Our studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was undertaken to examine the possible relationship between HO-2 and the recruitment of neutrophils following a corneal surface injury in wild type (WT) and HO-2 knockout (HO-2(-/-)) mice treated with Gr-1 monoclonal antibody to deplete peripheral neutrophils. Epithelial injury was performed by removing the entire corneal epithelium. Infiltration of inflammatory cell into the cornea in response to injury was higher in HO-2(-/-) than in WT. However, the rate of corneal wound closure following neutrophil depletion was markedly inhibited in both WT and HO-2(-/-) mice by 60% and 85%, respectively. Neutropenia induced HO-1 expression in WT but not in HO-2(-/-) mice. Moreover, endothelial cells lacking HO-2 expressed higher levels of the Midkine and VE-cadherin and displayed strong adhesion to neutrophils suggesting that perturbation in endothelial cell function caused by HO-2 depletion underlies the increased infiltration of neutrophils into the HO-2(-/-) cornea. Moreover, the fact that neutropenia worsened epithelial healing of the injured cornea in both WT and HO-2(-/-) mice suggest that cells other than neutrophils contribute to the exaggerated inflammation and impaired wound healing seen in the HO-2 null cornea.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117875 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021180 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
Inhibition of phosphodiesterase 10A mitigates neuronal injury by modulating apoptotic pathways in cold-induced traumatic brain injury.
Mol Cell Neurosci
December 2024
Department of Physiology, School of Medicine, Istanbul Medeniyet University, Istanbul, Türkiye; Regenerative and Restorative Medical Research Center (REMER), Research Institute for Health Sciences and Technologies (SABITA), Istanbul Medipol University, Istanbul, Türkiye.
Brain injury develops from a complex series of pathophysiological phases, resulting in acute necrotic or delayed apoptotic cell death after traumatic brain injury (TBI). Inhibition of apoptotic cell death is critical for the treatment of acute neurodegenerative disorders, such as TBI. Here, we investigated the role of phosphodiesterase 10A (PDE10A) in the development of neuronal injury, particularly in apoptotic cell death.
View Article and Find Full Text PDFExtracellular Vesicle ASC: A Novel Mediator for Lung-Brain Axis in Preterm Brain Injury.
Am J Respir Cell Mol Biol
October 2024
Division of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Holtz Children's Hospital.
Bronchopulmonary dysplasia (BPD) and neurodevelopmental impairment are among the most common morbidities affecting preterm infants. Although BPD is a predictor of poor neurodevelopmental outcomes, it is currently uncertain how BPD contributes to brain injury in preterm infants. Extracellular vesicles (EVs) are involved in interorgan communication in diverse pathological processes.
View Article and Find Full Text PDFIs Environmental Cadmium Exposure Causally Related to Diabetes and Obesity?
Cells
December 2023
Kidney Disease Research Collaborative, Translational Research Institute, Woolloongabba, Brisbane, QLD 4102, Australia.
Article Synopsis
- Cadmium (Cd) is a toxic metal commonly found in food, cigarette smoke, and air, and it accumulates in the kidneys, influencing its excretion through urine as cells die.
- Despite being less recognized, Cd has been linked to diabetes, showcasing diabetogenic effects in earlier studies while its connection to diabetes appears independent of obesity.
- The review emphasizes the roles of the liver and kidneys in glucose metabolism disruption due to Cd, highlighting cellular stress responses and potential protective mechanisms involving enzymes like heme oxygenase-1 and -2 (HO-1 and HO-2).
Deuterium Magnetic Resonance Spectroscopy Quantifies Tumor Fraction in a Mouse Model of a Mixed Radiation Necrosis / GL261-Glioblastoma Lesion.
Mol Imaging Biol
February 2024
Department of Radiology, Biomedical MR Center, Washington University, 660 South Euclid Avenue, MO 63110, St. Louis, MO, Mail Stop Code: MSC 8227-0082-02, USA.
Purpose: Distinguishing recurrent brain tumor from treatment effects, including late time-to-onset radiation necrosis (RN), presents an on-going challenge in post-treatment imaging of neuro-oncology patients. Experiments were performed in a novel mouse model that recapitulates the relevant clinical histologic features of recurrent glioblastoma growing in a RN environment, the mixed tumor/RN model. The goal of this work was to apply single-voxel deuterium (H) magnetic resonance spectroscopy (MRS), in concert with administration of deuterated glucose, to determine if the metabolic signature of aerobic glycolysis (Warburg effect: glucose → lactate in the presence of O), a distinguishing characteristic of proliferating tumor, provides a quantitative readout of the tumor fraction (percent) in a mixed tumor/RN lesion.
View Article and Find Full Text PDFGYY4137, a HS donor, ameliorates kidney injuries in diabetic mice by modifying renal ROS-associated enzymes.
Biomed Pharmacother
June 2023
The Core Laboratory for Clinical Research, Nanjing BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, China; Department of Nephrology, Nanjing BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, China. Electronic address:
Diabetic nephropathy (DN) is a common microvascular complication of both type 1 and type 2 diabetes mellitus and often advances to end-stage renal disease. Oxidative stress plays an important role in the pathogenesis and progress of DN. Hydrogen sulfide (HS) is considered as a promising candidate for the management of DN.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!