Biochemical and Biophysical Research Communications
Regular Article2,3,7,8-Tetrachlorodibenzo-p-dioxin Increases mRNA Levels for Interleukin-1β, Urokinase Plasminogen Activator, and Tumor Necrosis Factor-α in Human Uterine Endometrial Adenocarcinoma RL95-2 Cells☆
References (35)
- et al.
J. Biol. Chem.
(1994) - et al.
Tox. Appl. Pharmacol.
(1995) - et al.
Tox. Appl. Pharmacol.
(1986) - et al.
Fund. Appl. Toxicol.
(1993) - et al.
Toxicol. Appl. Pharmacol.
(1996) - et al.
Fertil. Steril.
(1996) - et al.
Am. J. Obstet. Gynecol.
(1992) - et al.
Fertil. Steril.
(1996) - et al.
Toxicol.
(1997) - et al.
Mol. Cell. Endocrinol.
(1990)
Fertil. Steril.
Clin. Biochem.
Pharmacol. Toxicol.
Pharmacol. Rev.
Science
Human Reprod.
Human Reprod.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced inflammatory activation is mediated by intracellular free calcium in microglial cells
2013, ToxicologyCitation Excerpt :COX-2 has been shown to be one of the major mediators of pro-inflammatory responses induced by TCDD (Dong et al., 2010; Sciullo et al., 2010). Additionally, TCDD also causes induction of TNF-α production (Charles and Shiverick, 1997), which appears to contribute greatly to the toxic manifestation of TCDD in mice (Taylor et al., 1992). Through binding to its specific receptor, TNF-α is capable of activating Nuclear factor kappaB (NF-κB), which is known to induce further activation of gene transcription of a number of pro-inflammatory cytokines and chemokines (Lappas et al., 2002).
Modulation of the chemokines KC and MCP-1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice
2007, Archives of Biochemistry and BiophysicsCitation Excerpt :For instance, TCDD has been shown to elicit inflammation in liver of TCDD-exposed mice, which is associated with infiltration of inflammatory cells especially macrophages [3]. The induction of proinflammatory cytokines such as TNFα or IL-1β mRNA has been demonstrated in liver [4] and other tissues of TCDD-exposed mice [5] which has been confirmed in numerous in vitro experiments [34–36]. The present study focused on the expression of chemokines such as KC and MCP-1 in different organs of mice after treatment with TCDD.
Aryl hydrocarbon receptor-mediated posttranscriptional regulation of IL-1β
2004, Archives of Biochemistry and BiophysicsOn the significance of the role of cellular stress response reactions in the toxic actions of dioxin
2003, Biochemical PharmacologyCitation Excerpt :Since the liver is the main site of activation of dioxin-induced detoxification enzymes, including those catalyzed by cytochrome P4501A1, it makes sense that oxidative stresses are observed in that organ. In addition to oxidative stress, however, there are many documented signs of other types of cellular stresses induced by dioxin in various cell types; for example, (a) prostaglandin synthesis (e.g. Puga et al. [14] in mouse hepatoma cells; Schuhmacher et al. [15] in ovine seminal vesicle cells; Olnes et al. [16] in rat thymocytes; Liu et al. [17] in HUVEC primary human epithelial cells; Vogel et al. [18,19] in liver, thymus, kidneys, and spleen of mice; and Wölfle et al. [20] in mouse fibroblasts), (b) production of inflammatory cytokines (e.g. Yin et al. [21] in human keratinocytes; Fan et al. [22] in rats; Charles and Shiverick [23] in human endometrial cells; Lang et al. [24] in human lung and blood cells; and Birnbaum and Tuomisto [25] in rats), (c) increased expression of stress markers such as NF-κB (Olnes et al. [26] in rat thymus; and Puga et al. [27] in murine hepatoma cells), (d) increased Ca2+ uptake (Puga et al. [14,28] in murine hepatoma cells), (e) the loss of intracellular pH maintenance (Legare et al. [29] in primary rat astroglia), and (f) reduced glutathione levels (e.g. Shertzer et al. [30] in mouse hepatoma cells; and Zhao and Ramos [31] in rat hepatocytes). The mention of specific cell/tissue types and species in such cases is important, since, as will be shown later, the action of dioxin varies depending on the affected cells.
Induction of apoptosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin following endotoxin exposure
2003, Toxicology and Applied PharmacologyThe aryl hydrocarbon receptor and its xenobiotic ligands: A fundamental trigger for cardiovascular diseases
2003, Nutrition, Metabolism and Cardiovascular Diseases
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TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxinDMSO, dimethyl sulfoxide; kDa, kilodalton; kb, kilobase; IL-1β, interleukin-1β; uPA, urokinase plasminogen activator; TNF-α, tumor necrosis factor-α; EGF, epidermal growth factor;
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Corresponding author: Kathleen T. Shiverick, Ph.D. FAX: (352) 392-9696. E-mail: [email protected].