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PubMed2003

[High-dose external ionizing radiation prevents intimal hyperplasia and limits secretion of growth factors PDGFbb, bFGF, and TGFb1. Experiments and results].

PURPOSE: To evaluate the ionizing radiation for intimal hyperplasia prevention and to assess the production of growth factors. METHODS: An oversized injury using an embolectomy catheter was performed on a rabbit distal aorta (N=23), associated (test group; N=12) or not (control group; N=11) with a post-operative external radiation (25 Gy). At t=45 days, histological studies and morphometric studies were performed on the aorta. Smooth muscular cells and endothelial cells were stained using immuno-histologic revelation. Immuno-histological analysis was performed on arteries for growth factors PDGFbb, bFGF and TGFb1. RESULTS: Twenty-one animals survived the procedure, 11 were in the test group and 10 in the control group. Intimal thickness and ratio intima/media were significantly lower after radiation (respectively p=0.008, p=0.008). There was no difference for the medial thickness (p=0.155). Immuno-histochemical positive staining for PDGF and TGFb1 was lower after radiation (respectively 18.44 +/- 2.963% versus 47.64 +/- 6.86%, p<0.001 and 10.11 +/- 3.18% versus 29.45 +/- 4.156%, p<0.001). There was no difference for the expression of bFGF growth factor. After radiation, the media was found to be reduced and replaced by interstitial fibrosis. CONCLUSION: After external radiation the thickness parameter of the intima and the ratio intima/media decreased significantly in comparison with the control group. PDGF and TGFb1 were also less expressed in the artery irradiated. Fibrosis recasting needs to be confirmed by further investigation.

Animals↗
PubMedDate not supplied

Alginate for endovascular treatment of aneurysms and local growth factor delivery.

BACKGROUND AND PURPOSE: Coil embolization is safe and effective but may be followed by aneurysm recurrence. Our purpose was to explore the use of alginate as a new embolic agent that could deliver growth factors and improve results of endovascular treatment of aneurysms. METHODS: We first assessed the potential of alginate as a vector for growth factor delivery by using in vitro binding and elution studies. Lateral wall (n = 68) and bifurcation (n = 4) aneurysms were then constructed in six pigs and 36 dogs. We explored iodine-125 transforming growth factor-beta(1) in vivo alginate delivery in 16 canine aneurysms. We next assessed the effects of adding alginate to gelatin sponges on angiographic and pathologic results at 3 weeks (n = 4 each) in an established model used for the study of recanalization and recurrence. We then explored techniques to control endovascular alginate delivery without protection (n = 4), with the protection of a balloon (n = 4), and with the protection of a single coil (n = 12) at the aneurysm neck in 12 porcine aneurysms, four canine lateral wall aneurysms, and four canine bifurcation aneurysms. The stability of cross-linked alginate was studied after intraoperative injections in eight aneurysms. Finally, to determine the value of the material with or without growth factor in promoting aneurysm healing, we compared angiographic results and neointima formation 3 weeks after intraoperative embolization of canine lateral wall aneurysms with alginate blocks with or without platelet-derived growth factor-BB or transforming growth factor-beta(1) (n = 5 each). RESULTS: Growth factors rapidly eluted from alginate in vitro and in vivo. Alginate coating of sponges led to improved angiographic results and thick neointima formation. Intraoperative alginate block embolization did not lead to recurrence, and growth factors delivered with alginate did not show added benefits. Endovascular alginate embolization was complicated by carotid emboli, and the polymer was unstable once injected, causing delayed neurologic deficits. CONCLUSION: Growth factor delivery can be performed with alginate, but formulation changes and improved endovascular control are necessary before contemplating its use in intracranial aneurysms.

Alginates↗
PubMed2003

Periodontal regeneration in human Class II furcations using purified recombinant human platelet-derived growth factor-BB (rhPDGF-BB) with bone allograft.

