Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/119545
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dc.contributor.authorHassanshahi, M.en
dc.contributor.authorSu, Y.en
dc.contributor.authorKhabbazi, S.en
dc.contributor.authorFan, C.en
dc.contributor.authorChen, K.en
dc.contributor.authorWang, J.en
dc.contributor.authorQian, A.en
dc.contributor.authorHowe, P.en
dc.contributor.authorYan, D.en
dc.contributor.authorZhou, H.en
dc.contributor.authorXian, C.en
dc.date.issued2019en
dc.identifier.citationJournal of Cellular Physiology, 2019; 234(7):11276-11286en
dc.identifier.issn0021-9541en
dc.identifier.issn1097-4652en
dc.identifier.urihttp://hdl.handle.net/2440/119545-
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.language.isoenen
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
dc.identifier.rmid0030106018en
dc.identifier.doi10.1002/jcp.27785en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/508046en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/508047en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1010752en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1127396en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1042105en
dc.identifier.pubid453659-
pubs.library.collectionPsychology publicationsen
pubs.library.teamDS10en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidHassanshahi, M. [0000-0002-4097-8527]en
dc.identifier.orcidHowe, P. [0000-0001-6546-7742]en
dc.identifier.orcidXian, C. [0000-0002-8467-2845]en
Appears in Collections:Psychology publications

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