A5041415357- Spinal Cord Injury Research
- Neurogenesis and neuroplasticity mechanisms
- Nerve injury and regeneration
- Neuroinflammation and Neurodegeneration Mechanisms
- Spinal Dysraphism and Malformations
- Peroxisome Proliferator-Activated Receptors
- Neurogenetic and Muscular Disorders Research
- Iron Metabolism and Disorders
- Neuropeptides and Animal Physiology
- Hemoglobinopathies and Related Disorders
- Cerebral Palsy and Movement Disorders
- Gastrointestinal motility and disorders
- Mesenchymal stem cell research
- Neuroscience of respiration and sleep
- Liver Disease and Transplantation
- Stroke Rehabilitation and Recovery
- Aortic Disease and Treatment Approaches
- Neuroscience and Neuropharmacology Research
- Trace Elements in Health
- Immune Response and Inflammation
- Liver Disease Diagnosis and Treatment
- Biochemical Analysis and Sensing Techniques
- Bone and Joint Diseases
- Cardiac Arrest and Resuscitation
- Ion channel regulation and function
The Ohio State University
2015-2024
The Ohio State University Wexner Medical Center
2012-2023
State Library of Ohio
2023
Thapar Institute of Engineering & Technology
2020
Marymount University
2010
Genetically engineered mice are used extensively to examine molecular responses spinal cord injury (SCI). Inherent strain differences may confound behavioral outcomes; therefore, characterization of several strains after SCI is warranted. The Basso, Beattie, Bresnahan Locomotor Rating Scale (BBB) for rats has been widely mice, but not accurately reflect their unique recovery pattern. This study's purpose was develop a valid locomotor rating scale and identify in SCI. We examined C57BL/6,...
Functional loss after spinal cord injury (SCI) is caused, in part, by demyelination of axons surviving the trauma. Neurotrophins have been shown to induce oligodendrogliagenesis vitro , but stimulation oligodendrocyte proliferation and myelination these factors vivo has not examined. We sought determine whether neurotrophins can formation new oligodendrocytes regenerating SCI adult rats. In this study, fibroblasts producing neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF),...
Given the numerous reparative roles glia may play after spinal cord injury (SCI), glial proliferation and cell number were examined in a model of traumatic SCI. Emphasis was placed on analysis oligodendrocytes NG2-positive (NG2+) cells, an endogenous population that be involved oligodendrocyte replacement. Overall, (assessed by bromodeoxyuridine incorporation) markedly elevated during first 2 weeks declined thereafter; large portion these dividing cells likely consisted...
Traumatic spinal cord injury (SCI) triggers a neuro-inflammatory response dominated by tissue-resident microglia and monocyte derived macrophages (MDMs). Since activated MDMs are morphologically identical express similar phenotypic markers in vivo, identifying responses specifically coordinated has historically been challenging. Here, we pharmacologically depleted use anatomical, histopathological, tract tracing, bulk single cell RNA sequencing to reveal the cellular molecular SCI controlled...
Following traumatic injury to the spinal cord, hematogenous inflammatory cells including neutrophils, monocytes, and lymphocytes infiltrate lesion in a distinct temporal sequence. To examine potential mechanisms for their recruitment, we measured chemokine mRNAs contused rat using specific sensitive reverse transcriptase polymerase chain reaction (RT-PCR) dot-blot hybridization assays. The neutrophil chemoattractant GRO-α was 30-fold higher than control values at 6 hr postinjury decayed...
Significance Oligodendrocytes have been implicated in disease pathology amyotrophic lateral sclerosis (ALS) using transgenic mouse models. To date there is no human coculture system available to investigate oligodendrocyte involvement motor neuron (MN) death ALS. Our data highlight that oligodendrocytes derived from patients with familial and sporadic ALS induced pluripotent stem cells neural progenitor play an active role MN death. Oligodendrocyte toxicity mediated through soluble factors...
Adult progenitor cells proliferate in the acutely injured spinal cord and their progeny differentiate into new oligodendrocytes (OLs) that remyelinate spared axons. Whether this endogenous repair continues beyond first week postinjury (wpi), however, is unknown. Identifying duration of response essential for guiding therapies targeting improved recovery from injury (SCI) by enhancing OL survival and/or remyelination. Here, we used two PDGFRα-reporter mouse lines rats injected with a...
