Linked Life Data

19006121

Source:http://linkedlifedata.com/resource/pubmed/id/19006121

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-12-29
pubmed:abstractText
High fluence low-power laser irradiation (HF-LPLI) can induce cell apoptosis via the mitochondria/caspase-3 pathway. Here, we further investigated the mechanism involved in the apoptotic process in human lung adenocarcinoma cells (ASTC-a-1) at a laser irradiation fluence of 120 J/cm(2) (633 nm). Cytochrome c release was ascribed to mitochondrial permeability transition (MPT) because the release was prevented by cyclosporine (CsA), a specific inhibitor of MPT. Furthermore, mitochondrial permeability for calcein (approximately 620 Da) was another evidence for the MPT induction under HF-LPLI treatment. A high-level intracellular reactive oxygen species (ROS) generation was observed after irradiation. The photodynamically produced ROS caused onset of MPT, as the ROS scavenger docosahexaenoic acid (DHA) prevented the MPT. However, CsA failed to prevented cell death induced by HF-LPLI, indicating the existence of other signaling pathways. Following laser irradiation, Bax activation occurred after mitochondrial depolarization and cytochrome c release, indicating Bax activation was a downstream event. In the presence of CsA, Bax was still activated at the end-stage of apoptotic process caused by HF-LPLI, suggesting that Bax was involved in an alternative-signaling pathway, which was independent of MPT. Under HF-LPLI treatment, cell viabilities due to pre-treatment with DHA, CsA, or Bax small interfering RNA (siRNA) demonstrated that the MPT signaling pathway was dominant, while Bax signaling pathway was secondary, and more importantly ROS mediated both pathways. Taken together, these results showed that HF-LPLI induced cell apoptosis via the CsA-sensitive MPT, which was ROS-dependent. Furthermore, there existed a secondary signaling pathway through Bax activation. The observed link between MPT and triggering ROS could be a fundamental phenomenon in HF-LPLI-induced cell apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1097-4652
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
218
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
603-11
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
High fluence low-power laser irradiation induces mitochondrial permeability transition mediated by reactive oxygen species.
pubmed:affiliation
MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't