Linked Life Data

21071887

Source:http://linkedlifedata.com/resource/pubmed/id/21071887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-3-22
pubmed:abstractText
Mitochondria are important regulators of both apoptosis and autophagy. One of the triggers for mitochondrial-mediated apoptosis is the production of reactive oxygen species (ROS), which include hydrogen peroxide, superoxide, hydroxyl radical, nitric oxide and peroxynitrite. Recently, several studies have indicated that ROS may also be involved in the induction of autophagy. In the present study, we used H(2)O(2) to induce mitochondrial stress, examined apoptotic- and autophagic-related gene expression and observed LC3 protein (autophagosome presence marker) expression in porcine parthenotes developing in vitro. In porcine four-cell parthenotes cultured for 5 days in NCSU37 medium containing 0.4% BSA, the developmental rate and mitochondrial distribution did not differ from that of the group supplemented with 100 µM H(2)O(2) but was significantly decreased in the group supplemented with 500 µM H(2)O(2) (P<0.05). Transmission electron microscopy (TEM) indicated that whereas normal shaped mitochondria were observed in blastocysts from the control group, abnormal mitochondria (mitophagy) and autophagic vacuoles were observed in blastocysts from the group that received 500 µM H(2)O(2). Furthermore, addition of H(2)O(2) (100 µM and 500 µM) decreased cell numbers (P<0.05) and increased both apoptosis (P<0.05) and LC3 protein expression in the blastocysts. Real-time RT-PCR showed that H(2)O(2) significantly decreased mRNA expression of anti-apoptotic gene Bcl-xL but increased pro-apoptotic genes, Caspase 3 (Casp3) and Bak, and autophagy-related genes, microtubule-associated protein 1 light chain 3 (Map1lc3b) and lysosomal-associated membrane protein 2 (Lamp2). However, the addition of H(2)O(2) had no effect on mRNA expression levels in nuclear DNA-encoded mitochondrial-related genes, cytochrome oxidase (Cox) 5a, Cox5b and Cox6b1, in blastocysts. These results suggest that H(2)O(2) leads to mitochondrial dysfunction that results in apoptosis and autophagy, which is possibly related to porcine early embryo development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1348-4400
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-50
pubmed:meshHeading
pubmed-meshheading:21071887-Animals, pubmed-meshheading:21071887-Apoptosis, pubmed-meshheading:21071887-Apoptosis Regulatory Proteins, pubmed-meshheading:21071887-Autophagy, pubmed-meshheading:21071887-Blastocyst, pubmed-meshheading:21071887-Cell Count, pubmed-meshheading:21071887-Ectogenesis, pubmed-meshheading:21071887-Electron Transport Complex IV, pubmed-meshheading:21071887-Embryo Culture Techniques, pubmed-meshheading:21071887-Gene Expression Regulation, pubmed-meshheading:21071887-Hydrogen Peroxide, pubmed-meshheading:21071887-Lysosomal-Associated Membrane Protein 2, pubmed-meshheading:21071887-Microtubule-Associated Proteins, pubmed-meshheading:21071887-Mitochondria, pubmed-meshheading:21071887-Oxidants, pubmed-meshheading:21071887-Oxidative Stress, pubmed-meshheading:21071887-Parthenogenesis, pubmed-meshheading:21071887-Protein Subunits, pubmed-meshheading:21071887-RNA, Messenger, pubmed-meshheading:21071887-Sus scrofa
pubmed:year
2011
pubmed:articleTitle
Mitochondrial dysfunction influences apoptosis and autophagy in porcine parthenotes developing in vitro.
pubmed:affiliation
Department of Animal Sciences, Chungbuk National University, Chungbuk, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't