knockout mice with hindlimb ischemia.

OBJECTIVE: Angiogenesis is the growth and proliferation of blood vessels from existing vascular structures, and therapeutic angiogenesis seeks to promote blood vessel growth to improve tissue perfusion. Vascular endothelial growth factor (VEGF) is a prototypic angiogenic agent that exists in vivo in multiple isoforms, and studies with VEGF to date had used single isoform therapy with disappointing results. We tested plasmid and adenoviral vectors encoding a zinc-finger DNA-binding transcription factor (ZFP-32E) that was designed to increase the expression of all major VEGF isoforms in a preclinical model of peripheral arterial obstructive disease (PAOD) in hypercholesterolemic (ApoE knock-out) mice. METHODS: Unilateral femoral artery ligation/excision was performed in 117 mice. At 7 days postoperatively, the ischemic tibialis anterior (TA) and gastrocnemius (GAS) muscles received either ZFP-32E treatment (125 microg of plasmid, 2.5 x 10(11) viral particle units [vpu] of adenovirus; some mice received a second plasmid injection 3 days later) or no-ZFP treatment (125 microg of beta-galactosidase [beta-gal], a plasmid-lacking insert, or an equal dose of adenoviral encoding beta-gal; some mice received a second plasmid injection 3 days later). Group 1 mice (n = 31) were euthanized 3 days later, and VEGF messenger RNA (mRNA) and protein levels were measured. Group 2 mice (n = 38) were euthanized 7 days later, and measures of capillary density, cell proliferation, and apoptosis were quantified. Group 3 mice (n = 48) were euthanized 28 days later, and changes in lower limb blood flow perfusion were measured. RESULTS: In group 1, VEGF mRNA and protein levels were significantly higher in those with ZFP-32E treatment vs beta-gal. In group 2, capillary density and proliferating cells were significantly greater and apoptosis was significantly lower in those with ZFP-32E treatment vs beta-gal. Finally, in group 3, changes in the perfusion ratio (ischemic/nonischemic limb) at 21 days after injection were significantly greater in those with ZFP-32E treatment vs no-ZFP treatment. CONCLUSION: The ability of this engineered zinc-finger VEGF-activating transcription factor to induce therapeutic angiogenesis in hypercholesterolemic mice suggests this approach warrants investigation as a novel approach to treat PAOD.

Adenoviridae↗

Intracavernosal basic fibroblast growth factor improves vasoreactivity in the hypercholesterolemic rabbit.

PURPOSE: We determined the effects of intracavernosal injection (ICI) of recombinant basic fibroblast growth factor (rbFGF) on corporal tissue in hypercholesterolemic rabbits. METHODS: Twenty New Zealand White rabbits were fed a 1% cholesterol diet for 6 weeks and were randomly divided into four groups. Group 1 (N = 5) received an ICI of phosphate buffered saline solution (PBS) once and again 3 weeks later. Group 2 (N = 4) received an ICI of 2.5 microg rbFGF once and PBS 3 weeks later. Group 3 (N = 6) received an ICI of 2.5 microg rbFGF once and again 3 weeks later. Group 4 (N = 5) received an ICI of 2.5 microg rbFGF once. All animals were maintained on the high cholesterol diet until sacrifice, 3 weeks after last injection. Strips of corporal tissue were submaximally contracted with norepinephrine, and dose-response curves were generated to evaluate endothelial-dependent (acetylcholine, ACH) and endothelial-independent (sodium nitroprusside, SNP) vasoreactivity. Protein levels of bFGF and vascular endothelial growth factor (VEGF) were assessed by enzyme-linked immunosorbent assay. Neuronal nitric oxide synthase (nNOS) protein and mRNA were detected by Western blot and semi-quantitative polymerase chain reaction, respectively. RESULTS: Vasoreactivity was improved by bFGF treatment as shown by higher ED50[-log(M)] of ACH and SNP in Groups 2, 3, and 4. The expression of bFGF protein, VEGF protein, nNOS protein, and mRNA were all increased after bFGF treatment. CONCLUSIONS: ICI of bFGF improved vasoreactivity in hypercholesterolemic rabbit corporal tissue, offering a new direction to explore for the treatment of erectile dysfunction.

