scholarly journals Alterations in Gastric Mucosal Expression of Calcitonin Gene-Related Peptides, Vanilloid Receptors, and Heme Oxygenase-1 Mediate Gastroprotective Action of Carbon Monoxide against Ethanol-Induced Gastric Mucosal Lesions

2018 ◽  
Vol 19 (10) ◽  
pp. 2960 ◽  
Author(s):  
Katarzyna Magierowska ◽  
Dagmara Wojcik ◽  
Anna Chmura ◽  
Dominik Bakalarz ◽  
Mateusz Wierdak ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Protein Expression ◽  
Alcian Blue ◽  
Heme Oxygenase ◽  
Mrna Level ◽  
Fold Change ◽  
Gastric Damage ◽  
Gastric Lesions ◽  
Calcitonin Gene ◽  
Enos Mrna

Carbon monoxide (CO) has been reported to contribute to the maintenance of gastric mucosal integrity, gastroprotection, and ulcer healing. However, involvement of transient receptor potential vanilloid receptor type 1 (TRPV1) located on afferent sensory fibers endings and sensory neuropeptide calcitonin gene-related peptide (CGRP) in CO-mediated gastroprotection against ethanol-induced gastric damage has not been explored. Male Wistar rats with and without denervation of afferent sensory neurons induced by capsaicin (total dose 125 mg/kg within 3 days) were pretreated with vehicle, CO donor tricarbonyldichlororuthenium (II) dimer (CORM-2, 5 mg/kg i.g.), administered alone or with CGRP-α (10 μg/kg i.p.) or TRPV1 antagonist capsazepine (5 mg/kg i.g.), followed 30 min later by intragastric (i.g.) administration of 75% ethanol. The area of gastric damage and gastric blood flow (GBF) were assessed planimetrically and by laser flowmetry, respectively. Microscopic evaluation of ethanol-induced gastric lesions was performed after haematoxylin/eosin (H&E) or alcian blue/periodic acid-Schiff/alcian blue (AB/PAS) staining. Gastric mucosal mRNA fold change for heme oxygenase (HMOX)-1, HMOX-2, CGRP-α, CGRP-β, inducible nitric oxide synthase (iNOS), endothelial (e)NOS, neuronal (n)NOS, cyclooxygenase (COX)-1, COX-2, and protein expression for HMOX-1 and TRPV1 was determined by real-time PCR or Western blot, respectively. Pretreatment with CORM-2 combined or not with CGRP reduced ethanol-induced gastric lesions and elevated GBF. Capsaicin-denervation or co-treatment with capsazepine or CGRP and CORM-2 in capsaicin-denervated animals failed to affect these beneficial effects of CO donor. In rats with intact sensory nerves, CORM-2 increased gastric mRNA level for HMOX-1 and CGRP-α. In capsaicin-denervated rats, CORM-2 increased eNOS mRNA fold change and TRPV1 protein expression while capsaicin denervation itself decreased HMOX-1 protein expression and eNOS mRNA level. We conclude that CO prevents gastric mucosa from ethanol-induced lesions due to activation of TRPV1/CGRP-α system and accompanying increase in gastric microcirculation but independently on afferent sensory nerve activity despite the stimulation of TRPV1 protein and CGRP-α mRNA expression.

scholarly journals Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages

2019 ◽  
Vol 20 (3) ◽  
pp. 503 ◽  
Author(s):  
Dominique Muschter ◽  
Anna-Sophie Beiderbeck ◽  
Tanja Späth ◽  
Christian Kirschneck ◽  
Agnes Schröder ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Level ◽  
Cyclic Stretch ◽  
Murine Bone Marrow ◽  
Raw264.7 Macrophages ◽  
Neurokinin Receptor ◽  
Calcitonin Gene ◽  
Gene And Protein Expression ◽  
Sensory Neuropeptides ◽  
Comparable Activity

