scholarly journals Age-Dependent Cognitive Deficits and Neuronal Apoptosis in Cyclooxygenase-2 Transgenic Mice

2001 ◽  
Vol 21 (20) ◽  
pp. 8198-8209 ◽  
Author(s):  
Katrin I. Andreasson ◽  
Alena Savonenko ◽  
Sveta Vidensky ◽  
Joseph J. Goellner ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Neuronal Apoptosis ◽  
Cyclooxygenase 2 ◽  
Age Dependent

MiR-335-5p Inhibits β-Amyloid (Aβ) Accumulation to Attenuate Cognitive Deficits Through Targeting c-jun-N-terminal Kinase 3 in Alzheimer’s Disease

2020 ◽  
Vol 17 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Dan Wang ◽  
Zhifu Fei ◽  
Song Luo ◽  
Hai Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Western Blot ◽  
Mrna Expression ◽  
Cognitive Deficits ◽  
Protein Levels ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
The Relationship

Objectives: Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs (miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progression of AD is still not clearly clarified. Methods: The protein and mRNA levels were measured by western blot and RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual-luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice were used as an in vivo AD model. Morris water maze test was performed to assess the effect of miR- 335-5p on the cognitive deficits in APP/PS1 transgenic mice. Results: The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated, and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients. The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, the dual Luciferase assay verified the relationship between miR-335- 5p and JNK3. Overexpression of miR-335-5p significantly decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved the cognitive abilities of APP/PS1 mice. Conclusion: The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, may be a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment.

Stroke-induced opposite and age-dependent changes of vessel-associated markers in co-morbid transgenic mice with Alzheimer-like alterations

2013 ◽  
Vol 250 ◽  
pp. 270-281 ◽  
Author(s):  
Cheryl A. Hawkes ◽  
Dominik Michalski ