Dopamine regulates endothelial progenitor cell mobilization from mouse bone marrow in tumor vascularization

Chakroborty, Debanjan; Chowdhury, Uttio Roy; Sarkar, Chandrani; Baral, Rathindranath; Dasgupta, Partha; Basu, Sujit

doi:10.1172/jci33125

Cited by 138 publications

(135 citation statements)

References 36 publications

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“…In this regard, it is known that most immune cell subtypes express DRD2 (McKenna et al 2002), and among them, macrophages are known to express large amounts of VEGF (Nap et al 2004). Moreover, the ability of macrophages to reduce angiogenesis when activated by dopamine has recently been described (Chakroborty et al 2008). Thus, in our experiments, it is likely that quinagolide decreased VEGF transcripts in implanted endometrial tissue by Quinagolide reduces endometriotic lesion size inhibiting the expression of this factor in macrophages through the activation of DRD2.…”

Section: Discussionmentioning

confidence: 58%

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

Delgado-Rosas¹,

Gómez²,

Ferrero³

et al. 2011

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Implantation of a retrogradely shed endometrium during menstruation requires an adequate blood supply, which allows the growth of endometriotic lesions. This suggests that the development of endometriosis can be impaired by inhibiting angiogenesis. The growth of endometriotic foci is impaired by commercial oncological antiangiogenic drugs used to block vascular endothelial growth factor (VEGF) signaling. The dopamine agonist cabergoline (Cb2) inhibits the growth of established endometriosis lesions by exerting antiangiogenic effects through VEGFR2 inactivation. However, the use of ergot-derived Cb2 is associated with an increased incidence of cardiac valve regurgitation. To evaluate the potential usage of non-ergot-derived dopamine agonists for the treatment of human endometriosis, we compared the efficacy of quinagolide with that of Cb2 in preventing angiogenesis and vascularization in a heterologous mouse model of endometriosis. Nude mice whose peritoneum had been implanted with eutopic human endometrial fragments were treated with vehicle, 50 mg/kg per day oral Cb2, or 50 or 200 mg/kg per day quinagolide during a 14-day period. At the end of the treatment period, the implants were excised in order to assess lesion size, cell proliferation, degree of vascularization, and angiogenic gene expression. Neoangiogenesis was inhibited and the size of active endometriotic lesions, cellular proliferation index, and angiogenic gene expression were significantly reduced by both dopamine agonists when compared with the placebo. Given that Cb2 and quinagolide were equally effective in inhibiting angiogenesis and reducing lesion size, these experiments provide the rationale for pilot studies to explore the use of non-ergot-derived dopamine agonists for the treatment of endometriosis in humans.

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Section: Discussionmentioning

confidence: 58%

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

Delgado-Rosas¹,

Gómez²,

Ferrero³

et al. 2011

Reproduction

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“…21,23 VEGF-A mainly acts through its VEGF receptor 2, present in the EC and endothelial progenitor cells, to stimulate migration and proliferation of these cells, the essential steps of the angiogenic process. 11,21,23 We have previously reported that stimulation of DA D 2 receptors can significantly inhibit VEGF-Aeinduced The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or CSIR.…”

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confidence: 99%

Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Chakroborty

Sarkar

et al. 2016

The American Journal of Pathology

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“…68 Complementary, quinagolide binding to DRD2 on macrophages has been reported to decreases the expression of VEGF-A mRNA levels. 69 Thus, it is likely that quinagolide also suppresses the endometriosisassociated angiogenesis in a paracrine fashion by decreasing the production of VEGF-A by immune cells within the lesions. 70 Since endometriosis-associated inflammation and angiogenesis are closely related processes, numerous studies have been focused on anti-inflammatory drugs and immunomodulators.…”

mentioning

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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Dopamine regulates endothelial progenitor cell mobilization from mouse bone marrow in tumor vascularization

Cited by 138 publications

References 36 publications

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

The effects of ergot and non-ergot-derived dopamine agonists in an experimental mouse model of endometriosis

Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Angiogenesis as a Therapeutic Target in Endometriosis

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