Vitamin A Depletion Induced by Cigarette Smoke Is Associated with the Development of Emphysema in Rats

Li, Ting; Molteni, Agostino; Latkovich, Predrag; Castellani, William J.; Baybutt, Richard

doi:10.1093/jn/133.8.2629

Cited by 43 publications

(47 citation statements)

References 36 publications

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“…The concentration we used was equivalent to the CS-40. We felt this concentration would be sufficient due to the fact that the only difference between treating with CS-40 and CS-80 specifically noted in the Miller study was a higher number of total cells in the BAL fluid, with that occurring mainly in young mice (4 weeks of age).Although CSE treatment times in the Miller study varied from 1 to 40 days, we chose to treat the mice for 6 weeks based on a study published by Gairola, in which a time course of CS exposure in C57BL/6 mice shows that 6 weeks is the time point at which an increase in BAL cells occurs [33], and on two other rodent studies showing the development of pathological changes in the lungs occurring at this time point using a similar smoke exposure regimen [22].Following a 6-week exposure, we found that CSE induced a greater influx of inflammatory cells into the lungs compared to the CS exposure. We think this is interesting and postulate that the degree of exposure occurring with each method is most likely not similar.…”

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confidence: 99%

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Elliott

Sisson

West

et al. 2006

Experimental Lung Research

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In this study the authors compared the affect of vapor phase cigarette smoke (CS) versus cigarette smoke extract (CSE) on the lungs and upper airway of C57BL/6 mice. The authors found that CSE treatment significantly increased neutrophil influx (P < .001), baseline ciliary beat frequency (CBF) (P < .05), and protein kinase C activity compared to CS and controls. Isoproterenol increased CBF with CS exposure, but decreased CBF with CSE (P < .01). Isoproterenol increased protein kinase A (PKA) activity in all groups except CSE. CSE exposure induced inflammatory cell bronchiolitis. These data indicate that CSE exposure has differential effects on the lungs and tracheal epithelium compared to CS exposure.Ciliary motility provides the driving force for mucociliary clearance. Normal function of the airway mucociliary clearance system prevents the attachment and colonization of pulmonary pathogens in the upper airways. Mucociliary dysfunction caused by impaired ciliary motility results in mucus accumulation, airway obstruction, and bacterial colonization, increasing the likelihood of infection in the lower airway [1][2][3]. Mucociliary clearance is affected by exposure to a number of environmental agents [4,5], including cigarette smoke. Exposure to cigarette smoke (CS) has been linked to the development of lung cancer, emphysema, chronic bronchitis, and chronic obstructive pulmonary disease (COPD) [6]. Smokers are at a higher risk for pulmonary infection [7]. Chronic exposure to tobacco smoke is associated with increased ciliary abnormality [8] and reduced mucociliary clearance [9]. The increased risk for infection seen in smokers may be due to alterations in ciliary function in the upper airway.Several studies have revealed that ciliary activity is controlled by phosphorylation of axonemal proteins [10][11][12]. Protein kinase C (PKC) and cyclic adenosine monophosphate (CAMP)-Address correspondence to Todd A. Wyatt, PhD, University of Nebraska Medical Center, 985300 Nebraska Medical Center, Omaha, NE 68198-5300, USA. E-mail: twyatt@unmc.edu. NIH Public Access Author ManuscriptExp Lung Res. Author manuscript; available in PMC 2007 November 21. Published in final edited form as:Exp Lung Res. 2006 ; 32(3-4): 99-118. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript dependent protein kinase (PKA) are important regulators of airway ciliary beat frequency (CBF). Agents that increase PKC are associated with decreased CBF [13][14][15]. Alternatively, agents associated with increased CBF also increase PKA activity [16]. In past studies, we have shown that exposure of ciliated epithelial cells to cigarette smoke extract (CSE) in culture and whole cigarette smoke in vivo induces an increase in epithelial cell PKC activity [15,[17][18][19]. Many animal models of exposure to cigarette smoke components exist. Most recently, Miller and colleagues have developed a method of exposure consisting of intranasal administration of CSE [20]. This method was shown to induce an inflammatory response similar to ...

