951 INTERLEUKIN 10-MEDIATED HEME OXYGENASE 1-INDUCED UNDERLYING MECHANISM IN INFLAMMATORY DOWNREGULATION BY NORFLOXACIN IN CIRRHOSIS

2011 ◽  
Vol 54 ◽  
pp. S380
Author(s):  
I. Gómez-Hurtado ◽  
P. Zapater ◽  
P. Bellot ◽  
S. Pascual ◽  
M. Pérez-Mateo ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Underlying Mechanism ◽  
Interleukin 10 ◽  
Heme Oxygenase 1

scholarly journals Interleukin-10-mediated heme oxygenase 1-induced underlying mechanism in inflammatory down-regulation by norfloxacin in cirrhosis

Hepatology ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 935-944 ◽  
Author(s):  
Isabel Gómez-Hurtado ◽  
Pedro Zapater ◽  
Pablo Bellot ◽  
Sonia Pascual ◽  
Miguel Pérez-Mateo ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Underlying Mechanism ◽  
Interleukin 10 ◽  
Heme Oxygenase 1 ◽  
Down Regulation

scholarly journals Heme Oxygenase-1-Mediated Autophagy Protects against Oxidative Damage in Rat Nucleus Pulposus-Derived Mesenchymal Stem Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Sheng Chen ◽  
Sheng Liu ◽  
Lei Zhao ◽  
Hui Lin ◽  
Kaige Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cell Viability ◽  
Nucleus Pulposus ◽  
Heme Oxygenase ◽  
Early Stage ◽  
Underlying Mechanism ◽  
Research Direction ◽  
Heme Oxygenase 1 ◽  
Ivd Degeneration

Although endogenous nucleus pulposus-derived mesenchymal stem cell- (NPMSC-) based regenerative medicine has provided promising repair strategy for intervertebral disc (IVD) degeneration, the hostile microenvironments in IVD, including oxidative stress, can negatively affect the survival and function of the NPMSCs and severely hinder the endogenous repair process. Therefore, it is of great importance to reveal the mechanisms of the endogenous repair failure caused by the adverse microenvironments in IVD. The aim of this study was to investigate the effect of oxidative stress on the rat NPMSCs and its underlying mechanism. Our results demonstrated that oxidative stress inhibited cell viability, induced apoptosis, and increased the production of reactive oxygen species (ROS) in NPMSCs. In addition, the results showed that the expression level of heme oxygenase-1 (HO-1) increased at an early stage but decreased at a late stage when NPMSCs were exposed to oxidative stress, and the oxidative damages of NPMSCs could be partially reversed by promoting the expression of HO-1. Further mechanistic analysis indicated that the protective effect of HO-1 against oxidative damage in NPMSCs was mediated by the activation of autophagy. Taken together, our study revealed that oxidative stress could inhibit cell viability, induce apoptosis, and increase ROS production in NPMSCs, and HO-1-mediated autophagy might act as a protective response to the oxidative damage. These findings might enhance our understanding on the mechanism of the endogenous repair failure during IVD degeneration and provide novel research direction for the endogenous repair of IVD degeneration.

scholarly journals Hemoglobin Scavenger Receptor CD163 Mediates Interleukin-10 Release and Heme Oxygenase-1 Synthesis

2004 ◽  
Vol 94 (1) ◽  
pp. 119-126 ◽  
Author(s):  
P. Philippidis ◽  
J.C. Mason ◽  
B.J. Evans ◽  
I. Nadra ◽  
K.M. Taylor ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Scavenger Receptor ◽  
Interleukin 10 ◽  
Heme Oxygenase 1

Heme oxygenase-1 expression inhibits dendritic cell maturation and proinflammatory function but conserves IL-10 expression

Blood ◽  
2005 ◽  
Vol 106 (5) ◽  
pp. 1694-1702 ◽  
Author(s):  
Christine Chauveau ◽  
Séverine Rémy ◽  
Pierre Joseph Royer ◽  
Marcelo Hill ◽  
Séverine Tanguy-Royer ◽  
...  
Keyword(s):  
Immune Responses ◽  
Heme Oxygenase ◽  
Human Monocyte ◽  
Cell Types ◽  
Interleukin 10 ◽  
Dendritic Cell Maturation ◽  
Heme Oxygenase 1 ◽  
Intracellular Enzyme

