Role of Vasoactive Intestinal Peptide in Hyperoxia-Induced Injury of Primary Type II Alveolar Epithelial Cells

Ao, Xiaoxiao; Fang, Fang; Xu, Feng

doi:10.1007/s12098-010-0248-1

Cited by 6 publications

(3 citation statements)

References 14 publications

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“…Since the inflammatory cells appear in the first few hours of hyperoxia exposure [ 43 ], early inhibition of the inflammatory response might prevent the lung injury and thus, this pathway is expected to contribute to the development of BHR. As confirmed by our findings (Figure 3 A, B), VIP was shown to protect alveolar epithelial cells against hyperoxia via decreasing neutrophil influx into the lung [ 27 , 44 ]. Thus, treatments with sildenafil or VIP protect against the deleterious consequences of hyperoxia-induced lung inflammation by inhibiting polymorphonuclear cell infiltration into the alveolar compartment and reducing the consecutive tissue destruction.…”

Section: Discussionsupporting

confidence: 84%

“…Thus, enhancing NO production in the lungs may counteract the elevated smooth muscle tone via a direct effect [ 23 ] or prevent against the development of chronic lung inflammation and subsequent airway remodeling [ 24 ]. Similar to NO, vasoactive intestinal peptide (VIP), which is also an inhibitory relaxant mediator of the non-adrenergic, non-cholinergic nervous pathway, may also exhibit dual bronchodilatory and anti-inflammatory potential [ 25 – 27 ]. Thus, we aimed at investigating whether the restoration of the NO-dependent processes with a phosphodiesterase type 5 (PDE5) inhibitor, such as sildenafil, or with VIP provides an effective protection against the development of BHR in the acute phase of hyperoxia.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of hyperoxia-induced bronchial hyperreactivity by sildenafil and vasoactive intestinal peptide: impact of preserved lung function and structure

et al. 2014

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Objective Hyperoxia exposure leads to the development of lung injury and bronchial hyperreactivity (BHR) via involvement of nitric oxide (NO) pathway. We aimed at characterizing whether the stimulation of the NO pathway by sildenafil or vasoactive intestinal peptide (VIP) is able to prevent the hyperoxia-induced development of BHR. The respective roles of the preserved lung volume and alveolar architecture, the anti-inflammatory and anti-apoptotic potentials of these treatments in the diminished lung responsiveness were also characterized. Materials and methods Immature (28-day-old) rats were exposed for 72 hours to room air (Group C), hyperoxia (>95%, Group HC), or hyperoxia with the concomitant administration of vasoactive intestinal peptide (VIP, Group HV) or sildenafil (Group HS). Following exposure, the end-expiratory lung volume (EELV) was assessed plethysmographically. Airway and respiratory tissue mechanics were measured under baseline conditions and following incremental doses of methacholine to assess BHR. Inflammation was assessed by analyzing the bronchoalveolar lavage fluid (BALF), while biochemical and histological analyses were used to characterize the apoptotic and structural changes in the lungs. Results The BHR, the increased EELV, the aberrant alveolarization, and the infiltration of inflammatory cells into the BALF that developed in Group HC were all suppressed significantly by VIP or sildenafil treatment. The number of apoptotic cells increased significantly in Group HC, with no evidence of statistically significant effects on this adverse change in Groups HS and HV. Conclusions These findings suggest that stimulating the NO pathway by sildenafil and VIP exert their beneficial effect against hyperoxia-induced BHR via preserving normal EELV, inhibiting airway inflammation and preserving the physiological lung structure, whereas the antiapoptotic potential of these treatments were not apparent in this process.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Prevention of hyperoxia-induced bronchial hyperreactivity by sildenafil and vasoactive intestinal peptide: impact of preserved lung function and structure

et al. 2014

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“…Recently, some studies have suggested that the survival and apoptosis of AECII cells may be involved in the pathological changes of hyperoxiainduced ALI and BPD, which determines the outcome of repair following lung injury (25,26). Previous studies have also found that the excessive apoptosis of AECII cells aggravated pulmonary pathological alteration, which may induce an inflammatory reaction and may aggravate the injury to residual lung tissue (23,(27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

CGRP attenuates hyperoxia-induced oxidative stress-related injury to alveolar epithelial type II cells via the activation of the Sonic hedgehog pathway

Dang

Liu

et al. 2017

International Journal of Molecular Medicine

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The aim of this study was to examine the effect of calcitonin gene-related peptide (CGRP) on primary alveolar epithelial type II (AECII) cells and expression of Sonic hedgehog (SHH) signaling pathway components following exposure to hyperoxia. The AECII cells were isolated and purified from premature rats and exposed to air (21% oxygen), air + CGRP, hyperoxia (95% oxygen) or hyperoxia + CGRP. The production of intracellular reactive oxygen species (ROS) was determined using the 2',7'-dichlorofluorescin diacetate molecular probe. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the culture supernatant were detected by spectrophotometry. The apoptosis of AECII cells was assayed by flow cytometry, and the mRNA and protein expression levels of Shh and Ptc1 in the AECII cells were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot analysis and immunofluorescence, respectively. The cellular pathological changes partly improved and apoptosis was markedly decreased upon treatment with CGRP under hyperoxic conditions. The levels of ROS in the hyperoxia + CGRP group were significantly lower than thoe in the hyperoxia group. In addition, the hyperoxia-induced increase in MDA levels and the decrease in SOD activity in the culture supernatant of the AECII cells were attenuated by CGRP. Compared with the cells exposed to air, hyperoxia markedly inhibited the mRNA and protein expression levels of Shh and Ptc1 in the AECII cells; however, this inhibition was partly attenuated by treatment with CGRP. On the whole, our data suggest that CGRP can partly protect AECII cells from hyperoxia-induced injury, and the upregulation of CGRP may be a potential therapeutic approach with which to combat hyperoxia-induced lung injury, which may be associated with the activation of the SHH signaling pathway.

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ROS-mediated MAPK activation aggravates hyperoxia-induced acute lung injury by promoting apoptosis of type II alveolar epithelial cells via the STAT3/miR-21–5p axis

Qin,

Liu,

Wang

et al. 2023

Molecular Immunology

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Role of Vasoactive Intestinal Peptide in Hyperoxia-Induced Injury of Primary Type II Alveolar Epithelial Cells

Abstract: VIP exerts a protective role in the hyperoxia-induced oxidative stress damage in AECIIs, which probably attributed to its anti-oxidant and anti-apoptosis property.

Cited by 6 publications

References 14 publications

Prevention of hyperoxia-induced bronchial hyperreactivity by sildenafil and vasoactive intestinal peptide: impact of preserved lung function and structure

Prevention of hyperoxia-induced bronchial hyperreactivity by sildenafil and vasoactive intestinal peptide: impact of preserved lung function and structure

CGRP attenuates hyperoxia-induced oxidative stress-related injury to alveolar epithelial type II cells via the activation of the Sonic hedgehog pathway

ROS-mediated MAPK activation aggravates hyperoxia-induced acute lung injury by promoting apoptosis of type II alveolar epithelial cells via the STAT3/miR-21–5p axis

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