Impaired defense mechanism against inflammation, hyperalgesia, and airway hyperreactivity in somatostatin 4 receptor gene-deleted mice

Helyes, Zsuzsanna; Pintér, Erika; Sándor, Katalin; Elekes, Krisztián; Bánvölgyi, Ágnes; Keszthelyi, Dániel; Szöke, Éva; Toth, Daniel; Szepes, Zoltán; Kereskai, László; Pozsgai, Gábor; Allen, Jeremy P.; Emson, Piers C.; Markovics, Adrienn; Szolcsányi, Janós

doi:10.1073/pnas.0900681106

Cited by 90 publications

(98 citation statements)

References 38 publications

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“…Mice in OA group were injected with pure OA (Sigma-Aldrich Co., USA) slowly through the tail veins at a volume of 0.6ml/kg by a Micro Sample instrument to induce acute lung injury, and saline was administered 30min before OA injection as vehicle treatment. In SOM+OA group, animals received SOM (1μg/g) 30min before OA (0.6ml/kg) injection [22,23]. All procedures were approved by Experimental Animal Ethics Committee at the Third Military Medical University (TMMU) and performed in accordance with the TMMU guidelines for the care and use of experimental animal which are consistent with the NIH guidelines.…”

Section: Animals and Drugs Treatmentmentioning

confidence: 99%

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Zhao

Zhang

Xiong

et al. 2016

Cell Physiol Biochem

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Background/Aims: Although it has been reported that somatostatin (SOM) upregulated the level of 90-kD heat shock protein (Hsp90), which participates in the inflammatory regulation by its client proteins, such as glucocorticoid receptor (GR), it remains unclear if it has a protective role against acute lung injury (ALI). Methods: ALI model was established by the injection of oleic acid (OA) into the tail vein of mice. Lung injury was assessed by histological analysis, lung water content and arterial blood gases. The levels of Hsp90 and GR, the binding capacity and the affinity of GR were examined. Results: It was showed that pretreatment with SOM significantly increased Hsp90 levels and alleviated lung injuries in OA-injected mice. Furthermore, SOM increased the GR expression and improved the affinity of the GR in animals with lung injury. However, little alteration was found in the maximum binding capacity of the GR in mice with or without SOM. Conclusion: The data indicate SOM exerts a protective effect by increasing Hsp90 abundant and further enhancing the affinity of the GR. The beneficial effects of SOM treatment provide a new strategy for modulation of GR efficiency and alleviation of acute lung injury.

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Section: Animals and Drugs Treatmentmentioning

confidence: 99%

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Zhao

Zhang

Xiong

et al. 2016

Cell Physiol Biochem

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“…Ϫ/Ϫ mice could also exacerbate systemic vascular water loss, based on studies showing that the release of this neuropeptide from intranasal LPS (and presumably endovanilloid)-stimulated airway sensory neurons is anti-inflammatory and protective against pulmonary and systemic injury (12,17,18). As such, a reduction in edema with TRPV1 inhibition would not be expected, rather it would be exacerbated, as implied by Fig.…”

Section: Trpv1 Agonistmentioning

confidence: 99%

“…It is proposed that selective inhibition of TRPV1 and/or specific agonist synthesis pathways may represent a feasible approach to prevent select components of lung injury, such as cytotoxicity via the ER stress response pathway, but that such therapies will require site-specific delivery, based on results that systemic Trpv1 inhibition is associated with adverse consequences, including increased lung (and other tissue) injury, morbidity, and mortality (8,12,17,18,38,43).…”