This human clinical trial evaluated the clinical and histologic response to recombinant human platelet-derived growth factor-BB (rhPDGF-BB) delivered in bone allograft for the treatment of advanced Class II furcation defects. Three mandibular and one maxillary molar furcation defects were treated: Two received 0.5 mg/mL and two received 1.0 mg/mL rhPDGF-BB, in all cases mixed with DFDBA. Clinical probing depths and attachment levels were obtained presurgically and 9 months postsurgical, after which the teeth and surrounding tissues were removed en bloc. Both concentrations of rhPDGF-BB resulted in substantially improved horizontal (mean 3.5 mm) and vertical (mean 4.25 mm) probing depths and attachment levels (mean 3.75 mm). Histologic evaluation revealed periodontal regeneration, including new bone, cementum, and periodontal ligament coronal to the reference notch. Regeneration was also present coronal to the original osseous crest In one case where an enamel projection extended into the fornix of the furcation, new calcified tissue with new inserting connective tissue fibers was observed over the enamel. This study documented the favorable tissue response to rhPDGF-BB treatment at both the clinical and microscopic levels, provided the first human histologic evidence that new calcified tissue with inserting collagen fibers can occur over enamel projections within furcations, and demonstrated for the first time that complete periodontal regeneration can be achieved in advanced Class II furcation defects using a combination of purified recombinant growth factor and bone allograft.

Adult↗
PubMed2003

Proliferative effect of growth factors TGF-beta1, PDGF-BB and rhBMP-2 on human gingival fibroblasts and periodontal ligament cells.

The regeneration of periodontal tissues lost due to periodontal disease requires cell migration, differentiation and proliferation. Several procedures have been proposed to promote wound healing events such as the application of growth factors including PDGF-BB, TGF-beta1 and rhBMP-2. The purpose of this study was to evaluate the mitogenic responses of human periodontal ligament cells and gingival fibroblasts to PDGF-BB, TGF-beta1 and rhBMP-2. Human periodontal ligament cells were isolated from the mid root of three maxillary third molars extracted from three adult patients with moderate periodontitis and gingival fibroblasts were obtained from two patients also affected by moderate periodontitis, who underwent periodontal surgery. Cells were grown in 24-well dishes. On day 2 of quiescence, new medium was added with PDGF-BB or TGF-beta1 or rhBMP-2 at the concentration of 10 ng/ml. To determine the effects of the test agents on cell proliferation, DNA synthesis was estimated by measuring [3H] thymidine incorporation. After 48h of incubation the cells were processed and subject to scintillation counting. Counts per minute (cpm/ well) were determined for each sample. The results of this study demonstrated that PDGF-BB acts like a strong mitogenic agent for human periodontal ligament cells and gingival fibroblasts, TGF-beta1 mostly supports the proliferation of these cells and rhBMP-2 had an opposite effect on cell mitosis.

Adult↗
PubMedDate not supplied

EGFR but not PDGFR-beta expression correlates to the antiproliferative effect of growth factor withdrawal in glioblastoma multiforme cell lines.

BACKGROUND: The aim of the current study was to investigate a putative relationship between (i) growth characteristics (proliferation and tumorigenicity) of nine glioblastoma multiforme (GBM) cell lines under different growth-stimulating conditions in vitro and (ii) their basal expression of a panel of growth factor receptors/autocrine cytokines. MATERIALS AND METHODS: Basal expressions of the epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor-beta (PDGFR-beta), platelet-derived growth factor-AA (PDGF-AA) and PDGF-BB, tumor growth factor-alpha (TGF-alpha) and TGF-beta as well as tumor necrosis factor-alpha (TNF-alpha) were determined by immunocytochemistry at standard cell culture conditions (10% fetal calf serum [FCS]). Proliferation and tumorigenicity at 10% FCS and relative serum starvation (0.5% FCS) were assessed by using Coulter counting and soft agar cloning, respectively. RESULTS: The ratio between cell multiplications at 10% and 0.5% FCS over a 10-day period was defined as a measure of growth factor dependence of cellular proliferation. Expression of EGFR (but not of PDGFR-beta) strongly correlated to this ratio (Spearman rank correlation coefficient R = 0.87). No considerable correlations were present among other appropriate pairs of variables with biologically founded putative relationships. CONCLUSION: Greater expression of EGFR is associated with increased growth factor dependence of cellular proliferation. Our results strengthen the role of EGFR as a rational molecular target of therapeutic intervention in GBM.

Becaplermin↗
PubMed2003

Complementary effects of platelet-derived growth factor autocrine stimulation and p53 or Ink4a-Arf deletion in a mouse glioma model.

