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Conference Paper: The Role of Mitochondria in Cigarette Smoke-induced Inflammation and Apoptosis in Cardiomyocytes

TitleThe Role of Mitochondria in Cigarette Smoke-induced Inflammation and Apoptosis in Cardiomyocytes
Authors
KeywordsCardiomyocytes
Cigarette smoke
Mitochondria
Issue Date2018
PublisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
22nd Annual Scientific Meeting of Institute of Cardiovascular Science and Medicine, Hong Kong, 10 November 2018. In Journal of the Hong Kong College of Cardiology, v. 26 n. 2, p. 108 How to Cite?
AbstractBackground: Smoking has been regarded as the major risk factor for cardiovascular diseases (CVD). Reactive oxygen species (ROS) production has been implicated in promoting inflammation and inducing apoptosis in pathogenesis of cigarette smoke (CS)-induced CVD. The mitochondria are important sources of ROS in the heart. Therefore, it is necessary to investigate the role of mitochondria in smoking-related cardiac injury and whether the therapeutic strategies specifically targeting mitochondrial ROS may have benefits. This study was aimed to investigate the role of mitochondria in cigarette smoke medium (CSM)-exposed human AC16 cardiomyocytes and to examine the effects of mitochondria-targeted antioxidant Mito-TEMPO in vitro. Materials and methods: The AC16 cell line was cultured in DMEM/F12 containing 12.5% fetal bovine serum, in a CO₂ incubator at 37 °C. CSM was prepared by bubbling smoke from two cigarettes into 20ml serum-free medium, which was regarded as 100%. After serum starvation with 1% fetal bovine serum for 24h, cells were pretreated with Mito-TEMPO (1 μM) for 30 mins before 4% CSM was added and incubated for an additional 24h. Supernatant was collected for determination of interleukin (IL)-8 by ELISA. Cells were collected to perform MitoSox Red assay to determine mitochondrial superoxide by flow cytometry. Apoptotic cells were measured with Annexin V apoptosis detection kit. Cell lysates were prepared for Western blot analysis. Results: Exposure of AC16 cells to CSM for 24h significantly induced mitochondrial superoxide production, which was prevented by Mito-TEMPO. Treatment with Mito-TEMPO inhibited CSM-induced IL-8 release and decreased cell apoptosis in cardiomyocytes. Mechanistic study revealed that the beneficial effect of Mito-TEMPO were associated with inhibition of NF-κB phosphorylation. Conclusions: Inhibition of mitochondrial ROS by Mito-TEMPO reduced CSM-induced inflammation and apoptosis via NF-κB pathway in cardiomyocytes in vitro. Thus, mitochondria-targeted antioxidants may be an effective therapy for smoking-related cardiac complications.
Persistent Identifierhttp://hdl.handle.net/10722/274147
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorLiang, Y-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2019-08-18T14:56:00Z-
dc.date.available2019-08-18T14:56:00Z-
dc.date.issued2018-
dc.identifier.citation22nd Annual Scientific Meeting of Institute of Cardiovascular Science and Medicine, Hong Kong, 10 November 2018. In Journal of the Hong Kong College of Cardiology, v. 26 n. 2, p. 108-
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/274147-
dc.description.abstractBackground: Smoking has been regarded as the major risk factor for cardiovascular diseases (CVD). Reactive oxygen species (ROS) production has been implicated in promoting inflammation and inducing apoptosis in pathogenesis of cigarette smoke (CS)-induced CVD. The mitochondria are important sources of ROS in the heart. Therefore, it is necessary to investigate the role of mitochondria in smoking-related cardiac injury and whether the therapeutic strategies specifically targeting mitochondrial ROS may have benefits. This study was aimed to investigate the role of mitochondria in cigarette smoke medium (CSM)-exposed human AC16 cardiomyocytes and to examine the effects of mitochondria-targeted antioxidant Mito-TEMPO in vitro. Materials and methods: The AC16 cell line was cultured in DMEM/F12 containing 12.5% fetal bovine serum, in a CO₂ incubator at 37 °C. CSM was prepared by bubbling smoke from two cigarettes into 20ml serum-free medium, which was regarded as 100%. After serum starvation with 1% fetal bovine serum for 24h, cells were pretreated with Mito-TEMPO (1 μM) for 30 mins before 4% CSM was added and incubated for an additional 24h. Supernatant was collected for determination of interleukin (IL)-8 by ELISA. Cells were collected to perform MitoSox Red assay to determine mitochondrial superoxide by flow cytometry. Apoptotic cells were measured with Annexin V apoptosis detection kit. Cell lysates were prepared for Western blot analysis. Results: Exposure of AC16 cells to CSM for 24h significantly induced mitochondrial superoxide production, which was prevented by Mito-TEMPO. Treatment with Mito-TEMPO inhibited CSM-induced IL-8 release and decreased cell apoptosis in cardiomyocytes. Mechanistic study revealed that the beneficial effect of Mito-TEMPO were associated with inhibition of NF-κB phosphorylation. Conclusions: Inhibition of mitochondrial ROS by Mito-TEMPO reduced CSM-induced inflammation and apoptosis via NF-κB pathway in cardiomyocytes in vitro. Thus, mitochondria-targeted antioxidants may be an effective therapy for smoking-related cardiac complications.-
dc.languageeng-
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiology-
dc.subjectCardiomyocytes-
dc.subjectCigarette smoke-
dc.subjectMitochondria-
dc.titleThe Role of Mitochondria in Cigarette Smoke-induced Inflammation and Apoptosis in Cardiomyocytes-
dc.typeConference_Paper-
dc.identifier.emailLiang, Y: winniell@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMak, JCW=rp00352-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros301009-
dc.identifier.volume26-
dc.identifier.issue2-
dc.identifier.spage108-
dc.identifier.epage108-
dc.publisher.placeHong Kong-

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