scholarly journals Evidence for Cytoprotective Effect of Carbon Monoxide Donor in the Development of Acute Esophagitis Leading to Acute Esophageal Epithelium Lesions

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1203 ◽  
Author(s):  
Katarzyna Magierowska ◽  
Dominik Bakalarz ◽  
Dagmara Wójcik ◽  
Edyta Korbut ◽  
Aleksandra Danielak ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Sensory Nerve ◽  
Cytokine Signaling ◽  
Zinc Protoporphyrin ◽  
Esophageal Mucosa ◽  
Annexin A1 ◽  
Esophageal Epithelium ◽  
Drug Induced ◽  
Mucus Production ◽  
Socs3 Mrna

Exposure to acidic gastric content due to malfunction of lower esophageal sphincter leads to acute reflux esophagitis (RE) leading to disruption of esophageal epithelial cells. Carbon monoxide (CO) produced by heme oxygenase (HMOX) activity or released from its donor, tricarbonyldichlororuthenium (II) dimer (CORM-2) was reported to protect gastric mucosa against acid-dependent non-steroidal anti-inflammatory drug-induced damage. Thus, we aimed to investigate if CO affects RE-induced esophageal epithelium lesions development. RE induced in Wistar rats by the ligation of a junction between pylorus and forestomach were pretreated i.g. with vehicle CORM-2; RuCl3; zinc protoporphyrin IX, or hemin. CORM-2 was combined with NG-nitro-L-arginine (L-NNA), indomethacin, capsazepine, or capsaicin-induced sensory nerve ablation. Esophageal lesion score (ELS), esophageal blood flow (EBF), and mucus production were determined by planimetry, laser flowmetry, histology. Esophageal Nrf-2, HMOXs, COXs, NOSs, TNF-α and its receptor, IL-1 family and IL-1 receptor antagonist (RA), NF-κB, HIF-1α, annexin-A1, suppressor of cytokine signaling (SOCS3), TRPV1, c-Jun, c-Fos mRNA/protein expressions, PGE2, 8-hydroxy-deoxyguanozine (8-OHdG) and serum COHb, TGF-β1, TGF-β2, IL-1β, and IL-6 content were assessed by PCR, immunoblotting, immunohistochemistry, gas chromatography, ELISA or Luminex platform. Hemin or CORM-2 alone or combined with L-NNA or indomethacin decreased ELS. Capsazepine or capsaicin-induced denervation reversed CORM-2 effects. COHb blood content, esophageal HMOX-1, Nrf-2, TRPV1 protein, annexin-A1, HIF-1α, IL-1 family, NF-κB, c-Jun, c-Fos, SOCS3 mRNA expressions, and 8-OHdG levels were elevated while PGE2 concentration was decreased after RE. CO donor-maintained elevated mucosal TRPV1 protein, HIF-1 α, annexin-A1, IL-1RA, SOCS3 mRNA expression, or TGF-β serum content, decreasing 8-OHdG level, and particular inflammatory markers expression/concentration. CORM-2 and Nrf-2/HMOX-1/CO pathway prevent esophageal mucosa against RE-induced lesions, DNA oxidation, and inflammatory response involving HIF-1α, annexin-A1, SOCS3, IL-1RA, TGF-β-modulated pathways. Esophagoprotective and hyperemic CO effects are in part mediated by afferent sensory neurons and TRPV1 receptors activity with questionable COX/PGE2 or NO/NOS systems involvement.

scholarly journals Inhaled carbon monoxide does not cause pulmonary vasodilation in the late-gestation fetal lamb

2000 ◽  
Vol 278 (4) ◽  
pp. L779-L784 ◽  
Author(s):  
Theresa R. Grover ◽  
Robyn L. Rairigh ◽  
Jeanne P. Zenge ◽  
Steven H. Abman ◽  
John P. Kinsella
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Vascular Tone ◽  
Ductus Arteriosus ◽  
Protoporphyrin Ix ◽  
Left Lung ◽  
Late Gestation ◽  
Zinc Protoporphyrin ◽  
Pulmonary Vasodilation