Section: Trpv1 Agonistmentioning

confidence: 99%

Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury

Thomas

Roberts

Deering-Rice

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Thomas KC, Roberts JK, Deering-Rice CE, Romero EG, Dull RO, Lee J, Yost GS, Reilly CA. Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury. Am J Physiol Lung Cell Mol Physiol 302: L111-L119, 2012. First published September 23, 2011 doi:10.1152/ajplung.00231.2011.-Endogenous agonists of transient receptor potential vanilloid-1 (TRPV1) (endovanilloids) are implicated as mediators of lung injury during inflammation. This study tested the hypothesis that endovanilloids produced following lipopolysaccharide (LPS) treatment activate TRPV1 and cause endoplasmic reticulum stress/GADD153 expression in lung cells, representing a mechanistic component of lung injury. The TRPV1 agonist nonivamide induced GADD153 expression and caused cytotoxicity in immortalized and primary human bronchial, bronchiolar/alveolar, and microvascular endothelial cells, proportional to TRPV1 mRNA expression. In CF-1 mice, Trpv1 mRNA was most abundant in the alveoli, and intratracheal nonivamide treatment promoted Gadd153 expression in the alveolar region. Treatment of CF-1 mice with LPS increased Gadd153 in the lung, lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, and lung wet-to-dry weight ratio. Cotreating mice with LPS and the TRPV1 antagonist LJO-328 reduced Gadd153 induction and LDH in BAL but did not inhibit increases in lung wet-to-dry ratio. In Trpv1 Ϫ/Ϫ mice treated with LPS, Gadd153 induction and LDH in BAL were reduced relative to wild-type mice, and the wet-to-dry weight ratios of lungs from both wild-type and Trpv1 Ϫ/Ϫ mice decreased. Organic extracts of blood collected from LPS-treated mice were more cytotoxic to TRPV1-overexpressing cells compared with BEAS-2B cells and extracts from control mice, however, most pure endovanilloids did not produce cytotoxicity in a characteristic TRPV1-dependent manner. Collectively, these data indicate a role for TRPV1, and endogenous TRPV1 agonists, in ER stress and cytotoxicity in lung cells but demonstrate that ER stress and cytotoxicity are not essential for pulmonary edema.capsaicin; lipopolysaccharides; lung injury; endovanilloids; transient receptor potential vanilloid-1 LUNG INJURY CAN ARISE FROM inflammatory responses elicited by diverse stimuli, including chemical exposures, trauma, endotoxic and hemorrhagic shock, sepsis, and burn injury (24,25,44,45). Limited advances in the treatment of lung injury and the more severe clinical manifestation, acute respiratory distress syndrome (ARDS), mandate a better understanding of the underlying biochemical processes that contribute to lung injury during systemic inflammation (24,44,45).Transient receptor potential vanilloid-1 (TRPV1) is a calcium-selective ion channel that is activated by capsaicin and its synthetic analog nonivamide as well as temperatures Ͼ42°C and H ϩ (pH Ͻ6.2 at 37°C) (7). TRPV1 also is purportedly activated by various inflammatory mediators, including hydrogen sulfide (H 2 S) (1, 5, 41), anandamide (AEA), 2-arachidonoyl glycerol (2-AG), leuk...

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“…A significant anti-inflammatory effect of SRIH has been demonstrated in different animal models in which the experimental induction of inflammation is associated with capsaicin-sensitive nerve terminal stimulation, such as arthritis, subacute pneumonia, and contact dermatitis [19,24]. Recently, elegant studies with SSTR4 –/– animals have revealed that this SSTR subtype is crucial for SRIH anti-inflammatory effects in mice [24,25].…”

Section: Regulation Of Immunity By the Desmentioning

confidence: 99%

“…Recently, elegant studies with SSTR4 –/– animals have revealed that this SSTR subtype is crucial for SRIH anti-inflammatory effects in mice [24,25]. …”

Section: Regulation Of Immunity By the Desmentioning

confidence: 99%

Diffuse Endocrine System, Neuroendocrine Tumors and Immunity: What’s New?

Ameri

Ferone²

2012

Neuroendocrinology

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During the last two decades, research into the modulation of immunity by the neuroendocrine system has flourished, unravelling significant effects of several neuropeptides, including somatostatin (SRIH), and especially cortistatin (CST), on immune cells. Scientists have learnt that the diffuse neuroendocrine system can regulate the immune system at all its levels: innate immunity, adaptive immunity, and maintenance of immune tolerance. Compelling studies with animal models have demonstrated that some neuropeptides may be effective in treating inflammatory disorders, such as sepsis, and T helper 1-driven autoimmune diseases, like Crohn’s disease and rheumatoid arthritis. Here, the latest findings concerning the neuroendocrine control of the immune system are discussed, with emphasis on SRIH and CST. The second part of the review deals with the immune response to neuroendocrine tumors (NETs). The anti-NET immune response has been described in the last years and it is still being characterized, similarly to what is happening for several other types of cancer. In parallel with investigations addressing the mechanisms by which the immune system contrasts NET growth and spreading, ground-breaking clinical trials of dendritic cell vaccination as immunotherapy for metastatic NETs have shown in principle that the immune reaction to NETs can be exploited for treatment.

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Impaired defense mechanism against inflammation, hyperalgesia, and airway hyperreactivity in somatostatin 4 receptor gene-deleted mice

Cited by 90 publications

References 38 publications

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury

Diffuse Endocrine System, Neuroendocrine Tumors and Immunity: What’s New?

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