Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Wolf, Yehuda G.; Rasmussen, Lars Melholt; Ruoslahti, Erkki

doi:10.1172/jci117070

Cited by 289 publications

(169 citation statements)

References 34 publications

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“…TGF-␤1 may also play a crucial role in the pathogenesis of neointimal formation. In vivo studies show that the administration of TGF-␤1 enhances intimal thickening, and the neointimal formation is suppressed markedly by the administration of the specific antibodies against TGF-␤1 in ballooninjured arteries (24,25). TGF-␤1 expression is also increased in the luminal and abluminal neointima of stenosed AV fistulas and correlates to the neointimal cell number (26 -28).…”

Section: Discussionmentioning

confidence: 99%

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Jin

Ueda²,

Takai³

et al. 2005

Journal of the American Society of Nephrology

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It was hypothesized that chymase may participate in hemodialysis vascular access dysfunction, as chymase has been known to be an effective enzyme in the conversion of angiotensin I (Ang I) to Ang II and in the latent TGF-␤1 to the active form. An arteriovenous (AV) fistula was created between the brachial artery and vein in dogs. In the AV anastomosis, when the walls of the venous and arterial sides were compared, the eccentric neointimal formation was most evident in the venous wall. Compared with the venous side downstream of the AV anastomosis, a severe neointimal hyperplasia was found in the venous side upstream of the AV anastomosis (intima/media, 153 ؎ 25%). The chymase-and TGF-␤-positive mast cells were markedly accumulated in the proliferous neointima and media. In association with the reduction of chymase expression, a marked decrease in Ang II-, AT 1 receptor-, and TGF-␤-positive areas was achieved by NK3201 (a chymase inhibitor) treatment, and the neointima formation (intima/media: region A, 53 ؎ 9%, P < 0.001; region B, 54 ؎ 14%, P < 0.001) was also significantly suppressed in this group. Although lisinopril treatment also provided some beneficial effects with regard to the prevention of neointimal formation, the degree was less than that seen with chymase inhibition. These findings indicate that mast cell-derived chymase plays an essential role in the pathogenesis of the AV fistula access failure and that chymase inhibition may be a therapeutic target for the treatment of hemodialysis vascular access dysfunction in clinic settings.

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Section: Discussionmentioning

confidence: 99%

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Jin

Ueda²,

Takai³

et al. 2005

Journal of the American Society of Nephrology

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“…For example, Wolf et al (1994) have demonstrated that neutralizing antibodies directed against recombinant TGF-1 could suppress neointimal formation in the rat carotid-injury model. Additionally, other TGF-isoforms are well-characterized stimuli for extracellular matrix protein production, in connective tissue cells (Roberts et al 1986, Roberts 1995.…”

Section: Activin a Expression Following Vascular Injury: Pathophysiolmentioning

confidence: 99%

Novel cardiovascular actions of the activins

Molloy¹,

Taylor²,

Pawlowski³

1999

Journal of Endocrinology

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Proliferation and directed migration of vascular cells are key components in vascular diseases such as atherosclerosis and restenosis following percutaneous transluminal coronary angioplasty. However, the precise cellular and molecular mechanisms involved in the control of vascular cell proliferation or migration at the tissue level remain largely undefined. Molecules contributing to these processes are elaborated by distinct cell types and act in both autocrine and paracrine modes. They include two broad classes, polypeptide growth factors and vasoactive G-protein-coupled receptor (GPCR) agonists. Examples of the former, such as platelet-derived growth factor, bind to and activate cell surface receptor tyrosine kinases, initiating intracellular biochemical signaling pathways associated with cell proliferation or migration. In contrast, recent evidence suggests that vasoactive GPCR agonists (e.g. angiotensin II, endothelin-1, -thrombin) elicit cell growth indirectly by inducing the production of autocrine or paracrine factors in vascular cells. Recent studies have identified activin A as a novel component of conditioned medium obtained from GPCR agonist-stimulated vascular smooth muscle cells (SMCs). Although activin A alone only weakly stimulated rat aortic SMC DNA synthesis, it demonstrated a potent co-mitogenic effect in combination with either epidermal growth factor (EGF) or heparin binding EGF-like growth factor in these cells, increasing DNA synthesis by up to 5-and 4-fold respectively. Furthermore, in a rat carotid-injury model, activin A mRNA was upregulated within 6 h after injury, followed by increases in immunoreactive protein detected in the expanding neointima 7 to 14 days later. Taken together, these results indicate that activin A is a common vascular SMC-derived growth factor induced by vasoactive agonists that may, either alone or in combination with other factors, contribute to fibroproliferative vascular diseases.

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“…30,31) Studies have demonstrated the relation between TGF-ß1 and neointimal hyperplasia. 32,33) In a study, it has been reported that YC-1, which is a partial PDE5 inhibitor, reduces neointimal hyperplasia after balloon angioplasty in rat carotid artery. 7) Verdanafil, which is also a selective PDE5 inhibitor, has been shown to be effective in decreasing neointimal hyperplasia after carotid endarterectomy in rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of Tadalafil on Neointimal Hyperplasia in a Rabbit Carotid Artery Anastomosis Model

Guzeloglu

Aykut

Albayrak

et al. 2013

ATCS

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Purpose: Intimal thickening, which results from the response to arterial damage caused by therapeutic interventions or other reasons, is usually called as neointima. Neointimal hyperplasia is a main step in the pathogenesis of late-term restenosis, which is developed after vascular interventions. Reduction in nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling plays a substantial role in the pathogenesis of neointima formation. Phosphodiesterase V is detected in the peripheral coronary and pulmonary vascular smooth muscle cells and in the cardiac tissue. Based on the effects of phosphodiesterase V inhibitors on vascular smooth muscle cells, in the present study, the effect of tadalafil, a new member of phosphodiesterase V inhibitors, on neointimal hyperplasia was investigated in the rabbit carotid artery anastomosis model. Materials and Methods: Fourteen male New Zealand white rabbits weighing between 2.5-3 kg, were used. The rabbits were randomly divided into two equal groups; tadalafil group received oral tadalafil (2 mg/kg/day), and PBS group received sterile PBS solution (normal saline; 2 mg/kg/day) for 28 days after the surgery. The right carotid arteries of all rabbits were anastomosed in an end-to-end fashion using 8/0 polypropylene suture. The rabbits were sacrificed at the end of the postoperative period of 28 days. After sacrificing, firstly anastomosis segment on the right carotid artery and secondly a part of the left carotid artery (as control) of each rabbit were removed. Morphometric examination of tissue sections was performed under a light microscope connected to an image capture system. Results: There was a significant difference between the right and left carotid arteries in terms of intimal area and intima/media ratio both in tadalafil and PBS groups (p <0.001 for each). Intimal area and intima/media ratio were increased in the right carotid arteries compared to the left carotid arteries (p <0.001 for each). Besides, when the right carotid arteries of both groups were compared using covariance analysis, it was observed that intimal area and intima/media ratio in the anastomosis site were significantly reduced with tadalafil treatment (p <0.001). Conclusion: The present study was promising in terms of tadalafil use as a new agent for the prevention of neointimal hyperplasia, which is the leading cause of late-term graft failure in vascular surgery.

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Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model.

Cited by 289 publications

References 34 publications

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Novel cardiovascular actions of the activins

Effect of Tadalafil on Neointimal Hyperplasia in a Rabbit Carotid Artery Anastomosis Model

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