INK4a-ARF and p53 inactivation are common but rarely concurrent findings in glioblastoma multiforme. Here we demonstrate that experimental deletion of either tumor suppressor gene cooperates with retrovirally expressed platelet-derived growth factor (PDGF)-B regarding both tumor latency and frequency in a mouse brain tumor model. We find indications of PTEN down-regulation and increased Akt phosphorylation in both types of null tumors (although more prominent in p53-/- tumors) suggesting a possible mechanism for this synergism. This is the first time that the cooperative tumorigenic effects of PDGF-B stimulation and p53 loss of function are demonstrated in an in vivo model, establishing a functional link between two common molecular changes of human secondary glioblastoma multiforme.

Animals↗
PubMed1998

[Growth factor a/b-FGF and PDGF have no effect on development of inflammatory tumor in chronic pancreatitis].

Extensive fibrosis combined with the development of pseudocysts, calcifications and concomittant loss of acinar cells are the characteristic features in the pathogenesis of chronic pancreatitis. In some patients an inflammatory mass is generated which is most frequently located in the pancreatic head. The inflammatory pancreatic head tumor has been postulated to be the pace maker of the course of the disease. Over expression of growth factors (GF) has been discussed to be the molecular basis of focal development of fibrosis. Aim of this study was to correlate the expression of GF-m-RNA (acidic und basic fibroblast growth factor: a/b FGF; plateled derived growth factor: PDGF-A/B) in pancreatic specimens from patients with chronic pancreatitis taken from different parts of the pancreatic gland to the generation of an inflammatory mass in the pancreatic head. Using quantitative PCR, northern blotting and in-situ-hybridisation m-RNA expression of a/b FGF and PDGF-A/B was nearly identical in the pancreatic head, corpus and tail. Furthermore the expression of these GF did not correlate to the development of an inflammatory mass in the pancreatic head. From the results of this study a causal relation between expression of these GF and the development of an inflammatory mass in the pancreatic head could not be confirmed.

Becaplermin↗
PubMed2003

[Experimental study on recombinant human platelet-derived growth factor gel in a diabetic rat model of cutaneous incisal wound healing].

OBJECTIVE: To investigate the effect of recombinant human platelet-derived growth factor (rhPDGF-BB) on cutaneous incisal wound healing in diabetic rats and this factor does-effect relationship. METHODS: Thirty Wistar diabetic rats were used in this study. Four full-thickness skin wounds of 2.54 cm(2) were incised in the back of each rat. The wounds were divided into five groups: three groups were treated with different dosage of rhPDGF-BB gel (14.0 microg/cm(2) wound, 7.0 microg/cm(2) wound, 3.5 microg/cm(2) wound), other two groups were treated with vehicle or untreated, respectively. rhPDGF-BB gel was topically applied to the wounds from 1 to 14 days. The wound healing effect was assessed by the measurements of the wound area, subcutaneous chamber and histological changes of each group. RESULTS: On 14 days, the wounds of the three groups treated with rhPDGF-BB contracted to (0.22+/-0.30)cm(2), (0.05+/-0.06)cm(2), (0.32+/-0.32)cm(2), respectively. The area of the middle dosage groups was significantly smaller than those treated with vehicle 0.23+/-0.22 cm(2) (P<0.05) and untreated (0.22+/-0.25) cm(2) (P<0.05). On 7 days, the subcutaneous chambers of the three treated groups contracted to (0.04+/-0.03)ml, (0.02+/-0.02)ml, (0.06+/-0.03)ml, and there was a statistic significance when comparing middle dosage group with vehicle group (0.06+/-0.03) ml (P<0.05) and untreated group (0.07+/-0.05 ml (P<0.05). As for histological examination, much more granulation formation was shown in the wound bed in middle dosage group than that in other four groups on 7 days, and some of the wounds treated with middle dosage were healing on 14 days. CONCLUSION: It suggested that topical application of rhPDGF-BB might improve wound healing in diabetic rats. The effective dosage of rhPDGF-BB is 7.0 microg/cm(2) wound.

Animals↗
PubMed2003

Inhibition of platelet-derived growth factor receptor phosphorylation by STI571 (Gleevec) reduces growth and metastasis of human pancreatic carcinoma in an orthotopic nude mouse model.

