[11C]PK11195 PET imaging of spinal glial activation after nerve injury in rats

Imamoto, Natsumi; Momosaki, Sotaro; Fujita, Masahide; Omachi, Shigeki; Yamato, Hiroko; Kimura, Mika; Kanegawa, Naoki; Shinohara, Shunji; Abe, Kohji

doi:10.1016/j.neuroimage.2013.04.039

Cited by 35 publications

(25 citation statements)

References 34 publications

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“…Microglia express Toll-like receptors (TLR) and NOD-like receptors (NLR), allowing them to detect bacterial pathogens and molecular signatures of injury, leading to the transcription of proinflammatory cytokine genes. Local [4] and systemic [5] infections, neurodegenerative conditions [6], and sterile injury [7] have been reported to activate microglia.…”

Section: Introductionmentioning

confidence: 99%

Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

Taylor

Sansing

2013

Clinical and Developmental Immunology

346

302

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Stroke is a leading cause of death worldwide. Ischemic stroke is caused by blockage of blood vessels in the brain leading to tissue death, while intracerebral hemorrhage (ICH) occurs when a blood vessel ruptures, exposing the brain to blood components. Both are associated with glial toxicity and neuroinflammation. Microglia, as the resident immune cells of the central nervous system (CNS), continually sample the environment for signs of injury and infection. Under homeostatic conditions, they have a ramified morphology and phagocytose debris. After stroke, microglia become activated, obtain an amoeboid morphology, and release inflammatory cytokines (the M1 phenotype). However, microglia can also be alternatively activated, performing crucial roles in limiting inflammation and phagocytosing tissue debris (the M2 phenotype). In rodent models, microglial activation occurs very early after stroke and ICH; however, their specific roles in injury and repair remain unclear. This review summarizes the literature on microglial responses after ischemic stroke and ICH, highlighting the mediators of microglial activation and potential therapeutic targets for each condition.

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Section: Introductionmentioning

confidence: 99%

Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

Taylor

Sansing

2013

Clinical and Developmental Immunology

346

302

View full text Add to dashboard Cite

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“…Early attempts with these tracers in preclinical animal models of pain showed increased [ 11 C] PK11195 uptake in PET images of the spinal cord of animals with neuropathic pain (partial sciatic nerve ligation). 75 Others have found temporally dependent increases in activated TSPO-expressing microglial cells in the spinal cord of rodent models of complex regional pain syndrome and spinal cord injury, respectively. 76 These imaging findings suggest that increased radiotracer uptake correlated to increased microglial cell activation that is realized in these animal models of pain.…”

Section: Pet Imaging Of Activated Glial Cells and Macrophagesmentioning

confidence: 99%

Identifying Musculoskeletal Pain Generators Using Clinical PET

Yoon

Kogan

Gold

et al. 2020

Semin Musculoskelet Radiol

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Identifying the source of a person's pain is a significant clinical challenge because the physical sensation of pain is believed to be subjective and difficult to quantify. The experience of pain is not only modulated by the individual's threshold to painful stimuli but also a product of the person's affective contributions, such as fear, anxiety, and previous experiences. Perhaps then to quantify pain is to examine the degree of nociception and pro-nociceptive inflammation, that is, the extent of cellular, chemical, and molecular changes that occur in pain-generating processes. Measuring changes in the local density of receptors, ion channels, mediators, and inflammatory/immune cells that are involved in the painful phenotype using targeted, highly sensitive, and specific positron emission tomography (PET) radiotracers is therefore a promising approach toward objectively identifying peripheral pain generators. Although several preclinical radiotracer candidates are being developed, a growing number of ongoing clinical PET imaging approaches can measure the degree of target concentration and thus serve as a readout for sites of pain generation. Further, when PET is combined with the spatial and contrast resolution afforded by magnetic resonance imaging, nuclear medicine physicians and radiologists can potentially identify pain drivers with greater accuracy and confidence. Clinical PET imaging approaches with fluorine-18 fluorodeoxyglucose, fluorine-18 sodium fluoride, and sigma-1 receptor PET radioligand and translocator protein radioligands to isolate the source of pain are described here.

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“…Imamoto et al showed that glial activation could be quantitatively imaged in the spinal cord of a rat model of neuropathic pain using [ 11 C]PK11195 PET [119]. It was suggested that high-resolution PET using TSPO-specific radioligands is useful for imaging to assess the role of glial activation, including neuroinflammatory processes, in the spinal cord.…”

Section: Other Models Of Neuroinflammationmentioning

confidence: 99%

Basic Science of PET Imaging for Inflammatory Diseases

Kubota

Ogawa

et al. 2019

PET/CT for Inflammatory Diseases

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FDG-PET/CT has recently emerged as a useful tool for the evaluation of inflammatory diseases too, in addition to that of malignant diseases. The imaging is based on active glucose utilization by inflammatory tissue. Autoradiography studies have demonstrated high FDG uptake in macrophages, granulocytes, fibroblasts, and granulation tissue. Especially, activated macrophages are responsible for the elevated FDG uptake in some types of inflammation. According to one study, after activation by lipopolysaccharide of cultured macrophages, the [ 14 C]2DG uptake by the cells doubled, reaching the level seen in glioblastoma cells. In activated macrophages, increase in the expression of total GLUT1 and redistributions from the intracellular compartments toward the cell surface have been reported. In one rheumatoid arthritis model, following stimulation by hypoxia or TNF-α, the highest elevation of the [ 3 H]FDG uptake was observed in the fibroblasts, followed by that in macrophages and neutrophils. As the fundamental mechanism of elevated glucose uptake in both cancer cells and inflammatory cells, activation of glucose metabolism as an adaptive response to a hypoxic environment has been reported, with transcription factor HIF-1α playing a key role. Inflammatory cells and cancer cells seem to share the same molecular mechanism of elevated glucose metabolism, lending support to the notion of usefulness of FDGPET/CT for the evaluation of inflammatory diseases, besides cancer.

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[11C]PK11195 PET imaging of spinal glial activation after nerve injury in rats

Cited by 35 publications

References 34 publications

Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

Identifying Musculoskeletal Pain Generators Using Clinical PET

Basic Science of PET Imaging for Inflammatory Diseases

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