As observed with nitric oxide (NO), carbon monoxide (CO) binds and may activate soluble guanylate cyclase and increase cGMP levels in smooth muscle cells in vitro. Because inhaled NO (INO) causes potent and sustained pulmonary vasodilation, we hypothesized that inhaled CO (ICO) may have similar effects on the perinatal lung. To determine whether ICOcan lower pulmonary vascular resistance (PVR) during the perinatal period, we studied the effects of ICOon late-gestation fetal lambs. Catheters were placed in the main pulmonary artery, left pulmonary artery (LPA), aorta, and left atrium to measure pressure. An ultrasonic flow transducer was placed on the LPA to measure blood flow to the left lung. After baseline measurements, fetal lambs were mechanically ventilated with a hypoxic gas mixture (inspired O2fraction < 0.10) to maintain a constant fetal arterial [Formula: see text]. After 60 min (baseline), the lambs were treated with ICO[5–2,500 parts/million (ppm)]. Comparisons were made with INO(5 and 20 ppm) and combined INO(5 ppm) and ICO(100 and 2,500 ppm). We found that ICOdid not alter left lung blood flow or PVR at any of the study doses. In contrast, low-dose INOdecreased PVR by 47% ( P < 0.005). The combination of INOand ICOdid not enhance the vasodilator response to INO. To determine whether endogenous CO contributes to vascular tone in the fetal lung, zinc protoporphyrin IX, an inhibitor of heme oxygenase, was infused into the LPA in three lambs. Zinc protoporphyrin IX had no effect on baseline PVR, aortic pressure, or the pressure gradient across the ductus arteriosus. We conclude that ICOdoes not cause vasodilation in the near-term ovine transitional circulation, and endogenous CO does not contribute significantly to baseline pulmonary vascular tone or ductus arteriosus tone in the late-gestation ovine fetus.

scholarly journals Heterogeneous vesicles in mucous epithelial cells of posterior esophagus of Chinese giant salamander (Andrias davidianus)

2015 ◽  
Vol 59 (3) ◽  
Author(s):  
H. Zhang ◽  
X. Guo ◽  
S. Zhong ◽  
T. Ge ◽  
S. Peng ◽  
...  
Keyword(s):  
Mucous Cell ◽  
Single Layer ◽  
Esophageal Mucosa ◽  
Mucous Cells ◽  
Esophageal Epithelium ◽  
Andrias Davidianus ◽  
Transmission Electron ◽  
Chinese Giant Salamander ◽  
Columnar Cells ◽  
Dense Vesicles

The Chinese giant salamander belongs to an old lineage of salamanders and endangered species. Many studies of breeding and disease regarding this amphibian had been implemented. However, the studies on the ultrastructure of this amphibian are rare. In this work, we provide a histological and ultrastructural investigation on posterior esophagus of Chinese giant salamander. The sections of amphibian esophagus were stained by hematoxylin &amp; eosin (H&amp;E). Moreover, the esophageal epithelium was observed by transmission electron microscopy (TEM). The results showed that esophageal epithelium was a single layer epithelium, which consisted of mucous cells and columnar cells. The esophageal glands were present in submucosa. The columnar cells were ciliated. According to the diverging ultrastructure of mucous vesicles, three types of mucous cells could be identified in the esophageal mucosa: i) electron-lucent vesicles mucous cell (ELV-MC); ii) electron-dense vesicles mucous cell (EDV-MC); and iii) mixed vesicles mucous cell (MV-MC).

Correlation of HO-1 expression with onset and reversal of hypoxia-induced vasoconstrictor hyporeactivity

2001 ◽  
Vol 281 (1) ◽  
pp. H298-H307 ◽  
Author(s):  
Nikki L. Jernigan ◽  
Theresa L. O'Donaughy ◽  
Benjimen R. Walker
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Chronic Hypoxia ◽  
Protoporphyrin Ix ◽  
Hypoxic Exposure ◽  
Zinc Protoporphyrin ◽  
Protein Levels ◽  
Hypoxic Induction ◽  
Vasoconstrictor Response ◽  
Renal Vascular

