Growth Hormone Increases Circulating Neutrophil Activation and Provokes Lung Microvascular Injury in Septic Peritonitis Rats

Liu, Zhi-Hai; Yu, Yanping; Jiang, Yining; Li, Jieshou

doi:10.1006/jsre.2002.6374

Cited by 26 publications

(24 citation statements)

References 34 publications

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“…The increase in NF-B activity in the MacGHR KO ATMs is consistent with the inhibitory effect of GH on LPS stimulated NF-B nuclear translocation in human monocytes (41) and our previous studies demonstrating GH-dependent inhibition of NF-B activity in J774A.1 M⌽ (27). In contrast in the lung, GH enhanced LPS stimulated NF-B activity (42), suggesting that the effect of GH on NF-B activation is tissue/cell type-specific.…”

Section: Discussionsupporting

confidence: 90%

Targeted Deletion of Growth Hormone (GH) Receptor in Macrophage Reveals Novel Osteopontin-mediated Effects of GH on Glucose Homeostasis and Insulin Sensitivity in Diet-induced Obesity

Lü

Kumar

Sun

et al. 2013

Journal of Biological Chemistry

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Background: Pituitary growth hormone (GH) is a key hormone in the maintenance of glucose homeostasis. Results: GH acts on the macrophage to blunt the deleterious effects of diet-induced obesity (DIO) on insulin sensitivity. Conclusion:The effect of GH on glucose homeostasis is tissue-specific. Significance: Administration of GH could have salutary effects on DIO-associated chronic inflammation and insulin resistance in humans.

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Section: Discussionsupporting

confidence: 90%

Targeted Deletion of Growth Hormone (GH) Receptor in Macrophage Reveals Novel Osteopontin-mediated Effects of GH on Glucose Homeostasis and Insulin Sensitivity in Diet-induced Obesity

Lü

Kumar

Sun

et al. 2013

Journal of Biological Chemistry

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“…For instance, large lungs (Bartlett, 1971), upper airflow obstruction (Trotman-Dickenson et al, 1991), and narrowing of the small airways (Harrison et al, 1978) accompany GH excess, whereas a decrease in muscle strength and a reduction in the maximum inspiratory and expiratory pressure (Merola et al, 1995(Merola et al, , 1996 are associated with GH deficiency. The possibility that the lung is a target site for GH action is also indicated by the GH-induced production of superoxide by alveolar macrophages (Edwards et al, 1992), the GH-induced increase in circulating lung neutrophil activation during sepsis, and the accompanying increase in microvascular injury (Liu et al, 2002a). Exogenous GH also induces NFB activation in the lung (Liu et al, 2002b), increases phosphorylase A activity (Jost et al, 1979), and stimulates the tyrosine phosphorylation of specific proteins in lung epithelial cells (Batchelor et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…The possibility that the lung is a target site for GH action is also indicated by the GH-induced production of superoxide by alveolar macrophages (Edwards et al, 1992), the GH-induced increase in circulating lung neutrophil activation during sepsis, and the accompanying increase in microvascular injury (Liu et al, 2002a). Exogenous GH also induces NFB activation in the lung (Liu et al, 2002b), increases phosphorylase A activity (Jost et al, 1979), and stimulates the tyrosine phosphorylation of specific proteins in lung epithelial cells (Batchelor et al, 1998). The GH receptor (GHR) gene is also expressed in pulmonary tissues (e.g., Tiong et al, 1989;Garcia-Aragon et al, 1992;Batchelor et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Growth hormone expression in the perinatal and postnatal rat lung

