Morphometric study of the stromal vascularization in peritoneal endometriosis

Nisolle, Michelle; Casanas-Roux, Franco̧ise; Anaf, Vincent; Mine, Jean-Michel; Donnez, Jacques

doi:10.1016/s0015-0282(16)55823-3

Cited by 247 publications

(17 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The mechanisms underlying the establishment of endometriotic lesions are not fully understood; however, there is no doubt that the long-term survival and proliferation of these lesions are crucially dependent on the formation of new blood vessels, which guarantee the supply of oxygen and essential nutrients 9,38–40 . Endometriotic lesions are typically characterized by dense vascularization 1,41,42 . Cross transplantation of endometrial tissues isolated from genetically engineered mice is a very useful strategy for clarifying the cellular origin and tissue-specific functions of proangiogenic factors.…”

Section: Discussionmentioning

confidence: 99%

VEGF Receptor 1-Expressing Macrophages Recruited from Bone Marrow Enhances Angiogenesis in Endometrial Tissues

Sekiguchi

Yoshiya

Hattori

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Angiogenesis is critical in maintenance of endometrial tissues. Here, we examined the role of VEGF receptor 1 (VEGFR1) signaling in angiogenesis and tissue growth in an endometriosis model. Endometrial fragments were implanted into the peritoneal wall of mice, and endometrial tissue growth and microvessel density (MVD) were determined. Endometrial fragments from wild-type (WT) mice grew slowly with increased angiogenesis determined by CD31 + MVD, peaking on Day 14. When tissues from WT mice were transplanted into VEGFR1 tyrosine kinase-knockout mice, implant growth and angiogenesis were suppressed on Day 14 compared with growth of WT implants in a WT host. The blood vessels in the implants were not derived from the host peritoneum. Immunostaining for VEGFR1 suggested that high numbers of VEGFR1 + cells such as macrophages were infiltrated into the endometrial tissues. When macrophages were deleted with Clophosome N, both endometrial tissue growth and angiogenesis were significantly suppressed. Bone marrow chimera experiments revealed that growth and angiogenesis in endometrial implants were promoted by host bone marrow-derived VEGFR1 + /CD11b + macrophages that accumulated in the implants, and secreted basic fibroblast growth factor (bFGF). A FGF receptor kinase inhibitor, PD173047 significantly reduced size of endometrial tissues and angiogenesis. VEGFR1 signaling in host-derived cells is crucial for growth and angiogenesis in endometrial tissue. Thus, VEGFR1 blockade is a potential treatment for endometriosis.

show abstract

Section: Discussionmentioning

confidence: 99%

VEGF Receptor 1-Expressing Macrophages Recruited from Bone Marrow Enhances Angiogenesis in Endometrial Tissues

Sekiguchi

Yoshiya

Hattori

et al. 2019

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Vasculature in pathological situations, such as endometriosis ( [26], Additional file 2: Figure S2A) and cancer [27], grow in a chaotic and disorganized manner, compared to the structured physiological neovascularization in reproductive organs (Additional file 2: Figure S2B, C). Vessels in pathological situations fail to recruit mural cells (pericytes and vascular smooth muscle cells), which provide structural support and pro-survival stimuli to endothelial cells [28].…”

Section: Discussionmentioning

confidence: 99%

Chronic effects of an anti-angiogenic thrombospondin-1 mimetic peptide, ABT-898, on female mouse reproductive outcomes