Rats exposed to chronic hypoxia (CH; 4 wk at 0.5 atm) exhibit attenuated renal vasoconstrictor reactivity to phenylephrine (PE). Preliminary studies from our laboratory suggest that this response is mediated by hypoxic induction of heme oxygenase (HO) and subsequent release of the endogenous vasodilator carbon monoxide. Because vascular HO mRNA is increased within hours of hypoxic exposure, we hypothesized that the onset of reduced reactivity may occur fairly rapidly and correlate with HO expression. Therefore, we examined the onset of attenuated vasoconstriction on CH exposure as well as the duration of hyporeactivity on return to a normoxic environment. Renal vascular resistance (RVR) responses to graded intravenous infusion of PE were measured in conscious rats under control conditions and after 24 h, 48 h, and 4 wk of CH exposure. Vasoreactivity responses were also determined in 4-wk CH rats 1, 5, 24, and 96 h after return to normoxia. We found that RVR responses to PE were significantly blunted after 48 h and 4 wk but not after 24 h of hypoxic exposure. Inhibition of HO with zinc protoporphyrin IX increased RVR and decreased renal blood flow in 48-h CH rats but not controls. Although reactivity to PE was gradually restored after 4 wk of CH, responsiveness was still slightly blunted at 96 h after return to normoxia. Western blot analysis demonstrated a correlation between HO-1 protein levels and attenuated vasoconstrictor response in CH and posthypoxic rats. These data suggest that the onset and offset of physiologically relevant vascular HO expression occur within 2–3 days.

Effects of Carbon Monoxide on the Vulnerability of the Ventricles to Drug-Induced Arrhythmias

1974 ◽  
Vol 14 (1) ◽  
pp. 25-31 ◽  
Author(s):  
BALKRISHENA KAUL ◽  
JOHN CALABRO ◽  
DUNCAN E. HUTCHEON
Keyword(s):  
Carbon Monoxide ◽  
Drug Induced

The association between smoking and LINE-1 hypomethylation (global DNA hypomethylation) in normal esophageal epithelium of patients with esophageal squamous cell carcinoma.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 41-41
Author(s):  
Shiro Iwagami ◽  
Yoshifumi Baba ◽  
Masayuki Watanabe ◽  
Hironobu Shigaki ◽  
Keisuke Miyake ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Cancer ◽  
Squamous Cell ◽  
Methylation Level ◽  
Continuous Variable ◽  
Smoking History ◽  
Esophageal Mucosa ◽  
Esophageal Epithelium ◽  
Dna Hypomethylation

41 Background: DNA methylation is a major epigenetic mechanism in X-chromosome inactivation, imprinting and repression of transposable elements and endogenous retroviral sequences. Global DNA hypomethylation appears to play an important role in genomic instability, leading to cancer development. DNA methylation in the long interspersed nucleotide element-1, L1 (LINE-1) repetitive element is a good indicator of global DNA methylation level. Smoking and alcohol is extremely important as the etiology of esophageal squamous cell carcinoma. Nonetheless, whether or not smoking and alcohol affect LINE-1 methylation level in normal esophageal epithelium of esophageal cancer patients remains uncertain. Methods: We quantified LINE-1 methylation of normal esophageal mucosa using pyrosequencing technology in 118 resected esophageal squamous cell carcinomas. The data on smoking (Brinkman index, absence or presence) and alcohol amount are available in all cases. We excluded preoperatively treated cases. Results: LINE-1 methylation in normal esophageal epithelium of esophageal cancer patients ranged from 57.1 to 92.8 of 0-100 scale (N=118; mean 81.2; median 80.0; standard deviation 7.2). LINE-1 methylation level (continuous variable) was significantly associated with Brickman index (continuous variable) (r=0.12, p=0.0002); heavy smoker had lower LINE-1 methylation level of normal esophageal mucosa. LINE-1 methylation level was lower in patients with smoking history (mean 79.7) than in patients without smoking history (mean 83.2) (p=0.034). Alcohol assumption was not associated with LINE-1 methylation level (r=0.003, p=0.58). Conclusions: Smoking was associated with LINE-1 hypomethylation in esophageal normal epithelium, suggesting the possibility of epigenetic field effects caused by cigarette in esophageal tumorigenesis. Considering that DNA methylation alterations are reversible and can thus be targets for chemoprevention, our findings may have clinical implication.

Does endogenous zinc protoporphyrin modulate carbon monoxide formation from heme? Implications for long-term potentiation, memory, and cognitive function

1993 ◽  
Vol 71 (10-11) ◽  
pp. 753-754 ◽  
Author(s):  
Gerald S. Marks ◽  
Kanji Nakatsu ◽  
James F. Brien
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Cell Function ◽  
Physiological Role ◽  
Long Term Potentiation ◽  
Biological Properties ◽  
Zinc Protoporphyrin ◽  
Term Potentiation ◽  
Oxygenase Activity

