Vasoactive intestinal peptide protects alveolar epithelial cells against hyperoxia via promoting the activation of STAT3

Ao, Xiaoxiao; Fang, Fang; Xu, Feng

doi:10.1016/j.regpep.2011.02.006

Cited by 16 publications

(13 citation statements)

References 23 publications

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“…Perhaps then, inactivation of STAT3 in this model limits its mitochondrial translocation, and may explain in part the increase in neuronal cell death observed following Stattic treatment. STAT3 is also required to maintain mitochondrial membrane potential and limit cell death in lung epithelial cells exposed to hyperoxia [65]. Again, while this study did not directly investigate mitochondrial STAT3’s actions, it suggests that STAT3 may protect the cell from oxidative stress by its actions in both the nucleus and the mitochondria.…”

Section: Signal Transducer and Activator Of Transcription 3 (Stat3)mentioning

confidence: 94%

Toward a new STATe: The role of STATs in mitochondrial function

Meier¹,

Larner²

2014

Seminars in Immunology

146

139

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Signal Transducers and Activators of Transcription (STATs) have been studied extensively and have been associated with virtually every biochemical pathway. Until recently, however, they were thought to exert these effects solely as a nuclear transcription factor. The finding that STAT3 localizes to the mitochondria and modulates respiration has opened up a new avenue through which STATs may regulate the cell. Recently, other members of the STAT family (STAT1, STAT2, STAT5, and STAT6) have also been shown to be present in the mitochondria. Coordinate regulation at the nucleus and mitochondria by these proteins places them in a unique position to drive cellular processes to achieve a specific response. This review summarizes recent findings that have led to our current understanding of how STATs influence mitochondrial function in health and disease.

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Section: Signal Transducer and Activator Of Transcription 3 (Stat3)mentioning

confidence: 94%

Toward a new STATe: The role of STATs in mitochondrial function

Meier¹,

Larner²

2014

Seminars in Immunology

146

139

View full text Add to dashboard Cite

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“…Ao and coworkers showed that the inhibitory nonadrenergic noncholinergic neurotransmitter VIP protects alveolar epithelial cells from the damaging effects of hyperoxia through STAT3-dependent mechanisms (39). Ao and coworkers showed that the inhibitory nonadrenergic noncholinergic neurotransmitter VIP protects alveolar epithelial cells from the damaging effects of hyperoxia through STAT3-dependent mechanisms (39).…”

Section: Regulation Of Epithelial Cell Apoptosismentioning

confidence: 99%

Stat3

Prêle¹,

Yao²,

O’Donoghue³

et al. 2012

Proc Am Thorac Soc

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“…In murine models, lung remodeling and airway hyperreactivity increased when VIP levels were low, suggesting a therapeutic effect of exogenous VIP [26,48]. In human epithelial cell lines VIP protected against hypoxia-induced tissue damage and increased experimental wound repair through cAMP-dependent regulatory signaling [24,25]. Regarding exacerbation caused by viral infection, VIP was protective in mice against cytomegalovirus-induced lung damage [19].…”

Section: Discussionmentioning

confidence: 99%

“…Such beneficial effects of VIP on bronchial and alveolar epithelial cells were supported by animal models, where VIP protected against oxidative stress via a second transcription factor, the signal transducers and activators of transcription 3 (STAT3) [25]. Furthermore, application of VIP prevented hyperoxia-induced pathologic lung function and tissue structural changes in rats [26].…”

Section: Introductionmentioning

confidence: 99%

Vasoactive Intestinal Peptide for Diagnosing Exacerbation in Chronic Obstructive Pulmonary Disease

et al. 2015

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Background: Vasoactive intestinal peptide (VIP) is the most abundant neuropeptide in the lung. VIP has been linked to pulmonary arterial hypertension and hypoxia. Objectives: We aimed to assess circulating VIP levels at exacerbation and at stable chronic obstructive pulmonary disease (COPD) and to evaluate the diagnostic performance in a well-characterized cohort of COPD patients. Methods: The nested cohort study included patients with Global Initiative for Chronic Obstructive Lung Disease stage II-IV. Patients were examined at stable state and at acute exacerbation of COPD (AE-COPD), and dedicated serum was collected at both conditions. Serum VIP levels were determined by enzyme-linked immunosorbent assay. Diagnostic accuracy was analyzed by receiver operating characteristic curve and area under the curve (AUC). Results: Patients with acute exacerbation (n = 120) and stable COPD (n = 163) had similar characteristics at baseline. Serum VIP levels did not correlate with oxygen saturation at rest (p = 0.722) or at exercise (p = 0.168). Serum VIP levels were significantly higher at AE-COPD (130.25 pg/ml, 95% CI 112.19-151.83) as compared to stable COPD (40.07 pg/ml, 95% CI 37.13-43.96, p < 0.001). The association of increased serum VIP with AE-COPD remained significant after propensity score matching (p < 0.001). Analysis of the Youden index indicated the optimal serum VIP cutoff value as 56.6 pg/ml. The probability of AE-COPD was very low if serum VIP was ≤35 pg/ml (sensitivity >90%) and very high if serum VIP was ≥88 pg/ml (specificity >90%). Serum VIP levels presented a robust performance to diagnose AE-COPD (AUC 0.849, 95% CI 0.779-0.899). Conclusions: Increased serum VIP levels are associated with AE-COPD.

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Vasoactive intestinal peptide protects alveolar epithelial cells against hyperoxia via promoting the activation of STAT3

Cited by 16 publications

References 23 publications

Toward a new STATe: The role of STATs in mitochondrial function

Toward a new STATe: The role of STATs in mitochondrial function

Stat3

Vasoactive Intestinal Peptide for Diagnosing Exacerbation in Chronic Obstructive Pulmonary Disease

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