PURPOSE: We evaluated the expression of platelet-derived growth factor (PDGF) ligands and receptors in clinical specimens of human pancreatic adenocarcinomas and determined the therapeutic effect of STI571 (Gleevec), a protein tyrosine kinase inhibitor of PDGF receptor (PDGFR), on human pancreatic carcinoma cells growing in the pancreas and liver of nude mice. EXPERIMENTAL DESIGN: Immunohistochemical staining for PDGF-AA and -BB ligands, PDGFR-alpha and -beta, and phosphorylated PDGFR-alpha and -beta was performed on 31 specimens of human pancreatic cancer and L3.6pl human pancreatic adenocarcinoma cell line. To determine the in vivo effects of STI571, nude mice with L3.6pl cells injected into the pancreas were randomized 7 days later to receive one of the following treatments: sterile water p.o. (control), STI571, gemcitabine, or a combination of STI571 and gemcitabine. RESULTS: In 29 of 31 clinical specimens of human pancreatic adenocarcinoma, both tumor cells and tumor-associated endothelial cells expressed phosphorylated PDGFR-alpha and -beta. L3.6pl cells growing in culture expressed moderate amounts of PDGF-AA and little to no PDGFR-alpha or -beta, whereas L3.6pl cells growing in the pancreas of nude mice expressed a high level of PDGF and receptors. Colocalization immunohistochemical analysis demonstrated expression of activated PDGFR-beta by tumor-associated endothelial cells in both the pancreas and in liver metastases. Tumors of mice treated for 4 weeks with STI571 (50 mg/kg or 100 mg/kg p.o. daily) were slightly smaller than controls. Tumors treated with gemcitabine and STI571 (50 mg/kg) were >70% smaller than tumors in control mice and 36% smaller than those in mice treated with gemcitabine only (P < 0.0002 and P < 0.04, respectively). Combination therapy also inhibited spontaneous metastasis to the liver. Tumors from mice treated with both STI571 and gemcitabine had decreased expression of activated (phosphorylated) PDGFR-alpha and -beta, decreased mean vessel density, decreased cell proliferation, and increased apoptosis of tumor cells. CONCLUSIONS: Collectively, these data show that activated PDGFR on tumor cells and tumor-endothelial cells can be a novel target for therapy of pancreatic carcinoma.

Adenocarcinoma↗
PubMed2004

[Perindopril attenuates the progression of CCl4-inducing rat hepatic fibrosis].

OBJECTIVES: The aim of the present study was to determine the effects of angiotensin-converting enzyme inhibitor, perindopril, on the progression of rat hepatic fibrosis induced by CCl4. METHODS: Male wistar rats weighting about 250g were treated with perindopril (2mg/kg, daily gavage), except for model group and control group. After 4, 6 weeks, morphological examination was based on microscopy. RT-PCR was utilized to detect gene expression of angiotensin II type 1 receptor (AT1 receptor) in the liver. Meanwhile, the protein expressions of AT1 receptor, transforming growth factor beta 1 (TGF-beta1) and platelet-derived growth factor-BB (PDGF-BB) in liver tissue were examined by Western blot. The activity of matrix metalloproteinase-2 (MMP-2) was assessed by zymography. Serum laminin (LN) and hyaluronic acid (HA) were measured using radio-immunity technique. RESULTS: RT-PCR and Western blot revealed that there was a up-regulation in AT1 receptor expression in model group compared with control group. Perindopril treatment significantly reduced mean fibrosis score, messenger RNA and protein levels of AT1 receptor, protein levels of TGF-beta1 and PDGF-BB, Serum levels of HA and LN, and MMP-2 activity. CONCLUSION: These results suggest that angiotensin II may play an important role in fibrosis of liver. Perindopril may have a inhibiting effect on CCl4-induced hepatic fibrogenesis of rat.

Angiotensin II↗
PubMed2004

[Construction and identification of yeast expression vectors containing human platelet-derived growth factor B-chain gene].

OBJECTIVE: To investigate the expression efficiency of human platelet-derived growth factor B-chain (PDGF-B) gene in yeast and assess the activity of the expressed product. METHODS: A full-length complementary DNA of human PDGF-B gene was amplified from the total RNA extracted from human vascular endothelial cells using reverse transcription (RT)-PCR and then cloned into pGEM-T vector. The PCR products with specific primers were recombined into yeast expression plasmids pMETB or pMETalphaA, followed by identification with restriction endonuclease. RESULTS: The 578 bp fragment encoding mature PDGF-BB peptide with signal peptide and the 340 bp fragment without signal peptide were identified and verified by restriction endonuclease mapping and sequencing, and two yeast expression vectors pMETB-PDGFB(1) and pMETalphaA-PDGFB(2) were reconstructed. CONCLUSION: The yeast expression vectors containing human PDGF-B gene have been successfully constructed for further studies of gene expression in yeast.

