Serum Heme Oxygenase-1 as a Marker of Lung Function Decline in Patients With Chronic Silicosis

Sato, Takashi; Saito, Yoshiaki; Inoue, Satoshi; Shimosato, Takeshi; Takagi, Shigeto; Kaneko, Takeshi; Ishigatsubo, Yoshiaki

doi:10.1097/jom.0b013e3182636e93

Cited by 20 publications

(21 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The protective properties of HO-1 are multifactorial and likely due to degradation of pro-oxidant heme, the generation of antioxidant biliverdin and bilirubin, and the production of carbon monoxide, which is a potent vasodilator with anti-inflammatory effects (7,9). Furthermore, previous studies have also observed reduced serum HO-1 in lung disease (31). The presence of HO-1 has recently been demonstrated in various intracellular and extracellular compartments, suggesting that this protein may exhibit other functions independently of its known enzymatic activity (18,20,32).…”

Section: Discussionmentioning

confidence: 99%

Plasma heme oxygenase-1 is decreased in peripheral artery disease patients

Signorelli

Volsi

Fiore

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

Peripheral artery disease (PAD) is a common manifestation of atherosclerosis. A number of emerging risk factors, including oxidative stress biomarkers, free radicals and heat shock proteins, may add to the established risk factors for cardiovascular disease (CVD). The present study assessed surrogate markers of oxidative stress, including total reduced glutathione (GSH), lipid hydroperoxides (LOOH), isoprostanes, heme oxygenase‑1 (HO‑1) and metabolic biomarkers, such as adiponectin and lactate, in PAD patients (n=27). Healthy age‑matched volunteers (n=27) served as controls. GSH and LOOH were evaluated by measuring total thiol groups and iron oxidation, respectively, by spectrophotometric analysis. Adiponectin, isoprostanes and HO‑1 levels were determined using commercially available ELISA kits and lactate level was determined colorimetrically. Results from patients with PAD demonstrated no significant difference in GSH content and LOOH formation when compared with healthy controls (5.1±7.6 vs. 6.9±9.1 nmol/ml and 6.8±14.2 vs. 8.3±14.9 nmol/ml, respectively), however, isoprostanes were demonstrated to be significantly reduced (3.8±4.8 pg/ml vs. 120±91 pg/mll; P<0.001). Furthermore, HO‑1, a protective heat shock protein, was significantly reduced in PAD patients (0.8±0.7 vs. 3.4±1.3 ng/ml; P<0.001). Adiponectin, an antiatherogenic adipokine, was not significantly different between the two groups (1.4±0.2 vs. 1.5±0.5 µg/ml), whereas serum lactate was significantly higher in PAD patients compared with controls (0.11±0.01 vs. 0.1±0.01 mM; P<0.05). Using multivariate analysis, HO‑1, hypertension, smoking and dyslipidemia were indicated to be independently associated with the presence of PAD, while only ankle‑brachial index was an independent predictor of severity of PAD. The oxidative pathway may be partially involved in the onset and progression of PAD and may represent a target to reduce the risk of ischemic events.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma heme oxygenase-1 is decreased in peripheral artery disease patients

Signorelli

Volsi

Fiore

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“… 32 – 34 Of interest, these findings suggest that serum HO-1 levels might be markers of disease severity in individuals exposed to silica. 35 …”

Section: Therapy Of Silicosismentioning

confidence: 99%

Silicosis and lung cancer: current perspectives

Sato¹,

Shimosato²,

Klinman³

2018

LCTT

Self Cite

View full text Add to dashboard Cite

“Silica” refers to crystalline particles formed by the combination of silicon with oxygen. Inhalation of silica particles promotes the development of pulmonary fibrosis that over prolonged periods increases the risk of lung cancer. The International Agency for Research on Cancer (IARC) classified crystalline silica as a human carcinogen in 1997. This categorization was questioned due to 1) the absence of dose–response findings, 2) the presence of confounding variables that complicated interpretation of the data and 3) potential selection bias for compensated silicosis. Yet, recent epidemiologic studies strongly support the conclusion that silica exposure increases the risk of lung cancer in humans independent of confounding factors including cigarette smoke. Based on this evidence, the US Occupational Safety and Health Administration (OSHA) lowered the occupational exposure limit for crystalline silica from 0.1 to 0.05 mg/m3 in 2013. Further supporting the human epidemiologic data, murine models show that chronic silicosis is associated with an increased risk of lung cancer. In animals, the initial inflammation induced by silica exposure is followed by the development of an immunosuppressive microenvironment that supports the growth of lung tumors. This work will review our current knowledge of silica-associated lung cancers, highlighting how recent mechanistic insights support the use of cutting-edge approaches to diagnose and treat silica-related lung cancer.

show abstract

“…In the present study, we measured the lung function of individuals to investigate the possible relationship between lung function loss and silicosis. We focus on FEV 1 and FVC, which were usually used to evaluate lung function loss in silicosis [35][36][37][38]. We found that FVC% pre, FEV 1 % pre, and FEV 1 /FVC (%) were decreased in the silicosis group.…”

Section: Discussionmentioning

confidence: 96%

Decreased Soluble Receptor of Advanced Glycation End Product Levels Correlated with Inflammation in Silicosis

Liu

Tian

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

Silicosis is a devastating disease caused by inhalation of silica dust that leads to inflammatory cascade and then scarring of the lung tissue. Increasing evidences indicate that soluble receptor for advanced glycation end products (sRAGE) is involved in inflammatory diseases. However, no data on the possible relationship between sRAGE and inflammation of silicosis are available. In this study, serum from subjects with silicosis (n=59) or from healthy controls (HC, n=14) was analyzed for the secretion of sRAGE, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), and oxidized low-density lipoprotein (ox-LDL). The associations between sRAGE and cytokines and ox-LDL and lung function were assessed by Pearson’s correlation analyses. Mean levels of serum sRAGE were lower in silicosis than those in controls (p<0.05). The subjects who had a longer term of occupational exposure had higher levels of sRAGE (p<0.05). The secretion of TNF-α, IL-1β, IL-6, TGF-β1, and ox-LDL was significantly higher in the silicosis group than that in the HC group (p<0.05). Furthermore, the levels of sRAGE were negatively correlated with TNF-α, IL-6, IL-1β, and ox-LDL. There is no correlation between sRAGE and TGF-β1 and lung function. The optimal point of sRAGE for differentiating silicosis from healthy controls was 14250.02 pg/ml by ROC curve analysis. A decrease in serum sRAGE and its association with inflammatory response might suggest a role for sRAGE in the pathogenesis of silicosis.

show abstract

Serum Heme Oxygenase-1 as a Marker of Lung Function Decline in Patients With Chronic Silicosis

Abstract: Serum HO-1 may be a predictor of lung function decline in silicosis patients.

Cited by 20 publications

References 37 publications

Plasma heme oxygenase-1 is decreased in peripheral artery disease patients

Plasma heme oxygenase-1 is decreased in peripheral artery disease patients

Silicosis and lung cancer: current perspectives

Decreased Soluble Receptor of Advanced Glycation End Product Levels Correlated with Inflammation in Silicosis

Contact Info

Product

Resources

About