Edwards

Olariu

Nakamura

et al. 2016

Reprod Biol Endocrinol

View full text Add to dashboard Cite

BackgroundAngiogenesis is an essential process in endometriosis disease progression. Earlier, we demonstrated that anti-angiogenic peptide, ABT-898 prevents neoangiogenesis of human endometriotic lesions in a xenograft mouse model. Since angiogenesis is essential for normal ovarian and uterine function, we evaluated effects of ABT-898 on normal female reproductive processes in mice.MethodsCycling female C57BL/6N mice were dosed with ABT-898 (100 mg/kg) or 5 % dextrose control for 21 consecutive days to cover multiple estrous cycles (average estrous cycle 4 to 5 days in mice). Pregnant female mice were dosed with ABT-898 (100 mg/kg) or control on alternate days over the course of gestation, beginning at gestation day 7.5 to 17.5 (gestation length 21 days). Histological analysis along with CD31 and Vimentin immunohistochemistry were performed on ovaries and uteri obtained from treated and control mice. To understand the influence of ABT-898 on systemic angiogenic factors, a Pro Mouse Cytokine 9-plex assay was performed on plasma samples obtained from mice prior to treatment, during the second week of ABAT-898 or control treatment and on the last day of treatment.ResultsABT-898 did not affect the number of estrous cycles over the 21 day treatment compared to control. Histological analysis of ovaries found no difference in the number of primordial, primary, secondary, and antral follicles between ABT-898 treated and control groups. Similarly, no difference was observed in the microvessel density between ABT-898 treated and control uteri, ovarian follicles or corpus luteum when assessed using CD31 or vimentin immunohistochemistry. Electron microscopy revealed similar capillary structure and appearance in both ABT-898 treated and control uteri. Although peripheral blood angiogenic cytokine profiles (IL-15, IL-18, M-CSF, b-FGF, PDGF-bb, MIG, MIP-2, LIF and VEGF) changed over the course of the intervention, there was no significant difference between ABT-898 and control groups at any of the studied time points. Treatment with ABT-898 during pregnancy had no effect on litter size at birth, pup weight at birth or pup weight at weaning.ConclusionOur findings suggest that ABT-898 may not alter angiogenesis dependent reproductive processes in female mice. However, an extensive reproductive toxicology screening is required to substantiate use of ABT-898 in future.Electronic supplementary materialThe online version of this article (doi:10.1186/s12958-016-0192-7) contains supplementary material, which is available to authorized users.

show abstract

“…Furthermore, once attached, the uterine fragment altered in appearance over time from a red, fibrin-rich tissue to a fluid-filled cyst that is typical of the human disease [15]. This alteration in macroscopic appearance coincided with histological remodelling of the uterine fragment with features such as luminal epithelium, stroma and glandular structures by day 7 post-surgery, suggesting a viable ectopic endometrial lesion.…”

Section: Discussionmentioning

confidence: 99%

Cellular Exchange in an Endometriosis-Adhesion Model Using GFP Transgenic Mice

Wilkosz¹,

Pullen

de-Giorgio-Miller

et al. 2011

Gynecol Obstet Invest

View full text Add to dashboard Cite

Background: Endometriosis is a debilitating disease that affects women of reproductive age and may lead to impaired fertility. Cell attachment, invasion of the underlying tissue, and vascular ingrowth are important processes in endometrial lesion development. However, the degree of cellular exchange between host peritoneum and endometrial tissue is unclear. Methods: An experimental endometriosis model was employed whereby uterine horn fragments from wild-type mice were implanted into genetically identical eGFP (enhanced green fluorescent protein) host mice and vice versa. Hormone sensitivity of the ectopic lesions was assessed and cellular exchange determined histologically. Results: White cyst-like lesions developed from implanted fibrin-rich fragments by day 7. Lesions consisted of a well-developed stroma with glandular and luminal epithelium. Both ovariectomy and treatment with a GnRH agonist, leuprorelin, resulted in the suppression of ectopic lesion growth, whereas estradiol treatment increased the size of the ectopic lesion (4 mice per group on day 14). Ingrowth and outgrowth of blood vessels was apparent as well as the exchange of cells between host peritoneum and lesion. Conclusion: These findings support the proposal that there is a close cellular interplay between host peritoneum and ectopic tissue and the suitability of this mouse model to study these interactions.

show abstract

Morphometric study of the stromal vascularization in peritoneal endometriosis

Cited by 247 publications

References 6 publications

VEGF Receptor 1-Expressing Macrophages Recruited from Bone Marrow Enhances Angiogenesis in Endometrial Tissues

VEGF Receptor 1-Expressing Macrophages Recruited from Bone Marrow Enhances Angiogenesis in Endometrial Tissues

Chronic effects of an anti-angiogenic thrombospondin-1 mimetic peptide, ABT-898, on female mouse reproductive outcomes

Cellular Exchange in an Endometriosis-Adhesion Model Using GFP Transgenic Mice

Contact Info

Product

Resources

About