Assessment of vitamin A status in chronic obstructive pulmonary disease patients and healthy smokers

Paiva, Sérgio Alberto Rupp de; Godoy, Irma; Vannucchi, Hélio; Fávaro, Rosa Maria Duarte; Geraldo, Rosana Regina Cardoso; Campana, Álvaro Oscar

doi:10.1093/ajcn/64.6.928

Cited by 65 publications

(45 citation statements)

References 38 publications

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“…In these patients, the prevalence of nutritional depletion, a dietary intake significantly higher than estimated energy needs and evidence suggesting ongoing inflammatory reaction, as shown by the finding of higher serum IL-6 concentration, are in agreement with previously available data obtained in clinically stable COPD patients [1,[17][18][19][20]. Although no significant relationship could be established, these findings may indicate that the higher levels of IL-6 are not related to a deficit of energy intake and that other factors may contribute to the elevated levels of this cytokine in COPD patients.…”

Section: Discussionsupporting

confidence: 90%

Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients

Godoy¹,

Campana

Geraldo³

et al. 2003

Eur Respir J

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Tumour necrosis factor (TNF)-a has been found to be increased in malnourished chronic obstructive pulmonary disease (COPD) patients; however, the main cause of this phenomenon remains undetermined. In normal subjects, TNF-a production may be induced by dietary energy deprivation. The aim of this study was to investigate if stable COPD patients present alterations of inflammatory mediators after 48 h of dietary energy restriction.Fourteen COPD patients were admitted to the hospital while receiving an experimental diet with an energy content of approximately one-third of their energy needs. Clinical evaluation, nutritional assessment and serum levels of interleukin (IL)-6, TNF-a and C-reactive protein, and secretion of TNF-a by peripheral blood monocytes were assessed on admission and after the experimental diet. For reference values of the laboratory parameters, blood was collected from 10 healthy, elderly subjects.COPD patients showed significantly higher serum concentrations of IL-6 than control subjects, however, the experimental diet was not associated with statistically significant changes in the inflammatory mediators.The findings of this study, although preliminary because of the limited degree and duration of the energy restriction, suggest that the elevated levels of tumour necrosis factor-a, previously described in undernourished or weight-losing chronic obstructive pulmonary disease patients, may not be linked to a decrease of dietary energy intake. Eur Respir J 2003; 22: 920-925.

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Section: Discussionsupporting

confidence: 90%

Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients

Godoy¹,

Campana

Geraldo³

et al. 2003

Eur Respir J

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“…Given the possibility that ATRA may negatively regulate pulmonary artery SMC mass, the decreased ATRA level in the plasma of pulmonary hypertension patients implies a potential role of this specific retinoid in pulmonary vascular remodeling. Decreased levels of plasma retinol, a precursor of ATRA, have been found in patients with chronic obstructive pulmonary disease; this disease, like asthma, often includes increased smooth muscle mass in airway remodeling (36). Further work is required to determine whether plasma levels of ATRA are involved in reduced inhibition of airway SMC migration in patients with asthma.…”

Section: Discussionmentioning

confidence: 99%

Retinoic Acid Inhibits Airway Smooth Muscle Cell Migration

Day

Lee²,

Park³

et al. 2006

Am J Respir Cell Mol Biol

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Airway remodeling in chronic asthma is characterized by increased smooth muscle mass that is associated with the reduction of the bronchial lumen as well as airway hyperresponsiveness. The development of agents that inhibit smooth muscle growth is therefore of interest for therapy to prevent asthma-associated airway remodeling. All-trans retinoic acid (ATRA) suppresses growth of vascular smooth muscle cells (SMCs) from the systemic and pulmonary circulation. The present study investigated the effects of ATRA on human bronchial (airway) SMCs. Human bronchial SMCs were found to express mRNAs for retinoic acid receptor (RAR)-␣, -␤, -␥, and retinoid X receptor (RXR)-␣, -␤, but not RXR-␥. Although ATRA was not effective in inhibiting proliferation or in inducing apoptosis in airway SMCs, we found that ATRA (0.2-2 M) inhibited the SMC migration in response to platelet-derived growth factor (PDGF), as determined in a modified Boyden chamber assay. Both RAR and RXR agonists also blocked PDGF-induced airway SMC migration. ATRA also inhibited PDGF-induced actin reorganization associated with migration. PDGF-induced actin reorganization and migration were blocked by inhibitors of phosphatidylinositol 3 kinase (PI3K) and Akt. However, migration was blocked by inhibitors of the MEK/ ERK pathway, with no effect on cytoskeletal reorganization. ATRA suppressed PDGF-induced Akt activation without influencing ERK activation. RAR was found to form protein-protein interactions with the p85 PI3K subunit. These results suggest that retinoic acid inhibits airway SMC migration through the modulation of the PI3K/Akt pathway.

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“…15 Furthermore, patients with more severe chronic obstructive pulmonary disease, who would be expected to have more pulmonary vascular involvement, have decreased levels of plasma retinol, a precursor of ATRA, compared with patients with mild chronic obstructive pulmonary disease. 16 Thus, decreased ATRA levels may predispose to increased pulmonary vascular remodeling, given the evidence that ATRA negatively regulates pulmonary artery smooth muscle cell proliferation. The relationship between retinoids and pulmonary hypertension, however, has not yet been defined.…”

mentioning

confidence: 99%

Retinoids and Pulmonary Hypertension

et al. 2005

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Background-Retinoic acid has antimitogenic effects on smooth muscle cells. Studies on the systemic circulation suggest that it may reduce vascular thickening. Relationships between retinoids and pulmonary hypertension/pulmonary vascular remodeling, however, have not been explored. Thus, the present study examined retinoid levels in plasma of patients with idiopathic pulmonary arterial hypertension and the effects of retinoic acid on human pulmonary artery smooth muscle cell growth. Methods and Results-We measured retinoid levels by gas chromatograph-mass spectrometer technique in plasma of idiopathic pulmonary arterial hypertension patients and in age-and sex-matched healthy control subjects. Patients had significantly lower levels of all-trans retinoic acid and 13-cis retinoic acid than control subjects but similar 9-cis retinoic acid and retinol levels. In cultured human pulmonary artery smooth muscle cells, all-trans retinoic acid suppressed serotonin-induced cell growth. These cells were found to express the retinoid acid receptors RAR␣, RAR␤, RAR␥, RXR␣, and RXR␤. Gene array analysis showed that retinoic acid induces the expression of GADD45A, a known cell growth suppressor. Contrary to expectations, plasma from pulmonary hypertension patients suppressed cell growth, likely influenced by factors other than retinoids. Conclusions-Idiopathic

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Assessment of vitamin A status in chronic obstructive pulmonary disease patients and healthy smokers

Cited by 65 publications

References 38 publications

Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients

Cytokines and dietary energy restriction in stable chronic obstructive pulmonary disease patients

Retinoic Acid Inhibits Airway Smooth Muscle Cell Migration

Retinoids and Pulmonary Hypertension

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