Becaplermin↗
PubMed2004

[The diagnostic value of eight serum indices for liver fibrosis].

OBJECTIVES: Using receiver operating characteristic (ROC) curve to compare the value of platelet derived growth factor-BB (PDGF-BB), transforming growth factor-beta1 (TGF-beta1), matrix metalloproteinase-1 (MMP-1), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), hyaluronic acid (HA), type III procollagen (PCIII), type IVcollagen (C-IV) and laminin (LN) in serum and message RNA (mRNA) expression of TIMP-1 and MMP-1 in peripheral blood mononucleocytes (PBMC) to diagnose liver fibrosis. METHODS: Serum samples from 60 chronic hepatitis B patients and 20 healthy blood donors were assayed for serum level of PDGF-BB, TGF-beta1, MMP-1 and TIMP-1 with ELISA, and for serum level of HA, PCIII, C-IV and LN, with RIA. The mRNA expression of TIMP-1 and MMP-1 in PBMC was detected by RT-PCR. Liver biopsy was performed in all those patients. The biopsy materials were examined histopathologically. RESULTS: Through the analysis by ROC curve, serum PDGF-BB is the most valuable marker, and its sensitivity was the highest among eight indices. The marker with the highest specificity was TIMP-1 mRNA in PBMCs. The area under the curve (AUC) of PDGF-BB, TIMP-1, HA, PCIII, C-IV, LN, TIMP-1 mRNA was 0.985, 0.726, 0.318, 0.728, 0.727, 0.583, 0.463, 0.876, respectively. The sensitivity and specificity of combination of PDGF-BB and TIMP-1 mRNA were 97.4%, 95.0%, respectively. CONCLUSION: Serum PDGF-BB is the most potential index among eight markers. The combination of serum PDGF-BB and TIMP-1 mRNA in PBMC might be more efficient to screen liver fibrosis.

Adult↗
PubMed2004

Mouse embryonic fibroblasts derived from Odin deficient mice display a hyperproliiferative phenotype.

Odin is a recently identified cytosolic phosphotyrosine binding (PTB) domain containing negative regulatory protein, that was discovered on the basis of its ability to undergo tyrosine phosphorylation upon stimulation by epidermal growth factor in HeLa cells. The protein was originally obtained as a KIAA clone (KIAA 0229) from the Kazusa DNA Research Institute which maintains the HUGE protein database--a database devoted to the analysis of long cDNA clones encoding large proteins (>50 kDa). Odin has been demonstrated to cause downregulation of c-Fos promoter activity and to inhibit PDGF-induced mitogenesis in cell lines. To further investigate the role of Odin in growth factor receptor signaling and to elucidate its biological function in vivo, we have generated mice deficient in Odin by gene targeting. Odin-deficient mice do not display any obvious phenotype, and histological examination of the kidney, lung and liver does not show any major abnormalities as compared to wild-type controls. However, mouse embryonic fibroblasts (MEFs) generated from Odin-deficient mice exhibit a hyperproliferative phenotype compared to wild-type-derived MEFs, consistent with its role as a negative regulator of growth factor receptor signaling. Our results confirm that although Odin expression in mice is not essential for any major developmental pathway, it could play a significant functional role to negatively regulate growth factor receptor signaling pathways.

Adaptor Proteins, Signal Transducing↗
PubMed2004

[Molecular cloning and expression of human PDGF-B chain mature peptide gene].

OBJECTIVE: To acquire sufficient PDGF-BB protein and provide the basis for the further studies of its role on the fracture healing and trauma reconstruction and its clinical applications. METHODS: Constructed the prokaryotic expression vector pQE-PDGF-B with the gene rearrangement technique, and the monomeric form of recombinant PDGF-B expressed in E. coli M15. RESULTS: PDGF-B mature peptide gene was inserted into prokaryotic expression vector pQE30, which was confirmed by PCR, enzyme digestion and sequencing identification; the expressed products of pQE-PDGF-B in E. coli showed a single protein on SDS-PAGE, and their expression level was about 15% of the total bacterial protein. The molecular weight of the purified PDGF-B protein was about 15 KDs on SDS-PAGE. CONCLUSIONS: The construction of recombinant plasmid and preparation of the monomeric protein of PDGF-B provides a solid foundation for further studying the function of PDGF-BB and producing biologically PDGF-BB protein.