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confidence: 99%

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Elliott

Sisson

West

et al. 2006

Experimental Lung Research

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“…The smoke exposure lasted for 4 weeks, 5d/wk. The cigarette smoke treatment has been previously described in detail [4]. Twelve rats were placed together in a plastic chamber measuring 65 cm long, 50 cm wide, and 45 cm high with three holes, two for holding the cigarette at one side of the chamber and another on the opposite side of the chamber that was connected to a tube attached to a Leeson vacuum pump (model # A6C17EB20.1; Labconco, Kansas City, MO) for drawing the smoke.…”

Section: Cigarette Smoke Exposure Conditionsmentioning

confidence: 99%

“…Rats in the control group were placed in another chamber, but were exposed to air only. The extent of exposure of rats to cigarette smoke was ascertained by measuring total particulate matter inhaled, and is reported in our previous study [4].…”

Section: Cigarette Smoke Exposure Conditionsmentioning

confidence: 99%

“…Vitamin A deficiency has been shown to be associated with bronchial metaplasia and an increased incidence of lung cancer [3]. From our previous study, we have found that exposure to cigarette smoke deceases vitamin A levels in the lungs and results in precancerous lesions in the trachea [4]. The molecular mechanisms by which lung cancer is induced by cigarette smoke and how that is related to vitamin A deficiency is complicated.…”

Section: Introductionmentioning

confidence: 99%

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Microarray Analysis reveals that Dietary Retinoic Acid Suppresses Cancer-Related Gene Expression of the Lungs of Cigarette Smoke Exposed Rats

Xue¹,

Meadors

Wang³

et al. 2012

J Nutr Food Sci

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Sciences Xue et al., J Nutr Food Sci 2012, S2 http://dx.doi.org/10.4172/2155 AbstractPreviously we found that cigarette smoke depleted vitamin A in the lungs and induced tracheal precancerous lesions. To understand the molecular consequences underlying cigarette smoke-induced vitamin A depletion and its associated lung cancer risk, this study investigated the lung cancer-related genes in cigarette smoke-exposed rats with or without dietary retinoic acid, the active metabolite of vitamin A. Twenty-four male weanling rats were fed either a control or a retinoic acid supplemented diet. Half of each group was exposed to 40 commercial cigarettes/ d, 5 d/ wk. After 4 weeks, the rats were sacrificed and their lungs were immediately frozen. Total RNA was extracted and purified, from which cDNA was synthesized and labeled for gene expression analysis. Expressions of 120 genes were measured via a customized microarray. In lungs exposed to cigarette smoke, most of the genes involved in cell division, transcription and cell adhesion were up-regulated. The dietary retinoic acid treatment of the cigarette smoke-exposed lungs was found to down-regulate most of the genes involved in similar functions. In addition, retinoic acid down-regulated four genes, Egr1, Fos, Icam1 and Mmp9, all of which were up-regulated by cigarette smoke. These findings suggest possible molecular mechanisms of cigarette smoke induced-lung cancer and define potential targets of retinoic acid anticarcinogenic actions.

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“…RA is the main active metabolite of vitamin A, and many clinical studies have demonstrated a positive relationship between vitamin A status and lung function (28,29). It was reported that CS exposure causes vitamin A depletion and that the deficiency of vitamin A induces the development of emphysema in rats (30,31). Previous studies have also shown that RA treatment can promote the repair and or realveolarization of parenchymal lesions in animal models of emphysema (32)(33)(34).…”

mentioning

confidence: 99%

Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection

Wang

Liu

Marion

et al. 2015

Am J Respir Cell Mol Biol

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Virus-induced exacerbations often lead to further impairment of lung function in chronic obstructive pulmonary disease. IL-15 is critical in antiviral immune responses. Retinoic acid (RA) signaling plays an important role in tissue maintenance and repair, particularly in the lung. We studied RA signaling and its relation to IL-15 in the lung during cigarette smoke (CS) exposure and influenza virus infection. In vivo studies show that RA signaling is diminished by long-term CS exposure or influenza virus infection alone, which is further attenuated during infection after CS exposure. RA receptor b (RARb) is specifically decreased in the lung of IL-15 transgenic (overexpression; IL-15Tg) mice, and a greater reduction in RARb is found in these mice compared with wild-type (WT) mice after infection. RARb is increased in IL-15 knockout (IL-15KO) mice compared with WT mice after infection, and the additive effect of CS and virus on RARb down-regulation is diminished in IL-15KO mice. IL-15 receptor a (IL-15Ra) is increased and RARb is significantly decreased in lung interstitial macrophages from IL-15Tg mice compared with WT mice. In vitro studies show that IL-15 downregulates RARb in macrophages via IL-15Ra signaling during influenza virus infection. These studies suggest that RA signaling is significantly diminished in the lung by CS exposure and influenza virus infection. IL-15 specifically down-regulates RARb expression, and RARb may play a protective role in lung injury caused by CS exposure and viral infections.

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Vitamin A Depletion Induced by Cigarette Smoke Is Associated with the Development of Emphysema in Rats

Cited by 43 publications

References 36 publications

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Differential in Vivo Effects of Whole Cigarette Smoke Exposure Versus Cigarette Smoke Extract on Mouse Ciliated Tracheal Epithelium

Microarray Analysis reveals that Dietary Retinoic Acid Suppresses Cancer-Related Gene Expression of the Lungs of Cigarette Smoke Exposed Rats

Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection

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