This study aimed to analyze if the sensory neuropeptide SP (SP) and the neurokinin receptor 1 (NK1R) are involved in macrophage mechano-transduction, similar to chondrocytes, and if alpha-calcitonin gene-related peptide (αCGRP) and the CGRP receptor (CRLR/Ramp1) show comparable activity. Murine RAW264.7 macrophages were subjected to a cyclic stretch for 1–3 days and 4 h/day. Loading and neuropeptide effects were analyzed for gene and protein expression of neuropeptides and their receptors, adhesion, apoptosis, proliferation and ROS activity. Murine bone marrow-derived macrophages (BMM) were isolated after surgical osteoarthritis (OA) induction and proliferation, apoptosis and osteoclastogenesis were analyzed in response to loading. Loading induced NK1R and CRLR/Ramp1 gene expression and altered protein expression in RAW264.7 macrophages. SP protein and mRNA level decreased after loading whereas αCGRP mRNA expression was stabilized. SP reduced adhesion in loaded RAW264.7 macrophages and both neuropeptides initially increased the ROS activity followed by a time-dependent suppression. OA induction sensitized BMM to caspase 3/7 mediated apoptosis after loading. Both sensory neuropeptides, SP and αCGRP, and their receptors are involved in murine macrophage mechano-transduction affecting neuropeptide impact on adhesion and ROS activity. OA induction altered BMM apoptosis in response to loading indicate that OA-associated biomechanical alterations might affect the macrophage population.

Tu1858 Role of Heme Oxygenase-1 and Nuclear Factor (Erythroid-Derived 2)-Like 2 Factor (NRF2) in Pathogenesis of Aspirin-Induced Gastric Damage and Protection by Carbon Monoxide

2016 ◽  
Vol 150 (4) ◽  
pp. S961-S962
Author(s):  
Marcin Magierowski ◽  
Katarzyna Magierowska ◽  
Slawomir Kwiecien ◽  
Juliusz Adamski ◽  
Zbigniew Sliwowski ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Gastric Damage ◽  
Heme Oxygenase 1 ◽  
Nuclear Factor

scholarly journals Heme oxygenase activity in placenta: direct dependence on oxygen availability

2002 ◽  
Vol 282 (6) ◽  
pp. H2055-H2059 ◽  
Author(s):  
Scott D. Appleton ◽  
Gerald S. Marks ◽  
Kanji Nakatsu ◽  
James F. Brien ◽  
Graeme N. Smith ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Catalytic Activity ◽  
Protein Expression ◽  
Heme Oxygenase ◽  
Progressive Decrease ◽  
Vascular Control ◽  
Chorionic Villi ◽  
Heme Oxygenase Activity ◽  
Oxygenase Activity ◽  
Mrna And Protein Expression

Carbon monoxide (CO), which is formed endogenously from heme catalyzed by heme oxygenase (HO), is proposed to play a role in vascular control. The mRNA and protein expression of the inducible isoform of HO (HO-1) increases in response to hypoxia, and it has been assumed that HO activity also increases. This assumption requires evaluation because the catalytic activity of HO requires three molecules of O2 for each molecule of CO formed from heme, and HO activity may be limited by O2 availability. To test the hypothesis that low physiological O2 concentrations limit HO activity, heme-derived CO formation by microsomal fractions of homogenates of chorionic villi of human placentas was determined after exposure to 0, 1, 5, or 21% O2. Results revealed that HO activity was directly dependent on O2 concentration. Thus, although hypoxia may increase HO protein and mRNA expression, there is a progressive decrease in HO activity with decreasing O2concentration and the dependence of HO activity on O2concentration is similar in chorionic villi from noninfarcted areas of preeclamptic and normotensive placenta.

scholarly journals The role of heme oxygenase and carbon monoxide in inflammatory bowel disease

Redox Report ◽  
2010 ◽  
Vol 15 (5) ◽  
pp. 193-201 ◽  
Author(s):  
Tomohisa Takagi ◽  
Yuji Naito ◽  
Kazuhiko Uchiyama ◽  
Toshikazu Yoshikawa
Keyword(s):  
Inflammatory Bowel Disease ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

2021 ◽  
Vol 22 (3) ◽  
pp. 1382
Author(s):  
Jelena Nesovic Ostojic ◽  
Milan Ivanov ◽  
Nevena Mihailovic-Stanojevic ◽  
Danijela Karanovic ◽  
Sanjin Kovacevic ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protein Expression ◽  
Hyperbaric Oxygen ◽  
Heme Oxygenase ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Kidney Injury ◽  
Heme Oxygenase 1 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.

scholarly journals Heme oxygenase-1 and carbon monoxide in pulmonary medicine

2003 ◽  
Vol 4 (1) ◽  
Author(s):  
Dirk-Jan Slebos ◽  
Stefan W Ryter ◽  
Augustine MK Choi
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Pulmonary Medicine
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