Angiogenesis lymphangiogenesis and neurogenesis in endometriosis

Hey-Cunningham, Alison J.; Peters, Kathleen Mary; Zevallos, Hector Barrera-Villa; Berbic, Marina; Markham, Robert; Fraser, Ian S.

doi:10.2741/e682

Cited by 54 publications

(44 citation statements)

References 196 publications

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“…6,7,28 Recent reports provide evidence that the vascularization of endometriotic lesions is not only driven by angiogenesis but also involves vasculogenesis. 14,15 The latter mechanism of blood vessel development is characterized by homing of circulating EPCs to the lesions, where they are incorporated into the Detailed information about the individual genes is provided in GenBank (http://www.ncbi.nlm.nih.gov/genbank) using the provided accession numbers.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Rudzitis‐Auth

Nenicu

Nickels

et al. 2016

The American Journal of Pathology

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The incorporation of endothelial progenitor cells (EPCs) into microvessels contributes to the vascularization of endometriotic lesions. Herein, we analyzed whether this vasculogenic process is regulated by estrogen. Estrogen- and vehicle-treated human EPCs were analyzed for migration and tube formation. Endometriotic lesions were induced in irradiated FVB/N mice, which were reconstituted with bone marrow from FVB/N-TgN (Tie2/green fluorescent protein) 287 Sato mice. The animals were treated with 100 μg/kg β-estradiol 17-valerate or vehicle (control) over 7 and 28 days. Lesion growth, cyst formation, homing of green fluorescent protein(+)/Tie2(+) EPCs, vascularization, cell proliferation, and apoptosis were analyzed by high-resolution ultrasonography, caliper measurements, histology, and immunohistochemistry. Numbers of blood circulating EPCs were assessed by flow cytometry. In vitro, estrogen-treated EPCs exhibited a higher migratory and tube-forming capacity when compared with controls. In vivo, numbers of circulating EPCs were not affected by estrogen. However, estrogen significantly increased the number of EPCs incorporated into the lesions' microvasculature, resulting in an improved early vascularization. Estrogen further stimulated the growth of lesions, which exhibited massively dilated glands with a flattened layer of stroma. This was mainly because of an increased glandular secretory activity, whereas cell proliferation and apoptosis were not markedly affected. These findings indicate that vasculogenesis in endometriotic lesions is dependent on estrogen, which adds a novel hormonally regulated mechanism to the complex pathophysiology of endometriosis.

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Section: Discussionmentioning

confidence: 99%

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Rudzitis‐Auth

Nenicu

Nickels

et al. 2016

The American Journal of Pathology

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“…74,77,78 Several angiogenic factors in the human endometrium have been identified that play important roles in physiological angiogenesis. [79][80][81][82] The important regulators for endometrial angiogenesis include VEGF, ANGPTs, fibroblast growth factor, thrombospondin, relaxin, adrenomedullin, prostaglandins, prokineticins, angiogenin, and stromal cell-derived factor 1. [83][84][85][86][87][88][89] The VEGF is a key mediator of physiological and pathological vascular remodeling.…”

Section: Angiogenesis (Vascular Maturation)mentioning

confidence: 99%

Decidualization of the human endometrium

Okada

Tsuzuki

Murata

2018

Reprod Medicine & Biology

265

176

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BackgroundDecidualization of the human endometrium, which involves a dramatic morphological and functional differentiation of human endometrial stromal cells (ESCs), is essential for the establishment of a successful pregnancy. Decidualization results from a complex interplay of transcription factors, morphogens, cytokines, cell cycle regulators, and signaling pathways.MethodsBased on a literature review, the regulation of, and the molecular mechanisms involved in, the decidualization of the endometrium are described.Main findingsProgesterone, together with proteins that are regulated by progesterone and/or cyclic adenosine monophosphate, including homeobox A10, forkhead box O1, signal transducers and activators of transcription, and heart and neural crest derivatives expressed transcript 2, forms a critical network for ESC decidualization and is a prerequisite to successful implantation. Decidualized ESCs contribute to the microenvironment at the feto–maternal interface and its direct or indirect influence on extracellular matrix remodeling, regulation of the local immune response, anti‐oxidative stress, and angiogenesis (vascular maturation). Impairment of this process is associated with a variety of pregnancy disorders, including infertility, recurrent miscarriages, and uteroplacental disorders.ConclusionA deeper understanding of the process of decidualization is expected to provide new insights into the fields of reproductive biology and reproductive medicine.

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“…3 Since the survival and proliferation of endometriotic implants require neovascularization, 4 the inhibition of angiogenesis has become an attractive strategy for improved control of endometriosis.…”

Section: Introductionmentioning

confidence: 99%

“…35 Platelet-derived growth factor B (PDGF-B) is regarded as the main promoter of the pericyte investment in neovessels, being significantly over-expressed by eutopic endometrium of endometriosis patients. 4 Many other ubiquitously expressed molecules have been found to enhance angiogenesis in vitro, in animal models of endometriosis and/ or in human samples. 12,[36][37][38][39][40] Such promoters include cytokines and growth factors secreted by immune and neuroendocrine cells (e.g., interleukins, IL-1β, 6 and 8, tumor necrosis factor-α, TNF-α, and transforming growth factor β, TGF-β).…”

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confidence: 99%

Angiogenesis as a Therapeutic Target in Endometriosis

Djokovic

Calhaz‐Jorge

2014

Acta Med Port

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RESUMOIntrodução: A angiogénese é um factor determinante no estabelecimento e desenvolvimento das lesões de endometriose. Material e Métodos:Foram revistos os artigos indexados na PubMed e incluídos os estudos mais relevantes, publicados até Janeiro de 2014, sobre a angiogénese nas lesões de endometriose e/ou estratégias anti-angiogénicas para o tratamento desta doença ginecológica.Resultados: O presente artigo fornece um resumo conciso dos mecanismos moleculares conhecidos que promovem a vascularização das lesões de endometriose, podendo servir como alvos terapêuticos potenciais. Apresenta-se também uma revisão sistemática dos agentes anti-angiogénicos, inclusivos e exclusivos, que já foram avaliados em culturas de células, modelos animais e/ou doentes com endometriose. Discussão e Conclusão: A integração das estratégias anti-angiogénicas na terapêutica multimodal de endometriose será condicionada pelos resultados de avaliações futuras da verdadeira eficácia desses tratamentos, do risco de desenvolvimento de resistência aos medicamentos e da incidência de efeitos colaterais inaceitáveis. Palavras-chave: Inibidores da Angiogénese/uso terapêutico; Endometriose/terapêutica. ABSTRACT Introduction:Angiogenesis is a key factor for the successful establishment and growth of endometriotic lesions. Material and Methods:We performed a literature search in PubMed and reviewed the most pertinent studies published until January 2014 and focused on the endometriosis-associated angiogenesis and/or anti-angiogenic strategies for the treatment of this gynecological disorder. Results:The present review provides a concise summary of the known molecular mechanisms that promote vascularization of endometriotic lesions and may serve as potential therapeutic targets. We also present a systematic overview of the inclusive and exclusive anti-angiogenic agents that have been already studied in cell cultures, animal models and/or endometriosis patients. Discussion and Conclusion:The integration of anti-angiogenic approaches in the multimodal management strategies for endometriosis patients will be conditioned by the outcomes of future assessments regarding the effectiveness of such treatments, the risk of drug resistance development and the incidence of unacceptable side effects.

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Angiogenesis lymphangiogenesis and neurogenesis in endometriosis

Cited by 54 publications

References 196 publications

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Decidualization of the human endometrium

Angiogenesis as a Therapeutic Target in Endometriosis

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