Abstract 4545: Positron emission tomography (PET) of TSPO expression in preclinical models of human cancer

2012 ◽  
Author(s):  
Dewei Tang ◽  
Matthew R. Hight ◽  
Eliot T. Mckinley ◽  
Allie Fu ◽  
Jason R. Buck ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Human Cancer ◽  
Emission Tomography ◽  
Preclinical Models ◽  
Positron Emission ◽  
Tspo Expression

scholarly journals Molecular Imaging of CXCR4 Receptor Expression in Human Cancer Xenografts with [64Cu]AMD3100 Positron Emission Tomography

2010 ◽  
Vol 70 (10) ◽  
pp. 3935-3944 ◽  
Author(s):  
Sridhar Nimmagadda ◽  
Mrudula Pullambhatla ◽  
Kristie Stone ◽  
Gilbert Green ◽  
Zaver M. Bhujwalla ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Molecular Imaging ◽  
Human Cancer ◽  
Receptor Expression ◽  
Emission Tomography ◽  
Positron Emission ◽  
Cxcr4 Receptor

scholarly journals From positron emission tomography to cell analysis of the 18-kDa Translocator Protein in mild traumatic brain injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Clément Delage ◽  
Nicolas Vignal ◽  
Coralie Guerin ◽  
Toufik Taib ◽  
Clément Barboteau ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Positron Emission Tomography ◽  
Flow Cytometry ◽  
Microglial Activation ◽  
Translocator Protein ◽  
Emission Tomography ◽  
Flow Cytometry Analysis ◽  
Positron Emission ◽  
The Brain ◽  
Tspo Expression

AbstractTraumatic brain injury (TBI) leads to a deleterious neuroinflammation, originating from microglial activation. Monitoring microglial activation is an indispensable step to develop therapeutic strategies for TBI. In this study, we evaluated the use of the 18-kDa translocator protein (TSPO) in positron emission tomography (PET) and cellular analysis to monitor microglial activation in a mild TBI mouse model. TBI was induced on male Swiss mice. PET imaging analysis with [18F]FEPPA, a TSPO radiotracer, was performed at 1, 3 and 7 days post-TBI and flow cytometry analysis on brain at 1 and 3 days post-TBI. PET analysis showed no difference in TSPO expression between non-operated, sham-operated and TBI mice. Flow cytometry analysis demonstrated an increase in TSPO expression in ipsilateral brain 3 days post-TBI, especially in microglia, macrophages, lymphocytes and neutrophils. Moreover, microglia represent only 58.3% of TSPO+ cells in the brain. Our results raise the question of the use of TSPO radiotracer to monitor microglial activation after TBI. More broadly, flow cytometry results point the lack of specificity of TSPO for microglia and imply that microglia contribute to the overall increase in TSPO in the brain after TBI, but is not its only contributor.

scholarly journals Feasibility of TSPO-Specific Positron Emission Tomography Radiotracer for Evaluating Paracetamol-Induced Liver Injury

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1661
Author(s):  
Daehee Kim ◽  
Byung Seok Moon ◽  
Sun Mi Park ◽  
Sang Ju Lee ◽  
Seo Young Kang ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Liver Injury ◽  
Rat Model ◽  
Early Phase ◽  
Hepatic Uptake ◽  
Emission Tomography ◽  
Expression Level ◽  
Control Group ◽  
Positron Emission ◽  
Tspo Expression

Macrophages are activated during the early phase of paracetamol-induced liver injury (PLI). [18F]GE180 is a radiolabeled ligand that recognizes the macrophage translocator protein (TSPO). In this study, we evaluated the feasibility of a TSPO-specific radiotracer in a rat model of PLI. A rat model of liver injury was induced by intraperitoneal administration of paracetamol. [18F]GE180 positron emission tomography (PET) images were obtained after 24 h. The maximal and mean standardized uptake values (SUVmax and SUVav) of the liver and serum biomarker levels were examined. The TSPO expression level was examined using real-time polymerase chain reaction and Western blot analysis. [18F]GE180 hepatic uptake in the PLI group was significantly higher than that in the control group (SUVmax p = 0.001; SUVav p = 0.005). Both mRNA and protein TSPO expression levels were higher in the PLI group. The mRNA expression level of TSPO was significantly correlated with [18F]GE180 hepatic uptake in both groups (SUVmax p = 0.019; SUVav p = 0.007). [18F]GE180 hepatic uptake in the PLI group showed a significant positive correlation with ALT24 and ALT48 (ALT24 p = 0.016; ALT48 p = 0.002). [18F]GE180 enabled visualization of PLI through TSPO overexpression. Our results support the potential utility of hepatic uptake by TSPO-PET as a non-invasive imaging biomarker for the early phase of PLI.

scholarly journals Positron emission tomography of cerebral angiogenesis and TSPO expression in a mouse model of chronic hypoxia

2017 ◽  
Vol 38 (4) ◽  
pp. 687-696 ◽  
Author(s):  
Iwao Kanno ◽  
Chie Seki ◽  
Hiroyuki Takuwa ◽  
Zhao-Hui Jin ◽  
Didier Boturyn ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Pet Imaging ◽  
Vascular Remodeling ◽  
Early Phase ◽  
Transient Increase ◽  
Emission Tomography ◽  
Vascular Density ◽  
Positron Emission ◽  
Imaging Results ◽  
Tspo Expression

The present study aimed to examine whether positron emission tomography (PET) could evaluate cerebral angiogenesis. Mice were housed in a hypoxic chamber with 8–9% oxygen for 4, 7, and 14 days, and the angiogenic responses were evaluated with a radiotracer, 64Cu-cyclam-RAFT-c(-RGDfK-)4, which targeted αVβ3 integrin and was imaged with PET. The PET imaging results showed little uptake during all of the hypoxic periods. Immunofluorescence staining of the β3 integrin, CD61, revealed weak expression, while the microvessel density assessed by CD31 staining increased with the hypoxic duration. These observations suggest that the increased vascular density originated from other types of vascular remodeling, unlike angiogenic sprouting. We then searched for any signs of vascular remodeling that could be detected using PET. PET imaging of 11C-PK11195, a marker of the 18-kDa translocator protein (TSPO), revealed a transient increase at day 4 of hypoxia. Because the immunofluorescence of glial markers showed unchanged staining over the early phase of hypoxia, the observed upregulation of TSPO expression probably originated from non-glial cells (e.g. vascular cells). In conclusion, a transient increase in TSPO probe uptake was detected with PET at only the early phase of hypoxia, which indicates an early sign of vascular remodeling induced by hypoxia.

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