Animals↗

Decreases in corporeal vascular endothelial growth factor expression precede vasoreactivity changes in cholesterol fed rabbits.

PURPOSE: We determined temporal changes in vasoreactivity and angiogenic growth factor levels in corporeal tissue at varying time points after the induction of hypercholesterolemia in rabbits. MATERIALS AND METHODS: A total of 42 New Zealand White rabbits were fed a 1% cholesterol (8 per group) or normal (6 per group) diet for 2, 4.5 or 7.5 weeks. Vascular endothelial growth factor (VEGF) mRNA expression in corpus cavernosum was assessed by real-time polymerase chain reaction analyses for the 3 isoforms VEGF121, VEGF165 and VEGF189. Isometric tension studies were performed and dose response curves were generated to evaluate endothelial dependent and endothelial independent vasoreactivity. RESULTS: Real-time polymerase chain reaction analysis showed 2.2 to 2.5 and 1.5 to 2.7-fold decreases in VEGF121 and VEGF165, respectively, in the corporeal tissues of the high cholesterol group vs the normal diet group at the 2 week time point. At 2 weeks VEGF189 was unchanged but it was decreased 1.5 to 2-fold at 4.5 weeks. Acetylcholine isometric tension studies revealed no difference in mean ED50 (-log [M]) +/- SD until 7.5 weeks of high cholesterol diet (5.10 +/- 0.64 vs 3.95 +/- 1.35, p = 0.0269). The response to sodium nitroprusside was not statistically different at any time point. Endothelial cell and smooth muscle content were decreased for the high cholesterol vs normal diet at 4.5 weeks (endothelial only) and 7.5 weeks (each cell). CONCLUSIONS: Alterations in corporeal tissue levels of VEGF occur before abnormalities in vasoreactivity. The results suggest that VEGF has a role in normal vasoreactivity in corporeal tissue and, thereby, in normal erectile function.

Acetylcholine↗

Cholesterol feeding reduces vascular endothelial growth factor signaling in rabbit corporal tissues.

PURPOSE: Hypercholesterolemia is a major risk factor for erectile dysfunction (ED), but the mechanisms are not completely understood. Vascular endothelial growth factor (VEGF) is reduced in rabbit corporal tissue with cholesterol feeding. VEGF signaling leads to the phosphorylation of Akt and endothelial nitric oxide synthase (p-Akt and p-eNOS). MATERIAL AND METHODS: New Zealand White rabbits (n = 50) were fed a 1% cholesterol (n = 8, 8, 8, 4) or normal (n = 6, 6, 6, 4) diet for 2, 4.5, 7.5, and 12 weeks. Akt, p-Akt, and p-Akt/Akt were measured by enzyme-linked immunosorbent assay. Levels of eNOS, p-eNOS, and neuronal and inducible nitric oxide synthase (nNOS and iNOS) mRNA and protein were assessed by polymerase chain reaction and Western analysis. RESULTS: Cholesterol feeding was associated with a significant decrease in p-Akt/Akt 2.16-fold (P < 0.05), 3.28-fold (P < 0.02), and 3.42-fold (P < 0.02) at 4.5, 7.5, and 12 weeks, respectively. The reduction in p-Akt/Akt with the cholesterol diet at 2 weeks was not significantly different, but the correlation between the duration of cholesterol feeding and the reduction in p-Akt/Akt was high (r( 2) = 0.858). eNOS protein or mRNA did not change with cholesterol feeding, but p-eNOS was significantly decreased at 4.5 weeks and all subsequent time points. nNOS mRNA and protein levels were decreased at 4.5 weeks and all subsequent time points, while iNOS was not different between groups. CONCLUSIONS: Hypercholesterolemia results in decreased VEGF signaling and decreased levels of the active form of eNOS in corporal tissue. Levels of nNOS were reduced by a different mechanism. VEGF signaling may provide a target to modulate ED.

Animals↗