Abstract Heme oxygenase-1 (HO-1) is an intracellular enzyme that degrades heme and inhibits immune responses and inflammation in vivo. In most cell types, HO-1 is inducible by inflammatory stimuli and oxidative stress. Here we demonstrate that human monocyte-derived immature dendritic cells (iDCs) and several but not all freshly isolated rat splenic DC subsets and rat bone marrow-derived iDCs, spontaneously express HO-1. HO-1 expression drastically decreases during human and rat DC maturation induced in vitro. In human tissues, iDCs also express HO-1, whereas mature DCs do not. Induction of HO-1 expression with cobalt protoporphyrin (CoPP) in human and rat DCs inhibits lipopolysaccharide (LPS)-induced phenotypic maturation and secretion of proinflammatory cytokines, resulting in the inhibition of alloreactive T-cell proliferation. CoPP-treated DCs, however, retain the ability to produce the anti-inflammatory cytokine interleukin 10 (IL-10). Reactive oxygen species induced by LPS in DCs were inhibited by induction of HO-1. In conclusion, we identify, for the first time, the capacity of HO-1 to block maturation of DCs and to inhibit proinflammatory and allogeneic immune responses while preserving IL-10 production. This novel immune function for HO-1 may be of interest for the inhibition of immune responses in autoimmune diseases, transplantation, and other conditions involving activation of the immune system. (Blood. 2005;106:1694-1702)

scholarly journals Increased Plasma Heme Oxygenase-1 Levels in Patients With Early-Stage Parkinson’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Wenhua Sun ◽  
Jinhua Zheng ◽  
Jianjun Ma ◽  
Zhidong Wang ◽  
Xiaoxue Shi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Heme Oxygenase ◽  
Early Stage ◽  
Area Under The Curve ◽  
Underlying Mechanism ◽  
Hippocampal Volume ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
Brain Volumes

Introduction: Heme oxygenase-1 (HO-1) is a 32 kDa stress-response protein implicated in the pathogenesis of Parkinson’s disease (PD). Biliverdin is derived from heme through a reaction mediated by HO-1 and protects cells from oxidative stress. However, iron and carbon monoxide produced by the catabolism of HO-1 exert detrimental effects on patients with PD. The purpose of this study was to determine whether plasma HO-1 levels represent a biomarker of PD and to further explore the underlying mechanism of increased HO-1 levels by applying voxel-based morphometry (VBM).Methods: We measured plasma HO-1 levels using an enzyme-linked immunosorbent assay (ELISA) in 156 subjects, including 81 patients with early- and advanced-stage PD and 75 subjects without PD. The analyses were adjusted to control for confounders such as age, sex, and medication. We analyzed T1-weighted magnetic resonance imaging (MRI) data from 74 patients with PD using VBM to elucidate the association between altered brain volumes and HO-1 levels. Then, we compared performance on MMSE sub-items between PD patients with low and high levels of HO-1 using Mann-Whitney U tests.Results: Plasma HO-1 levels were significantly elevated in PD patients, predominantly those with early-stage PD, compared with controls (p < 0.05). The optimal cutoff value for patients with early PD was 2.245 ng/ml HO-1 [area under the curve (AUC) = 0.654]. Plasma HO-1 levels were unaffected by sex, age, and medications (p > 0.05). The right hippocampal volume was decreased in the subset of PD patients with high HO-1 levels (p < 0.05). A weak correlation was observed between right hippocampal volume and plasma HO-1 levels (r = −0.273, p = 0.018). There was no difference in total MMSE scores between the low- and high-HO-1 groups (p > 0.05), but the high-HO-1 group had higher language scores than the low-HO-1 group (p < 0.05).Conclusions: Plasma HO-1 levels may be a promising biomarker of early PD. Moreover, a high plasma concentration of the HO-1 protein is associated with a reduction in right hippocampal volume.

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