15d-PGJ2 stimulates HO-1 expression through p38 MAP kinase and Nrf-2 pathway in rat vascular smooth muscle cells

Lim, Hyun-Joung; Lee, Kuy-Sook; Lee, Seahyoung; Park, Jin Hee; Choi, Hyun‐Chul; Go, Sang Hee; Kwak, Hyun-Jeong; Park, Hyun-Young

doi:10.1016/j.taap.2007.04.019

Cited by 67 publications

(45 citation statements)

References 42 publications

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“…In the present study, we demonstrated that 15d-PGJ2 could rescue the effect of TDI on the expression of HO-1/FTL. It has been proposed that the effect of 15d-PGJ2 on the induction of HO-1 is independent of PPAR-g [36]. We also observed that 15d-PGJ2 is more effective than rosiglitazone.…”

Section: Discussionsupporting

confidence: 70%

Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma

Kim¹,

Choi²,

Ye³

et al. 2010

Clinical and Experimental Immunology

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SummaryDiisocyanate is a leading cause of occupational asthma (OA). Diisocyanateinduced OA is an inflammatory disease of the airways that is associated with airway remodelling. Although the pathogenic mechanisms are unclear, oxidative stress may be related to the pathogenesis of diisocyanate-induced OA. In our previous report, we observed that the expression of ferritin light chain (FTL) was decreased in both of bronchoalveolar lavage fluid and serum of patients with diphenyl-methane diisocyanate (MDI)-induced OA compared to those of asymptomatic exposed controls and unexposed healthy controls. In this study of toluene diisocyanate (TDI)-OA, we found identical findings with increased transferrin and decreased ferritin levels in the serum of patients with TDI-OA. To elucidate whether diisocyanate suppresses FTL synthesis directly, we tested the effect of TDI on the FTL synthesis in A549 cells, a human airway epithelial cell line. We found that haem oxygenase-1 as well as FTL was suppressed by treatment with TDI in dose-and timedependent manners. We also found that the synthesis of other anti-oxidant proteins such as thioredoxin-1, glutathione peroxidase, peroxiredoxin 1 and catalase were suppressed by TDI. Furthermore, TDI suppressed nuclear translocation of Nrf2 through suppressing the phosphorylation of mitogenactivated protein kinases (MAPKs); extracellular-regulated kinase 1/2 (ERK1/ 2); p38; and c-Jun N-terminal kinase (JNK). Peroxisome proliferator-activated receptor-g (PPAR-g) agonists, 15-deoxy-D 12,14 -PGJ2 and rosiglitazone rescued the effect of TDI on HO-1/FTL expression. Collectively, our findings suggest that TDI suppressed HO-1/FTL expression through the MAPK-Nrf2 signalling pathway, which may be involved in the pathogenesis of TDI-induced OA. Therefore, elucidating these observations further should help to develop the therapeutic strategies of diisocyanate-induced OA.

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Section: Discussionsupporting

confidence: 70%

Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma

Kim¹,

Choi²,

Ye³

et al. 2010

Clinical and Experimental Immunology

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“…Oxidative agents, including heme, hyperoxia and ROS, induce HO-1 gene expression through activation of MAPKs (45). The role of MAPK pathways in the process of HO-1 expression has been demonstrated (9,46). In this study, kaempferol-induced HO-1 expression was directly related to the JNK pathway because a JNK inhibitor SP600125 and a JNK DN plasmid affected the kaempferol-induced change in the HO-1 protein level, while each inhibitor of ERK and p38 pathways did not (Fig.…”

Section: Discussionmentioning

confidence: 54%

Kaempferol Suppresses Cisplatin-Induced Apoptosis Via Inductions of Heme Oxygenase-1 and Glutamate-Cysteine Ligase Catalytic Subunit in HEI-OC1 cells

et al. 2009

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“…Confirming previous reports, we found that exogenous PGE 2 and 15dPGJ 2 are able to elicit HO-1 protein expression (Chen et al 2002;Kansanen et al 2009). HO-1 expression by 15dPGJ 2 acted through the p38, ERK, and Nrf-2 pathways (Kansanen et al 2009;Kim et al 2006;Lim et al 2007), while HO-1 induction by PGE 2 was through the Akt and ERK pathways (Chen et al 2002;Park et al 2009). In J774 macrophages, maximal extents of HO-1 upregulation by PGE 2 were less significant than the dramatic response to 15dPGJ 2 .…”

Section: Discussionmentioning

confidence: 99%

Celecoxib induces heme oxygenase-1 expression in macrophages and vascular smooth muscle cells via ROS-dependent signaling pathway

Wang

Kang

et al. 2010

Naunyn-Schmied Arch Pharmacol

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The multiple cytoprotective mechanisms of heme oxygenase (HO)-1 make it a promising therapeutic target. This study investigated whether the selective cyclooxygenase (COX)-2 inhibitor, celecoxib, can upregulate HO-1 expression. Murine J774 macrophages and rat aortic vascular smooth muscle cells (VSMCs) were used to study the effect of celecoxib on HO-1 expression. A signal transduction pathway involving reactive oxygen species (ROS) was also investigated. We found that celecoxib can upregulate HO-1 gene and protein expressions in J774 macrophages and VSMCs. This effect was not diminished by prostaglandin E(2) or 15dPGJ(2), while it was additive to hypoxia-induced HO-1 expression, suggesting an event independent of COX-2 activity or hypoxia-inducible factor-1α. Moreover, celecoxib activated ERK, p38, Akt, and Nrf2 as well as increased ROS production. All these events contributed to the increase in the expression of HO-1 caused by celecoxib. In this study, we also, for the first time, demonstrated that AMP-activated protein kinase (AMPK) can mediate HO-1 expression via the downstream activation of p38 and Akt. However, the HO-1-inducing actions of celecoxib and hypoxia were not associated with AMPK. This study demonstrates a COX-2-independent action of celecoxib in upregulating HO-1 in macrophages and VSMCs. This action is dependent on ROS, Akt, ERK, p38, and Nrf2 activation. These findings provide new insights into the action mechanism of celecoxib with broad implications for anti-inflammation therapy.

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15d-PGJ2 stimulates HO-1 expression through p38 MAP kinase and Nrf-2 pathway in rat vascular smooth muscle cells

Cited by 67 publications

References 42 publications

Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma

Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma

Kaempferol Suppresses Cisplatin-Induced Apoptosis Via Inductions of Heme Oxygenase-1 and Glutamate-Cysteine Ligase Catalytic Subunit in HEI-OC1 cells

Celecoxib induces heme oxygenase-1 expression in macrophages and vascular smooth muscle cells via ROS-dependent signaling pathway

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