Spinal cord injury (SCI) induces a centralized fibrotic scar surrounded by reactive glial at the lesion site. The origin of these scars is thought to be perivascular cells entering lesions on ingrowing blood vessels and astrocytes, respectively. However, two NG2-expressing cell populations, pericytes glia, may also influence formation. In periphery, new vessel growth requires proliferating NG2 + pericytes; if this were true in CNS, then would depend dividing pericytes. (also called...
Astrocytes are extensively coupled through gap junctions into a syncytium. However, the basic role of this major brain network remains largely unknown. Using electrophysiological and computational modeling methods, we demonstrate that membrane potential ( V M ) an individual astrocyte in hippocampal syncytium, but not single, freshly isolated cell preparation, can be well‐maintained at quasi‐physiological levels when recorded with reduced or K + free pipette solutions alter equilibrium to...
Abstract Oligodendrocyte (OL) loss and axon demyelination occur after spinal cord injury (SCI). OLs may be replaced, however, by proliferating NG2+ progenitor cells. Indeed, new have been noted in ventral white matter SCI. Since tissue adjacent to lesion cavities is exposed different mediators compared with outlying spared tissue, the authors used a rat SCI model compare NG2 cell proliferation OL genesis that closer meninges. cells proliferated throughout first week postinjury accumulated...
Injured CNS tissue often contains elevated iron and its storage protein ferritin, which may exacerbate damage through pro-oxidative mechanisms. Therefore, therapeutic studies target reduction as a neuroprotective strategy. However, be crucial for oligodendrocyte replacement remyelination. For instance, we previously showed that intraspinal toll-like receptor 4 macrophage activation induced the generation of new ferritin-positive oligodendrocytes, chelation significantly reduced this...
Impaired signaling via CX3CR1, the fractalkine receptor, promotes recovery after traumatic spinal contusion injury in mice, a benefit achieved part by reducing macrophage-mediated at lesion epicenter. Here, we tested hypothesis that CX3CR1-dependent changes microglia and macrophage functions also will enhance neuroplasticity, several segments below New data show presence of inflammatory stimuli, CX3CR1-deficient (CX3CR1 −/− ) macrophages adopt reparative phenotype increase expression genes...
Spinal cord injury (SCI) activates macrophages, endowing them with both reparative and pathological functions. The mechanisms responsible for these divergent functions are unknown but likely controlled through stochastic activation of different macrophage receptor subtypes. Various danger-associated molecular patterns released from dying cells in the injured spinal activate distinct subtypes pattern recognition receptors, including bacterial toll-like receptors (TLRs) fungal C-type lectin...
Traumatic spinal cord injury (SCI) causes major disruption to peripheral organ innervation and regulation. Relatively little work has investigated these post-SCI systemic changes, however, despite considerable evidence that multiple system dysfunction contributes chronic impairments in health. Because metabolic is common after SCI the liver a pivotal site for homeostasis, we sought determine if pathology occurs as result of rat contusion model. Histologic showed excess lipid accumulation at...
Acute oligodendrocyte (OL) death after traumatic spinal cord injury (SCI) is followed by robust neuron–glial antigen 2 (NG2)-positive OL progenitor proliferation and differentiation into new OLs. Inflammatory mediators are prevalent during both phases can influence the fate of NG2 cells Specifically, toll-like receptor (TLR) 4 signaling induces genesis in naive cord, lack TLR4 impairs white matter sparing functional recovery SCI. Therefore, we hypothesized that may regulate...
Oligodendrocyte progenitor cells (OPCs) are present throughout the adult brain and spinal cord can replace oligodendrocytes lost to injury, aging, or disease. Their differentiation, however, is inhibited by myelin debris, making clearance of this debris an important step for cellular repair following demyelination. In models peripheral nerve TLR4 activation lipopolysaccharide (LPS) promotes macrophage phagocytosis debris. Here we tested whether novel synthetic agonist E6020, a Lipid A...
Fibroblasts nonvirally programmed to convert into induced endothelial cells show therapeutic potential for ischemic stroke.