Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage

Hsieh, Ya Ching; Frink, Michael; Hsieh, Chieh; Choudhry, Mashkoor A.; Schwacha, Martin G.; Bland, Kirby I.; Chaudry, Irshad H.

doi:10.1152/ajplung.00479.2006

Cited by 51 publications

(40 citation statements)

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“…23) Moreover, MIF can elevate the neutrophil accumulation by upregulation of IL-6 and TNF-a. 24) Therefore, we investigated whether MIF could stimulate NF-kB and induce IL-6 and TNF-a expression in seawater induced injury. In the present study, we found that seawater exposure induced the elevation of MIF expression as well as phospho-NF-kB p65, IL-6 and TNF-a in vitro.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Attenuates Seawater Aspiration-Induced Lung Injury by Inhibiting Macrophage Migration Inhibitory Factor

Zhang

et al. 2011

Biological & Pharmaceutical Bulletin

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In drowning victims, acute respiratory failure and hypoxia are very common, 1) and hypoxia-induced organ damage due to pulmonary edema caused by aspiration of water has been recognized as a major cause of death in near-drowning victims. [2][3][4] But the exact mechanisms remain unclear. Previous clinical studies have shown that white blood cell and neutrophils apparently increased in most acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) drowning patients' plasma with bilateral diffuse or localized alveolar infiltrates on chest X-ray obtained shortly after arrival. 5) In seawater aspiration-induced ALI rabbits model, the infiltration of inflammatory cells are increased in alveolar spaces with evidence of increasing of myeloperoxidase (MPO) activity and tumor necrosis factor-a (TNF-a) concentration in lung tissue. 6) These results may provide a potential mechanism that inflammation could partly explain the lung injury following seawater aspiration.Danshen, a traditional medical ingredient herbal drug deriving from dried roots of Salvia miltiorrhiza BUNGE, has been widely used in the treatment of acute or chronic diseases as circulatory, cerebrovascular disorders. 7) Tanshinone IIA (TIIA), one of the major active components of Danshen, has been reported to protect against lipopolysaccharide (LPS)-induced lung injury in mice.8) It is also shown that TIIA has an anti-inflammatory effect through the inhibition of nuclear factor-kB (NF-kB) activity 9) and the expression of inflammatory mediators such as nitric oxide, TNF-a, interleukin-1 (IL-1) and interleukin-6 (IL-6) in macrophage cells.10) Whether TIIA plays a protective effect on lung injury following seawater aspiration is unknown.Macrophage migration inhibitory factor (MIF) is recognized as a proinflammatory cytokine which derived from many cell types including macrophages and T lymphocytes.11) It is reported that serum MIF levels are significantly increased in ALI patients or animal model compared to healthy controls, as revealed MIF is a putative biomarker in ALI.12) Additionally, after activating NF-kB, MIF can induce the production of subsequent cytokines.13) The selective inhibition of inflammatory cytokine activities may remain an important goal for the effective treatment of acute lung injury.In the present study, we reported that TIIA treatment significantly attenuated seawater aspiration-induced lung injury. It was probably associated with downregulation of MIF and the subsequent inhibition of NF-kB activity as well as expression of IL-6 and TNF-a. MATERIALS AND METHODSChemicals Tanshinone IIA (sulfonate, purity is 99%) was purchased from the National Institute for the Control of Pharmaceutical and Biological Products (NICPBP, Beijing, China). The kits for determination of myeloperoxidase activity were obtained from Jiancheng Bioengineering Institute (Nanjing, China). Anti-phospho-NF-kB p65 and anti-b-actin monoclonal antibodies were obtained from Santa Cruz Biotechnology Inc. (Santa Cruz, CA, U.S.A.). Anti-MIF monoclonal antibody was g...

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Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Attenuates Seawater Aspiration-Induced Lung Injury by Inhibiting Macrophage Migration Inhibitory Factor

Zhang

et al. 2011

Biological & Pharmaceutical Bulletin

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“…Using a murine model of combined ethanol and burn injury, Messingham et al (4) demonstrated that estradiol reduces macrophage production of proinflammatory IL-6 and enhances survival following bacterial challenge. Furthermore, estradiol has been shown to facilitate cutaneous wound healing through attenuation of macrophage migration inhibitory factor, and to downregulate proinflammatory TNF-␣ production in activated macrophages (3,16,25). More recently, estrogen has been shown to inhibit expression of keratinocyte-derived chemokine, the murine homolog of CXCL8, in activated splenocytes (26).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies indicate that 17␤-estradiol (E2) inhibits the production of proinflammatory cytokines, including IL-6 and macrophage inhibitory factor (3,4). Furthermore, clinical reports demonstrate that premenopausal women have significantly lower LPS-induced TNF-␣ levels compared with men or postmenopausal women (5).…”