Becaplermin↗
PubMed2005

Antiangiogenic and antitumor activity of a selective PDGFR tyrosine kinase inhibitor, CP-673,451.

CP-673,451 is a potent inhibitor of platelet-derived growth factor beta-receptor (PDGFR-beta) kinase- and PDGF-BB-stimulated autophosphorylation of PDGFR-beta in cells (IC(50) = 1 nmol/L) being more than 450-fold selective for PDGFR-beta versus other angiogenic receptors (e.g., vascular endothelial growth factor receptor 2, TIE-2, and fibroblast growth factor receptor 2). Multiple models have been used to evaluate in vivo activity of CP-673,451 and to understand the pharmacology of PDGFR-beta inhibition and the effect on tumor growth. These models include an ex vivo measure of PDGFR-beta phosphorylation in glioblastoma tumors, a sponge model to measure inhibition of angiogenesis, and multiple models of tumor growth inhibition. Inhibition of PDGFR-beta phosphorylation in tumors correlates with plasma and tumor levels of CP-673,451. A dose of 33 mg/kg was adequate to provide >50% inhibition of receptor for 4 hours corresponding to an EC(50) of 120 ng/mL in plasma at C(max). In a sponge angiogenesis model, CP-673,451 inhibited 70% of PDGF-BB-stimulated angiogenesis at a dose of 3 mg/kg (q.d. x 5, p.o., corresponding to 5.5 ng/mL at C(max)). The compound did not inhibit vascular endothelial growth factor- or basic fibroblast growth factor-induced angiogenesis at concentrations which inhibited tumor growth. The antitumor efficacy of CP-673,451 was evaluated in a number of human tumor xenografts grown s.c. in athymic mice, including H460 human lung carcinoma, Colo205 and LS174T human colon carcinomas, and U87MG human glioblastoma multiforme. Once-daily p.o. x 10 days dosing routinely inhibited tumor growth (ED(50) < or = 33 mg/kg). These data show that CP-673,451 is a pharmacologically selective PDGFR inhibitor, inhibits tumor PDGFR-beta phosphorylation, selectively inhibits PDGF-BB-stimulated angiogenesis in vivo, and causes significant tumor growth inhibition in multiple human xenograft models.

Angiogenesis Inhibitors↗
PubMed2005

Coexpression of angiogenic factors in brain arteriovenous malformations.

OBJECTIVE: Brain arteriovenous malformations (BAVMs) are structurally unstable blood vessels that display an angiogenic phenotype, possibly maintained by concerted effects of key angiogenic factors. Therefore, we hypothesized that there are close correlations among key angiogenic factors in BAVMs and that levels of key angiogenic factors are associated with BAVM clinical characteristics that are linked with vascular instability. METHODS: We measured the expression of angiopoietin-2 (Ang-2), matrix metalloproteinase-9, vascular endothelial growth factor (VEGF), and platelet-derived growth factor-AA and -BB by use of enzyme-linked immunosorbent assay in 27 BAVM surgical specimens. Tissues were also collected from 14 structurally normal brain specimens obtained during epilepsy surgery. RESULTS: Ang-2, VEGF, and matrix metalloproteinase-9 were highly expressed in BAVM samples (11.9 +/- 15.5 ng/mg protein, 137 +/- 102 pg/mg protein, and 379 +/- 455 pg/mg protein, respectively). Platelet-derived growth factor-BB was detectable in 7 of 21 BAVM samples. There were close correlations between Ang-2 and VEGF (R2 = 0.79). Higher Ang-2 and VEGF levels seemed to be associated with draining vein characteristics linked with BAVM hemorrhage but not with feeding artery pressure or BAVM size. In the structurally normal brain specimens, levels of Ang-2, VEGF, and matrix metalloproteinase-9 were low (0.8 +/- 2.3 ng/mg protein, 38 +/- 25 pg/mg protein, and 52 +/- 43 pg/mg protein, respectively). CONCLUSION: There were close correlations among angiogenic factors in BAVMs. Concerted effects of angiogenic factors may maintain the angiogenic phenotype in BAVMs and thereby determine the clinical course of BAVMs.

Angiopoietin-2↗