Modulation of the expression of vascular endothelial growth factor in human fibroblasts

Diamond, Michael P.; El-Hammady, Eslam; Munkarah, Adnan; Bieber, Eric J.; Saed, Ghassan M.

doi:10.1016/j.fertnstert.2004.06.073

Cited by 60 publications

(45 citation statements)

References 19 publications

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“…The use of a VEGF receptor inhibitor would make up-regulation ineffective and prevent adhesion formation. Our finding that the VEGF staining scores of the treatment group were much lower than in the control group correlates well the findings of previous studies (21,(39)(40)(41)(42)(43). We found that bevacizumab decreased the number and percentage of cells positive for Ki-67 in a concentration-dependent manner and that the KI-67 staining scores of the treatment groups were statistically significantly lower than the control group.…”

Section: Groupsupporting

confidence: 92%

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Effect of bevacizumab on postoperative adhesion formation in a rat uterine horn adhesion model and the correlation with vascular endothelial growth factor and Ki-67 immunopositivity

Moraloğlu

Işık²,

Kılıç

et al. 2011

Fertility and Sterility

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Section: Groupsupporting

confidence: 92%

“…Also, VEGF is released from injured tissues and aids tissue growth and vascular remodeling. The recent studies demonstrated the expression of VEGF in the endothelium, fibroblasts of pelvic adhesions in females (39)(40)(41). In another study, fewer adhesions developed in mice injected with an anti-VEGF antibody (42,43).…”

Section: Groupmentioning

confidence: 97%

Effect of bevacizumab on postoperative adhesion formation in a rat uterine horn adhesion model and the correlation with vascular endothelial growth factor and Ki-67 immunopositivity

Moraloğlu

Işık²,

Kılıç

et al. 2011

Fertility and Sterility

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“…These observations were further supported by the reduced human fibroblast expression of VEGF after in vitro treatment with another COX-2 inhibitor, i.e. NS-358, and by stimulation of aerobic metabolism with dichloroacetic acid [52]. Although it was withdrawn from the market for the teratogenic side effects, the antiangiogenesis inhibitor thalidomide was shown to reduce adhesions formation after colonic anastomosis in rabbits [53].…”

Section: Antiangiogenic Therapy For Peritoneal Adhesion Preventionmentioning

confidence: 88%

Angiogenic factors in peritoneal adhesion formation

Molinas¹,

Binda

Koninckx

2006

Gynecol Surg

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Abdominal surgery is considered as the leading cause of peritoneal adhesions and almost universally as adhesiogenic. Peritoneal injury at the time of surgery initiates an inflammatory reaction determining fibrin deposition on the wound surface. Depending on the balance between the different components of the plasminogen system, this fibrin can be either lysed, leading to normal peritoneal healing, or organised, serving as a scaffold for fibroblast ingrowth, extracellular matrix deposition and angiogenesis, leading to adhesion formation. The mechanism underlying the predisposition to form adhesions in some patients and in some specific anatomic sites and not in others after similar surgical procedures remains unknown. In spite of the many attempts proposed over the years for reducing the incidence of adhesion formation, peritoneal adhesions remain a major clinical problem, inducing intestinal obstruction, pelvic pain, female infertility and difficulties at the time of re-operation. The available evidence indicates that understanding the adhesion formation process at the molecular level is essential for developing successful strategies for preventing adhesions. Fortunately, the advancement in molecular biology during the last years has led to the identification of many molecules with the potential of regulating inflammatory and immune responses, tissue remodelling and angiogenesis, key events in peritoneal healing and adhesion formation. This review focuses on the role of angiogenesis and angiogenic factors in peritoneal adhesion formation.

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“…Such adhesion phenotype can be induced when normal human peritoneal fibroblasts are cultured in vitro under hypoxic conditions. Work in our laboratory and those of others show that compared with normal peritoneal fibroblasts, adhesion fibroblasts produce elevated basal levels of transforming growth factor beta1 (TGF-b1), [23][24][25] vascular endothelial growth factor (VEGF), 26 a-smooth muscle actin (a-SMA), 27 and components of the ECM such as type I collagen and fibronectin, 28 decreased ratios of plasminogen activator/plasminogen activator inhibitor 1 (tPA/PAI-1), 29 and matrix metalloproteinase 1/tissue inhibitor of metalloproteinase (MMP-1/TIMP-1). 21,30 In addition, the expression of cyclooxgenase 2 (COX-2) messenger RNA (mRNA) and protein in adhesion fibroblasts, and the induction of COX-2 in peritoneal fibroblasts in response to hypoxia indicate a possible inflammatory response 31 ( Figure 2).…”

Section: Pathophysiology Of Adhesion Developmentmentioning

confidence: 99%

Postoperative Adhesion Development Following Cesarean and Open Intra-Abdominal Gynecological Operations

et al. 2011

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In this review, we discuss the pathophysiology of adhesion development, the impact of physiological changes associated with pregnancy on markers of adhesion development, and the clinical implications of adhesion development following cesarean delivery (CD). Although peritoneal adhesions develop after the overwhelming majority of intra-abdominal and pelvic surgery, there is evidence in the literature that suggests that patients having CD may develop adhesions less frequently. However, adhesions continue to be a concern after CD, and are likely significant, albeit on average less than after gynecological operations, but with potential to cause significant delay in the delivery of the baby with serious, lifelong consequences. Appreciation of the pathophysiology of adhesion development described herein should allow a more informed approach to the rapidly evolving field of intra-abdominal adhesions and should serve as a reference for an evidence-based approach to consideration for the prevention and treatment of adhesions.

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Modulation of the expression of vascular endothelial growth factor in human fibroblasts

Cited by 60 publications

References 19 publications

Effect of bevacizumab on postoperative adhesion formation in a rat uterine horn adhesion model and the correlation with vascular endothelial growth factor and Ki-67 immunopositivity

Effect of bevacizumab on postoperative adhesion formation in a rat uterine horn adhesion model and the correlation with vascular endothelial growth factor and Ki-67 immunopositivity

Angiogenic factors in peritoneal adhesion formation

Postoperative Adhesion Development Following Cesarean and Open Intra-Abdominal Gynecological Operations

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