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confidence: 99%

Estradiol Attenuates Lipopolysaccharide-Induced CXC Chemokine Ligand 8 Production by Human Peripheral Blood Monocytes

Pioli

Jensen

Weaver

et al. 2007

The Journal of Immunology

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Regulation of the inflammatory response is imperative to the maintenance of immune homeostasis. Activated monocytes elaborate a broad variety of proinflammatory cytokines that mediate inflammation, including CXCL8. Release of this chemokine attracts neutrophils to sites of bacterial invasion and inflammation; however, high levels of CXCL8 may result in excessive neutrophil infiltration and subsequent tissue damage. In this study, we demonstrate that 17β-estradiol (E2) attenuates LPS-induced expression of CXCL8 in human peripheral blood monocytes. Treatment of monocytes with estradiol before administration of LPS reduces CXCL8 message and protein production through an estrogen receptor-dependent mechanism, and luciferase reporter assays demonstrate that this inhibition is mediated transcriptionally. Importantly, the ability of estradiol-pretreated LPS-activated monocytes to mobilize neutrophils is impaired. These results implicate a role for estradiol in the modulation of the immune response, and may lead to an enhanced understanding of gender-based differences in inflammatory control mechanisms.

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“…However, reduced expression of GSK3b (GSK3B), TNFa, TNF-R I, TNF-R II, and IL10 can be observed in HCC and in other liver diseases (Zekri et al 2009). It is also well accepted that estrogen functions as an immunomodulator with a bidirectional effect on cytokine production: at high concentrations, E 2 decreases the production of pro-inflammatory cytokines including TNFa and IL1b (ILB1) (Ito et al 2001, Hsieh et al 2007), whereas at low concentrations, it increases the production of TNFa and IL1b (Roby & Hunt 1994). In breast cancer cells, TNFa partly controls the growth by downregulating the expression of ERa (ESR1) through PI3K/Akt signaling (Lee & Nam 2008), whereas in ERb (ESR2)-overexpressing colon cancer cells, E 2 treatment induces apoptosis without altering the expression of TNFa (Hsu et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor α (ESR1) over-expression mediated apoptosis in Hep3B cells by binding with SP1 proteins

Tu¹,

Velmurugan

Day

et al. 2013

Journal of Molecular Endocrinology

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Previous studies have reported that estrogen receptors (ERs) are expressed in normal human liver, chronic hepatitis, and benign hepatic tumor tissues. However, decreased expression of ERs can be observed in hepatocellular carcinoma (HCC) and the role of ERs in HCC is not fully understood. Thus, the present study aimed to investigate the molecular mechanism induced by the overexpression of ERa (ERa (ESR1)) in Hep3B cells. We first detected the induction of apoptosis in ER-negative Hep3B cells using DNA fragmentation assay and flow cytometry. We found that ERa and ERa plus 17b-estradiol treatment increased apoptosis in Hep3B cells. Additionally, western blotting showed increased expression of active caspase 3 and tumor necrosis factor a (TNFa (TNF)) in ERa-transfected cells. To further understand the importance of SP1-binding sites in the TNFa promoter, ERa-negative Hep3B cells were co-transfected with ERa and a wild-type TNFa plasmid or TNFa with deleted SP1 regions. Deletion of both distant and primal SP1 sites abolished the activity of ERa, and similar results were observed by blocking the expression of SP1 protein using mithramycin (MA). This result indicates that SP1 protein is essential for ERa-activated TNFa promoter activity. Co-immunoprecipitation assay further confirmed the binding interaction between ERa and SP1 in a ligand-dependent manner.In general, we demonstrate that the overexpression of ERa mediates apoptosis in ERa-negative Hep3B cells by the binding of ERa to SP1 protein. Additionally, this ERa-SP1 complex binds to the proximal and distal sites of the TNFa gene promoter and further induces the expression of active caspase 3 in a ligand-dependent manner.

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Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage

Abstract: IH. Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage.

Cited by 51 publications

References 50 publications

Tanshinone IIA Attenuates Seawater Aspiration-Induced Lung Injury by Inhibiting Macrophage Migration Inhibitory Factor

Tanshinone IIA Attenuates Seawater Aspiration-Induced Lung Injury by Inhibiting Macrophage Migration Inhibitory Factor

Estradiol Attenuates Lipopolysaccharide-Induced CXC Chemokine Ligand 8 Production by Human Peripheral Blood Monocytes

Estrogen receptor α (ESR1) over-expression mediated apoptosis in Hep3B cells by binding with SP1 proteins

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