Pelvic Adhesions Contain Sex Steroid Receptors and Produce Angiogenesis Growth Factors

Wiczyk, Halina; Grow, Daniel R.; Adams, B S Lorrie A; O’Shea, Donna; Reece, M T

doi:10.1016/s0015-0282(97)00529-3

Cited by 54 publications

(25 citation statements)

References 17 publications

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“…These findings support the data of Roy et al who found evidence of macrophage oxidative metabolism in human adhesions and stated that this was suggestive of ongoing inflammatory activity typical of a regenerating, dynamic structure. 30 Expression of VEGFA in human adhesion tissue confirmed results of previous studies 19,30 ; however, this is the first study that also detected expression of VEGF receptor, flk-1. Adhesions, which expressed VEGFA and flk-1, showed significantly more CD105-positive vessels, supporting the concept that new vessel production occurs in established human adhesions.…”

Section: Discussionsupporting

confidence: 81%

“…17 Through binding to its receptor, flk-1 (VEGFR2) on vascular endothelial cells, VEGFA increases vascular permeability, cellular proliferation and migration, and can alter cell morphology and cytoskeletal structure. 18 The expression of VEGFA has been demonstrated in adhesions from patients with endometriosis 19 and altered levels of VEGFA mRNA (messenger ribonucleic acid) has been detected during adhesion formation in a rodent model. 20 In addition, manipulation of the VEGFA pathway in animal models has been shown to influence adhesion formation.…”

mentioning

confidence: 99%

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Human Peritoneal Adhesions Show Evidence of Tissue Remodeling and Markers of Angiogenesis

Epstein¹,

Wilson²,

Wilkosz³

et al. 2006

Diseases of the Colon &Amp; Rectum

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All adhesions contained functional blood vessels and most showed evidence of cell proliferation. The presence of vascular endothelial growth factor A and its receptor in human adhesions suggests ongoing angiogenic activity. This study demonstrates that adhesions are vascular structures with evidence of tissue remodeling and suggests potential for new prevention strategies involving antiangiogenic therapies.

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Section: Discussionsupporting

confidence: 81%

mentioning

confidence: 99%

Human Peritoneal Adhesions Show Evidence of Tissue Remodeling and Markers of Angiogenesis

Epstein¹,

Wilson²,

Wilkosz³

et al. 2006

Diseases of the Colon &Amp; Rectum

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“…Angiogenesis is an important feature in adhesion formation, not only supplying the injured tissue with nutrients and oxygen during the healing process, but al- so enabling the fi brovascular adhesive bands to grow [4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Coincidence of Connective Tissue Growth Factor Expression with Fibrosis and Angiogenesis in Postoperative Peritoneal Adhesion Formation

Thaler

Mack

Berho³

et al. 2005

Eur Surg Res

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Purpose: To investigate the relationship between connective tissue growth factor (CTGF) and fibrosis and angiogenesis in postoperative peritoneal adhesion formation. Methods: Adhesions were performed in 35 rats by creation of a peritoneal patch. Animals were sacrificed at 7 different time-points over 3 weeks. Adhesions and uninjured peritoneum from all animals were assessed by Northern blotting for CTGF and collagen-I mRNA and by immunohistochemistry for CTGF localization, degree of fibrosis and angiogenesis. Results: Persistent adhesions formed in all animals. CTGF and collagen-I mRNA were increased in adhesions compared to uninjured peritoneum (p < 0.05 for both). The temporal expression pattern depicted delayed peak levels of collagen-I mRNA with increasing tendency for both transcripts at the end of the observation period. Fibrosis within adhesions correlated positively with time after surgery (r = 0.85; p < 0.001) and showed typical signs of chronic tissue fibrosis at later time points. Angiogenesis was detected in adhesions but not in uninjured peritoneum (p = 0.001) and coincided with the spatial and temporal expression of CTGF protein in fibroblasts and vascular endothelial cells. Conclusions: The co-expression of CTGF with increasing fibrosis and angiogenesis in postoperative peritoneal adhesions suggests a role for CTGF as critical molecule in fibrous adhesive disease and target for future adhesion prevention.

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“…Formation of all types of adhesions are dependent on angiogenesis (17,18). Fibroblasts from these adhesions express the COX-2 enzyme while fibroblasts in non-adhesion-bearing areas do not express this enzyme (19).…”

Section: Discussionmentioning

confidence: 99%

“…However, previous studies have suggested that, although COX-2 may play an active role in one or more biological responses during cutaneous wound healing, these enzymes are not essential, possibly due to the presence of other additional pathways with compensatory mechanisms (21). In view of the fact that an adhesion is understood to be an aberrant form of the normal tissue healing process (17), specific additional pathways with compensatory mechanisms could also exist in adhesion formation. It is possible that, apart from its effect on COX-2, celecoxib may inhibit adhesion formation through other mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting ERK1/2 and SMAD2/3 phosphorylation

Fan

Zeng

et al. 2011

Mol Med Report

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Abstract. This study aimed to investigate whether celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2) and SMAD2/3 phosphorylation. Celecoxib was added to NIH/3T3 fibroblasts stimulated by fibroblast growth factor-2 (FGF-2) or transforming growth factor-β1 (TGF-β1). NIH/3T3 fibroblast proliferation and viability were assessed by MTT assays; ERK1/2 expression and SMAD2/3 expression were assessed by quantitative RT-PCR and Western blot analysis. The results indicated that celecoxib suppressed cell proliferation (IC 50 FGF + group, 75±1.9 µmol/l) stimulated by FGF-2, and also inhibited cell viability (IC 50 FGF -group, 252±2.3 µmol/l) by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. In addition, celecoxib treatment led to the apoptosis of NIH/3T3 fibroblasts (IC 50 FGF -group, 35±1.4 µmol/l). Celecoxib also suppressed collagen expression (0.35-fold COL3 and 0.43-fold COL1 with 320 µmol/l celecoxib relative to the untreated group following stimulation for 3 h, p<0.01) when stimulated by TGF-β1, by inhibiting SMAD2/3 phosphorylation but not SMAD2/3 expression. Celecoxib is capable of inhibiting ERK1/2 and SMAD2/3 phosphorylation, which is responsible for NIH/3T3 fibroblast proliferation and collagen expression.

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Pelvic Adhesions Contain Sex Steroid Receptors and Produce Angiogenesis Growth Factors

Cited by 54 publications

References 17 publications

Human Peritoneal Adhesions Show Evidence of Tissue Remodeling and Markers of Angiogenesis

Human Peritoneal Adhesions Show Evidence of Tissue Remodeling and Markers of Angiogenesis

Coincidence of Connective Tissue Growth Factor Expression with Fibrosis and Angiogenesis in Postoperative Peritoneal Adhesion Formation

Celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting ERK1/2 and SMAD2/3 phosphorylation

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