A peptide inhibitor of synuclein-  reduces neovascularization of human endometriotic lesions

Edwards AK, Andrew Kenneth Edwards, Andrew K. Edwards, Sharanya Ramesh, Ramesh S, S. Ramesh, Singh V, Vinay Singh, Vijender Singh, Tayade C, Chandrakant Tayade
Molecular human reproduction · 2014 · vol. 20(10) , pp. 1002–1008 · doi:10.1093/molehr/gau054 · PMID:25024138 · PMC4172171 · W2154153572
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A novel peptide inhibitor of synuclein-γ, SP012, reduced the growth and vascularization of human endometriotic lesions in a mouse model.

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Abstract

Endometriosis is a chronic painful gynecological condition characterized by adherence and growth of endometrium outside of the uterine cavity. Neovascularization is essential to the developing endometriosis lesion to support its growth. Synuclein-γ (SNCG), a protein implicated in cellular proliferation, is associated with a broad range of malignancies as well as endometriosis. We hypothesized that SNCG plays an important role in the neovascularization and growth of endometriosis and blocking of SNCG will interfere with survival of endometriotic lesions in a mouse model. We developed SP012, a novel 12 amino acid peptide inhibitor of SNCG. SP012 inhibited three-dimensional endothelial cell tube formation in a dose-dependent manner. Using intravital microscopy, SP012 was shown to be successfully delivered to human endometriotic lesions in a xenograft mouse model in vivo. Alymphoid (BALB/c-Rag2-/-Il2rγ-/- lacking T, B and NK cells) mice were surgically induced with human endometriotic lesions and treated with SP012 or phosphate-buffered saline control. SP012 treated endometriotic lesions had decreased growth, development and vascularization at the time of necroscopy. Endometriotic lesions treated with SP012 also had fewer isolectin (+) microvessels. These results, using a mouse model, indicate that SNCG plays a role in the neovascularization and subsequent growth of human endometriotic lesions. Targeting SNCG function using peptide inhibitor might provide a potential therapeutic option for the treatment of endometriosis in the future.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium gamma-Synuclein Neoplasm Proteins Neovascularization, Pathologic Animals Cell Proliferation Disease Models, Animal Endometriosis Endometriosis Endometrium Endometrium Endometrium Female gamma-Synuclein Humans Human Umbilical Vein Endothelial Cells Lectins Lectins Mice

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References (20)

Cited by (9)

SciLite annotations

chemicals 28
peptide amino acid peptide peptide estrogen peptide wax xylene ethanol water sodium diethylcarbamazine citrate hydrogen peroxide haematoxylin peptide sulfamides 2',7'-difluorofluorescein isothiocyanate phenylindole ketamine xylazine estradiol acetate campest-22e-en-3beta,4beta,5alpha,6alpha,8beta,14alpha,15alpha,25r,26-nonol alexa fluor 488 iodonitrotetrazolium salt
organisms 17
transgenic mice human mus sp. human transgenic mice human human transgenic mice human transgenic mice multicellular animals rodents mus sp. somali wild ass naine d'afrique de l'ouest perennial horse gram brassaiopsis simplicifolia

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