Beyea

Olson

Harvey

2005

Developmental Dynamics

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It is now established that the lung is a target site for pituitary growth hormone (GH) action, because pathophysiological states of pituitary GH excess and deficiency are associated with impaired pulmonary function. The onset of lung development and differentiation is, however, before the ontogenic differentiation of pituitary somatotrophs. GH may be involved, nevertheless, in lung development, because it is present in extrapituitary tissues of preimplantation mouse embryos and in the lung buds of embryonic chickens. The possibility that GH may be expressed in the rat lung during fetal and neonatal development, therefore, has been assessed. GH mRNA was detected in the lung, and its 693-bp sequence was identical to that in the pituitary gland. By in situ hybridization, this transcript was found to be abundantly expressed in the lungs of embryonic day (ED) 17 rats in mesenchymal, mucosal epithelial, and smooth muscle cells. This transcript was expressed in neonates until at least day 14 postnatally and was localized to type I and II epithelial cells and to pulmonary tissue macrophages and alveolar macrophages. GH immunoreactivity paralleled GH mRNA cellular localization throughout the time course studied. This immunoreactivity was specific and was lost after antibody preabsorption. The perinatal and postnatal lung is, therefore, an extrapituitary site of GH gene expression during development. Given that the GH receptor is present in the lung from early development, lung GH may have autocrine and/or paracrine roles in lung growth or differentiation or in pulmonary function.

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“…Nuclear extracts of the intestine tissue was prepared by hypotonic lysis followed by high salt extraction [20][21][22] . EMSA was performed using a commercial kit (Gel Shift Assay System; Promega, Madison, WI) as previously described.…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%

Ketamine suppresses intestinal NF-kappa B activation and proinflammatory cytokine in endotoxic rats

Sun¹,

Xiao-dong²,

Hong³

et al. 2004

WJG

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AIM:To investigate the protective effect of ketamine on the endotoxin-induced proinflammatory cytokines and NFkappa B activation in the intestine. METHODS:Adult male Wistar rats were randomly divided into 6 groups: (a) normal saline control, (b) challenged with endotoxin (5 mg/kg) and treated by saline, (c) challenged with endotoxin (5 mg/kg) and treated by ketamine (0.5 mg/kg), (d) challenged with endotoxin (5 mg/kg) and treated by ketamine (5 mg/kg ), (e) challenged with endotoxin (5 mg/kg) and treated by ketamine (50 mg/kg), and (f) saline injected and treated by ketamine (50 mg/kg). After 1, 4 or 6 h, TNF-α and IL-6 mRNA were investigated in the tissues of the intestine (jejunum) by RT-PCR. TNF-α and IL-6 were measured by ELISA. We used electrophoretic mobility shift assay (EMSA) to investigate NF-kappa B activity in the intestine.RESULTS: NF-kappa B activity, the expression of TNF-α and IL-6 were enhanced in the intestine by endotoxin. Ketamine at a dose of 0.5 mg/kg could suppress endotoxininduced TNF-α mRNA and protein elevation and inhibit NFkappa B activation in the intestine. However the least dosage of ketamine to inhibit IL-6 was 5 mg/kg in our experiment. CONCLUSION:Ketamine can suppress endotoxin-induced production of proinflammatory cytokines such as TNF-α and IL-6 production in the intestine. This suppressive effect may act through inhibiting NF-kappa B.Sun J, Wang XD, Liu H, Xu JG. Ketamine suppresses intestinal NF-kappa B activation and proinflammatory cytokine in endotoxic rats.

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Growth Hormone Increases Circulating Neutrophil Activation and Provokes Lung Microvascular Injury in Septic Peritonitis Rats

Cited by 26 publications

References 34 publications

Targeted Deletion of Growth Hormone (GH) Receptor in Macrophage Reveals Novel Osteopontin-mediated Effects of GH on Glucose Homeostasis and Insulin Sensitivity in Diet-induced Obesity

Targeted Deletion of Growth Hormone (GH) Receptor in Macrophage Reveals Novel Osteopontin-mediated Effects of GH on Glucose Homeostasis and Insulin Sensitivity in Diet-induced Obesity

Growth hormone expression in the perinatal and postnatal rat lung

Ketamine suppresses intestinal NF-kappa B activation and proinflammatory cytokine in endotoxic rats

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