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Int J Med Sci 2016; 13(5):357-364. doi:10.7150/ijms.14592 This issue Cite

Research Paper

Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts

Moon-Soo Kim1, Jeong-Won Yun1, Jin-Ho Park1, Bong-Wook Park1, Young-Hoon Kang1, Young-Sool Hah2, Sun-Chul Hwang3, Dong Kyun Woo4, ✉, June-Ho Byun1,✉

1. Department of Oral and Maxillofacial Surgery, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, Institute of Health Sciences, Gyeongsang National University, Chilam-dong, Jinju, 660-702, Republic of Korea
2. Clinical Research Institutue of Gyeongsang National University Hospital, Jinju, Republic of Korea
3. Department of Orthopaedic Surgery, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju, Republic of Korea
4. College of Pharmacy and Research Institute of Pharmaceutical Sciences, Gyeongsang National University, Jinju, Republic of Korea

✉ Corresponding authors: June-Ho Byun (Department of Oral and Maxillofacial Surgery, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital, Institute of Health Sciences, Gyeongsang National University, Chilam-do More

Citation:
Kim MS, Yun JW, Park JH, Park BW, Kang YH, Hah YS, Hwang SC, Woo DK, Byun JH. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts. Int J Med Sci 2016; 13(5):357-364. doi:10.7150/ijms.14592. https://www.medsci.org/v13p0357.htm
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Abstract

The deleterious role of cigarette smoke has long been documented in various human diseases including periodontal complications. In this report, we examined this adverse effect of cigarette smoke on human gingival fibroblasts (HGFs) which are critical not only in maintaining gingival tissue architecture but also in mediating immune responses. As well documented in other cell types, we also observed that cigarette smoke promoted cellular reactive oxygen species in HGFs. And we found that this cigarette smoke-induced oxidative stress reduced HGF viability through inducing apoptosis. Our results indicated that an increased Bax/Bcl-xL ratio and resulting caspase activation underlie the apoptotic death in HGFs exposed to cigarette smoke. Furthermore, we detected that cigarette smoke also triggered autophagy, an integrated cellular stress response. Interesting, a pharmacological suppression of the cigarette smoke-induced autophagy led to a further reduction in HGF viability while a pharmacological promotion of autophagy increased the viability of HGFs with cigarette smoke exposures. These findings suggest a protective role for autophagy in HGFs stressed with cigarette smoke, highlighting that modulation of autophagy can be a novel therapeutic target in periodontal complications with cigarette smoke.

Keywords: cigarette smoke, oxidative stress, apoptosis, autophagy, gingival fibroblast

Citation styles

APA
Kim, M.S., Yun, J.W., Park, J.H., Park, B.W., Kang, Y.H., Hah, Y.S., Hwang, S.C., Woo, D.K., Byun, J.H. (2016). Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts. International Journal of Medical Sciences, 13(5), 357-364. https://doi.org/10.7150/ijms.14592.

ACS
Kim, M.S.; Yun, J.W.; Park, J.H.; Park, B.W.; Kang, Y.H.; Hah, Y.S.; Hwang, S.C.; Woo, D.K.; Byun, J.H. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts. Int. J. Med. Sci. 2016, 13 (5), 357-364. DOI: 10.7150/ijms.14592.

NLM
Kim MS, Yun JW, Park JH, Park BW, Kang YH, Hah YS, Hwang SC, Woo DK, Byun JH. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts. Int J Med Sci 2016; 13(5):357-364. doi:10.7150/ijms.14592. https://www.medsci.org/v13p0357.htm

CSE
Kim MS, Yun JW, Park JH, Park BW, Kang YH, Hah YS, Hwang SC, Woo DK, Byun JH. 2016. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts. Int J Med Sci. 13(5):357-364.

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