scholarly journals Assessment of microvascular patterns and density in glioblastoma and their correlation with matrix metalloproteinase-9, p53, glial fibrillary acidic protein, and Ki-67

Glioma ◽  
2018 ◽  
Vol 1 (6) ◽  
pp. 201
Author(s):  
Sujata Chaturvedi ◽  
Karuna Jha ◽  
Ishita Pant ◽  
Ritika Singh ◽  
AjayKumar Bansal
2013 ◽  
Vol 34 (2) ◽  
pp. 297-306 ◽  
Author(s):  
Seema Yousuf ◽  
Iqbal Sayeed ◽  
Fahim Atif ◽  
Huiling Tang ◽  
Jun Wang ◽  
...  

We evaluated the neuroprotective effects of delayed progesterone (PROG) treatment against ischemic stroke-induced neuronal death, inflammation, and functional deficits. We induced transient focal cerebral ischemia in male rats and administered PROG (8 mg/kg) or vehicle intraperitoneally at 3, 6, or 24 hours post occlusion, subcutaneously 5 hours later and then every 24 hours for 7 days. Behavioral outcomes were evaluated over 22 days. Infarct size and other biomarkers of injury were evaluated by cresyl violet staining, and matrix metalloproteinase-9 (MMP-9), glial fibrillary acidic protein (GFAP), and vascular endothelial growth factor (VEGF) by immunofluorescence. Progesterone treatment started at 3 and 6 hours post occlusion significantly ( P<0.05) improved behavioral performance at all time points (74.01%) and reduced infarction volume (61.68%) compared with vehicle. No significant difference was observed between the 3 and 6 hour PROG treatment groups. Matrix metalloproteinase-9 and VEGF were upregulated in the PROG groups compared with vehicle. Glial fibrillary acidic protein expression was increased in the vehicle group but markedly lower in the PROG groups. Treatment delayed for 24 hours did not significantly improve functional outcomes or reduce infarction volume. We conclude that, under the right treatment conditions, PROG treatment delayed up to 6 hours can improve functional deficits and reduce brain infarction, possibly by modulating GFAP, VEGF, and MMP-9 expression.


2019 ◽  
Vol 14 ◽  
pp. 117727191985151 ◽  
Author(s):  
Ségolène Mrozek ◽  
Louis Delamarre ◽  
Florence Capilla ◽  
Talal Al-Saati ◽  
Olivier Fourcade ◽  
...  

Glial fibrillary acidic protein (GFAP), ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), and matrix metalloproteinase 9 (MMP-9) are potential biomarkers of traumatic brain injury (TBI) but also of secondary insults to the brain. The aim of this study was to describe the cerebral distribution of GFAP, UCH-L1, and MMP-9 in a rat model of diffuse TBI associated with standardized hypoxia-hypotension (HH). Adult male Sprague-Dawley rats were allocated to Sham (n = 10), TBI (n = 10), HH (n = 10), and TBI+HH (n = 10) groups. After 4 hours, brains were rapidly removed and immunostaining of GFAP, UCH-L1, and MMP-9 was performed. Areas of interest that have been described as particularly sensitive to hypoxic insults were analyzed. For GFAP, in the neocortex, immunostaining revealed a significant decrease in strong staining for HH and TBI+HH groups compared with TBI group ( P < .0001). For UCH-L1, the total immunostaining (6 regions of interest) reported a significant increase in strong staining ( P < .0001) and decrease in weak staining ( P < .0001) for the HH and TBI+HH groups compared with the Sham and TBI groups. For MMP-9, for the HH and TBI+HH groups, a significant increase in moderate ( P < .0001) and weak staining ( P < .0001) and a decrease in negative staining ( P < .0001) compared with the Sham and TBI groups were observed. UCH-L1 and MMP-9 immunostainings increased after HH alone or HH combined with TBI compared with TBI alone. GFAP immunostaining decreased particularly in the neocortex after HH alone or HH combined with TBI compared with TBI alone. These three biomarkers could therefore be considered as potential biomarkers of HH insults independently of TBI.


2007 ◽  
Vol 6 (1) ◽  
pp. 102-102
Author(s):  
E VELOT ◽  
I ERNENS ◽  
B HAAS ◽  
C JEANTY ◽  
D ROUY ◽  
...  

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