Heat Stress Activates Interleukin-8 and the Antioxidant System via Nrf2 Pathways in Human Dental Pulp Cells

Chang, Seok Woo; Lee, Sang‐im; Bae, Won Kyung; Min, Kyung-San; Shin, Eun-Sang; Oh, Gi‐Su; Pae, Hyun‐Ock; Kim, Eun-Cheol

doi:10.1016/j.joen.2009.06.005

Cited by 27 publications

(21 citation statements)

References 38 publications

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“…In addition, HO-1 and hBD-2 messenger RNA and protein expression increased transiently in HDPCs from 0 to 2 or 6 hours after exposure to LPS and heat stress, returning to time 0 post-treatment levels at 24 hours. These results are consistent with the results of our previous study, which showed that IL-8, IL-8 receptor, and antioxidant enzymes such as HO-1 returned to near-basal levels by 24 hours after heat stress (23). Our results show the recovery of immune and defense gene expression after exposure to LPS and heat stress, indicating that HDPCs have thermotolerance and self-cytoprotective ability.…”

Section: Discussionsupporting

confidence: 93%

“…Similar data were obtained in 3 independent experiments. production was increased by heat stress in Chinese hamster ovary cells, bovine endothelial cells (29), and HDPCs (23) and by LPS in macrophages (30). We examined the induction of IL-8 and TNF-a messenger RNA expression in HDPCs by LPS and heat stress.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, we showed that heat stress activates chemokines such as IL-8 and defense genes such as hemeoxygenase-1 (HO)-1 in HDPCs (23). However, the role of SIRT1 in the regulation of the defense responses to environmental stressors such as LPS and heat is not known.…”

mentioning

confidence: 99%

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Role of SIRT1 in Heat Stress- and Lipopolysaccharide-induced Immune and Defense Gene Expression in Human Dental Pulp Cells

Lee

Min

Bae

et al. 2011

Journal of Endodontics

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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Role of SIRT1 in Heat Stress- and Lipopolysaccharide-induced Immune and Defense Gene Expression in Human Dental Pulp Cells

Lee

Min

Bae

et al. 2011

Journal of Endodontics

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“…Strong correlation has also been observed between activation of heat shock proteins and generation of CXC chemokines in response to heat shock in vitro as well as in vivo model systems; and activation of such a HS response during febrile range hyperthermia, inflammation, infections, and injury augments neutrophil delivery to the site of infection and injury (Nagarsekar et al 2005). Heat stroke induces IL-8 production in blood leukocytes (Huisse et al 2008) and activates expression of IL-8 and its receptor genes in human dental pulp cells (Chang et al 2009). In the present study, higher IL-8 levels observed during parturition and in postpartum period in the hot-humid season confirms that IL-8 is indeed heat stress responsive in buffaloes.…”

Section: Discussionmentioning

confidence: 99%

Temporal changes in circulating levels of plasma interleukin-8 during peripartum period in Murrah buffaloes (Bubalus bubalis) under subtropical climate

Kumar

Mohan³

et al. 2010

Trop Anim Health Prod

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The objective of this study was to elucidate the changes in circulating levels of plasma interleukin-8 (IL-8) during peripartum period in Murrah buffaloes (Bubalus bubalis). IL-8 was estimated in blood plasma of healthy peripartum Murrah buffaloes (n=6) on days ± 30, ± 15, ± 5, ± 3, ± 1 and 0 pre- and postpartum with respect to the day of parturition (day 0) in each of the two different seasons (hot-humid and spring). The mean microclimate Temperature-Humidity Index (THI) during spring season was significantly lower (p<0.01) than the corresponding THI in hot-humid season. In both the seasons, plasma IL-8 remained lower in prepartum period (≤ 46.56 ± 14.08 pg/ml during spring and ≤ 73.18 ± 18.56 pg/ml during hot-humid season) than in the postpartum period (≥ 51.41 ± 13.82 pg/ml during spring and ≥ 84.13 ± 16.97 pg/ml in hot humid season). During spring, the IL-8 levels were significantly higher (P<0.05) on days+5 and +15 postpartum in comparison to the IL-8 levels on days -30, -5, and -3 prepartum. During hot-humid season, IL-8 level was significantly higher (P<0.05) on day +30 as compared to the IL-8 levels on days -30 and -5 prepartum. The correlation between IL-8 and mean microclimate THI was significant (r=0.25, P<0.01). From the results, it is concluded that peripartum period in buffaloes is associated with an inflammatory response leading to significantly higher plasma IL-8 during parturition and postpartum period than in the pre-partum period.

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“…Heme oxygenase 1 (HMOX1) functions as an adaptive mechanism to protect cells from oxidative damage during stress, and is induced by HT in U937 cells [18]. HT has been reported to induce oxidative stress accompanied by an elevation of ROS [8] and an increase in the expression level of NRF2 [51]. Although heat is a principal activator of HSF1, previous findings suggested that this transcription factor can be activated directly by oxidative stress [52].…”

Section: Induction Of Genes Involved In Apoptosis By the Combination mentioning

confidence: 99%

Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification

Tabuchi

Ahmed

Kondo

2016

Hyperthermic Oncology From Bench to Bedside

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Hyperthermia (HT) is considered to be a possible treatment modality for various cancers, and its pleiotropic effects support its combined use with radiotherapy and/or chemotherapy. However, clinical results by HT alone have not always been satisfactory. In mammalian cells, HT elicits a wide spectrum of alterations in cellular morphology, biochemistry and function. One of these HT-induced alterations, oxidative stress, has been attributed to the increased production of reactive oxygen spaces (ROS), and is known to play an important role as an intracellular mediator of HT-induced cell death, including apoptosis. Indeed, it has been well established that increases in intracellular oxidative stress significantly enhance HT-induced apoptosis. Attention has therefore been focused on the development of heat sensitizers to modulate the intracellular ROS. Interestingly, the modification of oxidative stress via addition of ROS-generating compounds significantly enhanced the apoptosis elicited by HT. In this chapter, we describe the induction of oxidative stress by HT and enhancement of HT-induced apoptosis by oxidative stress modification, and we discuss the possible mechanisms underlying this enhancement.

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Heat Stress Activates Interleukin-8 and the Antioxidant System via Nrf2 Pathways in Human Dental Pulp Cells

Cited by 27 publications

References 38 publications

Role of SIRT1 in Heat Stress- and Lipopolysaccharide-induced Immune and Defense Gene Expression in Human Dental Pulp Cells

Role of SIRT1 in Heat Stress- and Lipopolysaccharide-induced Immune and Defense Gene Expression in Human Dental Pulp Cells

Temporal changes in circulating levels of plasma interleukin-8 during peripartum period in Murrah buffaloes (Bubalus bubalis) under subtropical climate

Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification

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