Oxygen radicals in the nonvagal component of noncholinergic airway constriction

Zhang, H.-Q.; Tai, Hsin Hsiung; Lai, Yijie

doi:10.1016/0034-5687(96)00004-7

Cited by 4 publications

(2 citation statements)

References 21 publications

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“…CEES may affect transcription, translation, and degradation of β 2 -ARs as a result of desensitization of β-AR by increasing production of TNF-α, generation of ROS, and endogenous catecholamine. Zang et al [55] have shown that oxygen radicals play an important role in the nonvagal component of the noncholinergic bronchoconstriction in guinea pigs in vivo . Morken et al [56] have shown that there is an immediate and sustained systemic elevation of catecholamines including epinephrine, which may set the stage for development of neutrophils-mediated acute lung injury.…”

Section: Discussionmentioning

confidence: 99%

Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog

Kabir

Mukherjee

Rajaratnam

et al. 2009

J Biochem & Molecular Tox

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Abstract2-Choloroethyl Ethyl Sulfide (CEES) exposure causes inflammatory lung diseases, including acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. This may be associated with oxidative stress, which has been implicated in the desensitization of beta-adrenergic receptors (β-ARs). The objective of this study was to investigate whether lung injury induced by intratracheal CEES exposure (2 mg/kg body weight) causes desensitization of β-ARs. The animals were sacrificed after 7 days and lungs were removed. Lung injury was established by measuring the leakage of iodinated-bovine serum albumin ([ 125 I]-BSA) into lung tissue. Receptor-binding characteristics were determined by measuring the binding of [ 3 H] dihydroalprenolol ([ 3 H] DHA) (0.5-24 nM) to membrane fraction in the presence and absence of DL-propranolol (10 μM). Both high-and low-affinity β-ARs were identified in the lung. Binding capacity was significantly higher in low-affinity site in both control and experimental groups. Although CEES exposure did not change K D and B max at the high-affinity site, it significantly decreased both K D and B max at low affinity sites. A 20% decrease in β 2 -AR mRNA level and a 60% decrease in membrane protein levels were observed in the experimental group. Furthermore, there was significantly less stimulation of adenylate cyclase activity by both cholera toxin and isoproterenol in the experimental group in comparison to the control group. Treatment of lungs with 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of phosphodiesterase (PDE) could not abolish the difference between the control group and the experimental group on the stimulation of the adenylate cyclase activity. Thus, our study indicates that CEES-induced lung injury is associated with desensitization of β 2 -AR.

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Section: Discussionmentioning

confidence: 99%

Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog

Kabir

Mukherjee

Rajaratnam

et al. 2009

J Biochem & Molecular Tox

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“…Inhibition of vagus nerve has been shown to increase systemic metastases of 4THM breast carcinoma, while activation of vagus nerve reduces BC metastasis 54,58 . This antimetastatic effect of the vagus nerve has been related to its ability in increasing the neprilysin activity and further degradation of SP to its bioactive fragments 59 . Thus, it can be concluded that stimulating the vagal nerve to alter the level of SP as well as the neprilysin‐like activity may be effective for treating advanced cancers.…”

Section: Sp‐degrading Enzymes and Bc Tumorigenesismentioning

confidence: 99%

New insight into the role of substance P/neurokinin‐1 receptor system in breast cancer progression and its crosstalk with microRNAs

et al. 2020

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The neuropeptide substance P (SP) triggers a variety of tumor-promoting signaling pathways through the activation of neurokinin-1receptor (NK1R), a class of neurokinin G protein-coupled receptors superfamily. Recent researches in our and other laboratories have shown the overexpression of both SP and NK1R in breast cancer (BC) patients. SP/NK1R signaling is strongly implicated in the pathogenesis of BC through affecting cell proliferation, migration, metastasis, angiogenesis, and resistance. Therefore, SP/NK1R signaling responses must be rigorously regulated; otherwise, they would contribute to a more aggressive BC phenotype. Recently, microRNAs (miRNAs) as a specific class of epigenetic regulators have been shown to regulate NK1R and thus, controlling SP/NK1R signaling responses in BC. This review summarizes the current knowledge of the role of SP/NK1R signaling and its therapeutic potentials in BC. We also provide an overview regarding the effects of miRNA-mediated NK1R regulatory mechanisms in controlling BC tumorigenesis to gain a clearer view and thus better management of cancer.

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Vagotomy enhances experimental metastases of 4THMpc breast cancer cells and alters Substance P level

Erin

Barkan

Harms

et al. 2008

Regulatory Peptides

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Oxygen radicals in the nonvagal component of noncholinergic airway constriction

Cited by 4 publications

References 21 publications

Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog

Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog

New insight into the role of substance P/neurokinin‐1 receptor system in breast cancer progression and its crosstalk with microRNAs

Vagotomy enhances experimental metastases of 4THMpc breast cancer cells and alters Substance P level

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