Mdivi-1, mitochondrial fission inhibitor, impairs developmental competence and mitochondrial function of embryos and cells in pigs

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dc.contributor.authorJ Y Yeon-
dc.contributor.authorS H Min-
dc.contributor.authorH J Park-
dc.contributor.authorJ W Kim-
dc.contributor.authorY H Lee-
dc.contributor.authorS Y Park-
dc.contributor.authorPil-Soo Jeong-
dc.contributor.authorH Park-
dc.contributor.authorD S Lee-
dc.contributor.authorSun-Uk Kim-
dc.contributor.authorKyu Tae Chang-
dc.contributor.authorD B Koo-
dc.date.accessioned2017-04-19T10:03:45Z-
dc.date.available2017-04-19T10:03:45Z-
dc.date.issued2015-
dc.identifier.issnI000-0068-
dc.identifier.uri10.1262/jrd.2014-070ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12586-
dc.description.abstractMitochondria are highly dynamic organelles that undergo constant fusion/fission as well as activities orchestrated by large dynamin-related GTPases. These dynamic mitochondrial processes influence mitochondrial morphology, size and function. Therefore, this study was conducted to evaluate the effects of mitochondrial fission inhibitor, mdivi-1, on developmental competence and mitochondrial function of porcine embryos and primary cells. Presumptive porcine embryos were cultured in PZM-3 medium supplemented with mdivi-1 (0, 10 and 50 μM) for 6 days. Porcine fibroblast cells were cultured in growth medium with mdivi-1 (0 and 50 μM) for 2 days. Our results showed that the rate of blastocyst production and cell growth in the mdivi-1 (50 μM) treated group was lower than that of the control group (P < 0.05). Moreover, loss of mitochondrial membrane potential in the mdivi-1 (50 μM) treated group was increased relative to the control group (P < 0.05). Subsequent evaluation revealed that the intracellular levels of reactive oxygen species (ROS) and the apoptotic index were increased by mdivi-1 (50 μM) treatment (P < 0.05). Finally, the expression of mitochondrial fission-related protein (Drp 1) was lower in the embryos and cells in the mdivi-1-treated group than the control group. Taken together, these results indicate that mdivi-1 treatment may inhibit developmental competence and mitochondrial function in porcine embryos and primary cells. Key words: Embryos, Fibroblast cells, Mdivi-1, Mitochondria, Pig.-
dc.publisherSociety Reproduction & Development-Srd-
dc.titleMdivi-1, mitochondrial fission inhibitor, impairs developmental competence and mitochondrial function of embryos and cells in pigs-
dc.title.alternativeMdivi-1, mitochondrial fission inhibitor, impairs developmental competence and mitochondrial function of embryos and cells in pigs-
dc.typeArticle-
dc.citation.titleJournal of Reproduction and Development-
dc.citation.number2-
dc.citation.endPage89-
dc.citation.startPage81-
dc.citation.volume61-
dc.contributor.affiliatedAuthorPil-Soo Jeong-
dc.contributor.affiliatedAuthorSun-Uk Kim-
dc.contributor.affiliatedAuthorKyu Tae Chang-
dc.contributor.alternativeName연지영-
dc.contributor.alternativeName민성훈-
dc.contributor.alternativeName박효진-
dc.contributor.alternativeName김진우-
dc.contributor.alternativeName이용희-
dc.contributor.alternativeName박수용-
dc.contributor.alternativeName정필수-
dc.contributor.alternativeName박흠대-
dc.contributor.alternativeName이동석-
dc.contributor.alternativeName김선욱-
dc.contributor.alternativeName장규태-
dc.contributor.alternativeName구덕본-
dc.identifier.bibliographicCitationJournal of Reproduction and Development, vol. 61, no. 2, pp. 81-89-
dc.identifier.doi10.1262/jrd.2014-070-
dc.subject.keywordEmbryos-
dc.subject.keywordFibroblast cells-
dc.subject.keywordMdivi-1-
dc.subject.keywordMitochondria-
dc.subject.keywordPig-
dc.subject.localEmbryo-
dc.subject.localembryos-
dc.subject.localembryo-
dc.subject.localEmbryos-
dc.subject.localFibroblast cells-
dc.subject.localMdivi-1-
dc.subject.localMitochondria-
dc.subject.localmitochondria-
dc.subject.localPigs-
dc.subject.localpigs-
dc.subject.localPig-
dc.subject.localpig-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
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