Vanadium pentoxide (V<sub>2</sub>O<sub>5</sub>) induced mucin production by airway epithelium

Yu, Dongfang; Walters, Dianne M.; Zhu, Lingxiang; Lee, Pak Kei; Chen, Yin

doi:10.1152/ajplung.00301.2010

Cited by 19 publications

(11 citation statements)

References 40 publications

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“…Interestingly, these hyperplastic cells did not stain positive for mucus in the 2 strains we examined (data not shown). This contrasts with studies in other strains of mice and rats, in which V 2 O 5 exposure induced goblet cell metaplasia, mucous production, thickening of airway smooth muscle, and peribronchiolar fibrosis (17, 28).…”

Section: Discussioncontrasting

confidence: 83%

“…For the dose-response study, 0, 0.1, 0.5, 1, 2, or 4 mg/kg V 2 O 5 was aspirated, and mice were euthanized on study d 14 (nϭ6 -8 mice/dose). For kinetic studies, 4 mg/kg V 2 O 5 was aspirated and mice were euthanized on study d 1,2,4,6,8,10,12,14,21,28,56,84, and 112 (nϭ4 -8/group). BXD RI strains were aspirated with 4 mg/kg V 2 O 5 or PBS on study d 0 and 7 and euthanized on study d 14 (nϭ4 -8/group).…”

Section: O 5 Exposurementioning

confidence: 99%

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Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)

Walters¹,

White²,

Patel³

et al. 2013

FASEB j.

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Interstitial lung diseases (ILDs) are characterized by injury, inflammation, and scarring of alveoli, leading to impaired function. The etiology of idiopathic forms of ILD is not understood, making them particularly difficult to study due to the lack of appropriate animal models. Consequently, few effective therapies have emerged. We developed an inbred mouse model of ILD using vanadium pentoxide (V2O5), the most common form of a transition metal found in cigarette smoke, fuel ash, mineral ores, and steel alloys. Pulmonary responses to V2O5, including dose-dependent increases in lung permeability, inflammation, collagen content, and dysfunction, were significantly greater in DBA/2J mice compared to C57BL/6J mice. Inflammatory and fibrotic responses persisted for 4 mo in DBA/2J mice, while limited responses in C57BL/6J mice resolved. We investigated the genetic basis for differential responses through genetic mapping of V2O5-induced lung collagen content in BXD recombinant inbred (RI) strains and identified significant linkage on chromosome 4 with candidate genes that associate with V2O5-induced collagen content across the RI strains. Results suggest that V2O5 may induce pulmonary fibrosis through mechanisms distinct from those in other models of pulmonary fibrosis. These findings should further advance our understanding of mechanisms involved in ILD and thereby aid in identification of new therapeutic targets.

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Section: Discussioncontrasting

confidence: 83%

Section: O 5 Exposurementioning

confidence: 99%

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)

Walters¹,

White²,

Patel³

et al. 2013

FASEB j.

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“…AB/PAS staining was used to detect mucous (goblet) cells as described previously [19]. Alcian blue stains acidic mucins and PAS stains neutral mucins.…”

Section: Methodsmentioning

confidence: 99%

Mucin Deficiency Causes Functional and Structural Changes of the Ocular Surface

Floyd

Evans

et al. 2012

PLoS ONE

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MUC5AC is the most abundant gel-forming mucin in the ocular system. However, the specific function is unknown. In the present study, a Muc5ac knockout (KO) mouse model was subject to various physiological measurements as compared to its wide-type (WT) control. Interestingly, when KO mice were compared to WT mice, the mean tear break up time (TBUT) values were significantly lower and corneal fluorescein staining scores were significantly higher. But the tear volume was not changed. Despite the lack of Muc5ac expression in the conjunctiva of KO mice, Muc5b expression was significantly increased in these mice. Corneal opacification, varying in location and severity, was found in a few KO mice but not in WT mice. The present results suggest a significant difference in the quality, but not the quantity, of tear fluid in the KO mice compared to WT mice. Dry eye disease is multifactorial and therefore further evaluation of the varying components of the tear film, lacrimal unit and corneal structure of these KO mice may help elucidate the role of mucins in dry eye disease. Because Muc5ac knockout mice have clinical features of dry eye, this mouse model will be extremely useful for further studies regarding the pathophysiology of the ocular surface in dry eye in humans.

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“…The protocol was performed as described previously [20,21]. Briefly, BALB/c mice were anesthetized with isoflorane.…”

Section: Mouse Model Of Synergismmentioning

confidence: 99%

Synergistic Up-Regulation of CXCL10 by Virus and IFN γ in Human Airway Epithelial Cells

Oslund

Lee

et al. 2014

PLoS ONE

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Airway epithelial cells are the first line of defense against viral infections and are instrumental in coordinating the inflammatory response. In this study, we demonstrate the synergistic stimulation of CXCL10 mRNA and protein, a key chemokine responsible for the early immune response to viral infection, following treatment of airway epithelial cells with IFN γ and influenza virus. The synergism also occurred when the cells were treated with IFN γ and a viral replication mimicker (dsRNA) both in vitro and in vivo. Despite the requirement of type I interferon (IFNAR) signaling in dsRNA-induced CXCL10, the synergism was independent of the IFNAR pathway since it wasn’t affected by the addition of a neutralizing IFNAR antibody or the complete lack of IFNAR expression. Furthermore, the same synergistic effect was also observed when a CXCL10 promoter reporter was examined. Although the responsive promoter region contains both ISRE and NFκB sites, western blot analysis indicated that the combined treatment of IFN γ and dsRNA significantly augmented NFκB but not STAT1 activation as compared to the single treatment. Therefore, we conclude that IFN γ and dsRNA act in concert to potentiate CXCL10 expression in airway epithelial cells via an NFκB-dependent but IFNAR-STAT independent pathway and it is at least partly regulated at the transcriptional level.

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Vanadium pentoxide (V₂O₅) induced mucin production by airway epithelium

Abstract: Yu D, Walters DM, Zhu L, Lee P-K, Chen Y. Vanadium pentoxide (V2O5) induced mucin production by airway epithelium.

Cited by 19 publications

References 40 publications

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)

Mucin Deficiency Causes Functional and Structural Changes of the Ocular Surface

Synergistic Up-Regulation of CXCL10 by Virus and IFN γ in Human Airway Epithelial Cells

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Vanadium pentoxide (V2O5) induced mucin production by airway epithelium

Abstract: Yu D, Walters DM, Zhu L, Lee P-K, Chen Y. Vanadium pentoxide (V2O5) induced mucin production by airway epithelium.

Cited by 19 publications

References 40 publications

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V2O5)

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V2O5)

Mucin Deficiency Causes Functional and Structural Changes of the Ocular Surface

Synergistic Up-Regulation of CXCL10 by Virus and IFN γ in Human Airway Epithelial Cells

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Product

Resources

About

Vanadium pentoxide (V₂O₅) induced mucin production by airway epithelium

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)

Genetic susceptibility to interstitial pulmonary fibrosis in mice induced by vanadium pentoxide (V₂O₅)