Carbon monoxide, which is formed endogenously from heme catabolism catalyzed by heme oxygenase and shares some of the chemical and biological properties of nitric oxide, may play a similar role as a widespread signal transduction mechanism for the regulation of cell function and communication. Zinc protoporphyrin, an inhibitor of heme oxygenase, prevents induction of long-term potentiation. Zinc protoporphyrin is an endogenous substance and we suggest that it has a physiological role, by modulating heme oxygenase activity and, therefore, formation of carbon monoxide from heme. This in turn would modulate long-term potentiation, memory, and cognitive function.Key words: zinc protoporphyrin, carbon monoxide, heme oxygenase, long-term potentiation.

scholarly journals Therapeutic Potential of Annexin A1 Modulation in Kidney and Cardiovascular Disorders

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3420
Author(s):  
Mahmood S. Mozaffari
Keyword(s):  
Cardiovascular System ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Stone Formation ◽  
Kidney Injury ◽  
Cardiovascular Disorders ◽  
Annexin A1 ◽  
Drug Induced ◽  
Vascular Abnormalities ◽  
Functional Features

Renal and cardiovascular disorders are very prevalent and associated with significant morbidity and mortality. Among diverse pathogenic mechanisms, the dysregulation of immune and inflammatory responses plays an essential role in such disorders. Consequently, the discovery of Annexin A1, as a glucocorticoid-inducible anti-inflammatory protein, has fueled investigation of its role in renal and cardiovascular pathologies. Indeed, with respect to the kidney, its role has been examined in diverse renal pathologies, including acute kidney injury, diabetic nephropathy, immune-mediated nephropathy, drug-induced kidney injury, kidney stone formation, and renal cancer. Regarding the cardiovascular system, major areas of investigation include the role of Annexin A1 in vascular abnormalities, atherosclerosis, and myocardial infarction. Thus, this review briefly describes major structural and functional features of Annexin A1 followed by a review of its role in pathologies of the kidney and the cardiovascular system, as well as the therapeutic potential of its modulation for such disorders.

Ultrastructure of esophageal epithelium of rats fed Zn-deficient diet

1986 ◽  
Vol 44 ◽  
pp. 336-337
Author(s):  
S. Yamashiro ◽  
T. Bast ◽  
T.M. Bray ◽  
W.J. Bettger
Keyword(s):  
Corn Oil ◽  
Choline Chloride ◽  
Basal Diet ◽  
Egg White ◽  
Esophageal Mucosa ◽  
Esophageal Epithelium ◽  
Deficient Diet ◽  
Male Wistar Rats ◽  
Ad Libitum ◽  
Epithelial Lesions

It has been shown that animals fed a Zn-deficient diet developed various epithelial lesions. These include parakeratosis of the tongue, larynx and nasal sinuses in the ducks and hypertrophy of esophageal mucosa in the rats and pigs.Twenty-one weanling, male Wistar rats were equally divided into three groups. Seven rats were fed a diet containing less than 1.1 ppm Zn ad libitum for 3 weeks. Control rats were either pair-fed or fed ad libitum a diet supplemented with 100 ppm Zn. The basal diet was composed of 20% egg white, 10% corn oil, 63.55% glucose hydrate, 1% vitamin premix, 4% mineral premix, 0.25% choline chloride, 0.4% sodium phytate and 0.8% calcium carbonate. Minerals and vitamins additions were according to the AIN-76 recommendations (5).

Infliximab-induced interstitial lung disease

2021 ◽  
Vol 14 (10) ◽  
pp. e245726
Author(s):  
Theodoros Karampitsakos ◽  
Ourania Papaioannou ◽  
Fotios Sampsonas ◽  
Argyrios Tzouvelekis
Keyword(s):  
Carbon Monoxide ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Pulmonary Function Tests ◽  
Functional Improvement ◽  
Productive Cough ◽  
Diffusing Capacity ◽  
Drug Induced ◽  
The Past ◽  
Reticular Pattern

A 70-year-old man was referred to our respiratory department with non-productive cough over the past 6 months. High-resolution CT revealed reticular pattern with basal and peripheral predominance, centrilobular nodules and mild ground glass opacities. Serology tests were normal and bronchoalveolar lavage revealed lymphocytosis. Pulmonary function tests showed functional impairment and reduced diffusing capacity for carbon monoxide. Meticulous evaluation of patient’s medical history unveiled longitudinal administration of infliximab due to diagnosis of psoriasis. The working diagnosis of drug-induced interstitial lung disease was proposed following multidisciplinary discussion. Considerable radiological and functional improvement was determined 6 months following infliximab discontinuation without implementation of corticosteroids. To this end, the patient has reported remission of cough and functional improvement.

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