Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Full metadata record
DC FieldValueLanguage
dc.contributor.authorHassanshahi, M.en
dc.contributor.authorSu, Y.W.en
dc.contributor.authorKhabbazi, S.en
dc.contributor.authorFan, C.M.en
dc.contributor.authorChen, K.M.en
dc.contributor.authorWang, J.F.en
dc.contributor.authorQian, A.en
dc.contributor.authorHowe, P.R.en
dc.contributor.authorYan, D.W.en
dc.contributor.authorZhou, H.D.en
dc.contributor.authorXian, C.J.en
dc.identifier.citationJournal of Cellular Physiology, 2019; 234(7):11276-11286en
dc.description.abstractCancer chemotherapy can cause significant damage to the bone marrow (BM) microvascular (sinusoidal) system. Investigations must now address whether and how BM sinusoidal endothelial cells (SECs) can be protected during chemotherapy. Herein we examined the potential protective effects of genistein, a soy-derived flavonoid, against BM sinusoidal damage caused by treatment with methotrexate (MTX). The groups of young adult rats were gavaged daily with genistein (20 mg/kg) or placebo. After 1 week, rats also received daily injections of MTX (0.75 mg/kg) or saline for 5 days and were killed after a further 4 days. Histological analyses showed that BM sinusoids were markedly dilated ( p < 0.001) in the MTX-alone group but were unaffected or less dilated in the genistein+MTX group. In control rats, genistein significantly enhanced expression of vascular endothelial growth factor (VEGF; p < 0.01), particularly in osteoblasts, and angiogenesis marker CD31 ( p < 0.001) in bone. In MTX-treated rats, genistein suppressed MTX-induced apoptosis of BM SECs ( p < 0.001 vs MTX alone group) and tended to increase expression of CD31 and VEGF ( p < 0.05). Our in vitro studies showed that genistein in certain concentrations protected cultured SECs from MTX cytotoxic effects. Genistein enhanced tube formation of cultured SECs, which is associated with its ability to induce expression of endothelial nitric oxide synthase and production of nitric oxide. These data suggest that genistein can protect BM sinusoids during MTX therapy, which is associated, at least partially, with its indirect effect of promoting VEGF expression in osteoblasts and its direct effect of enhancing nitric oxide production in SECs.en
dc.description.statementofresponsibilityMohammadhossein Hassanshahi, Yu‐Wen Su, Samira Khabbazi, Chia‐Ming Fan, Ke‐Ming Chen, Ju‐Fang Wang, Airong Qian, Peter R. Howe, De‐Wen Yan, Hou‐De Zhou, Cory J. Xianen
dc.publisherWiley Online Libraryen
dc.rights© 2018 Wiley Periodicals, Inc.en
dc.subjectangiogenesis; apoptosis; bone marrow sinusoidal endothelial cells (BM SECs); genisteinen
dc.titleFlavonoid genistein protects bone marrow sinusoidal blood vessels from damage by methotrexate therapy in ratsen
dc.typeJournal articleen
pubs.library.collectionPsychology publicationsen
dc.identifier.orcidHassanshahi, M. [0000-0002-4097-8527]en
dc.identifier.orcidKhabbazi, S. [0000-0002-5410-795X]en
dc.identifier.orcidHowe, P.R. [0000-0001-6546-7742]en
dc.identifier.orcidXian, C.J. [0000-0002-8467-2845]en
Appears in Collections:Psychology publications

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.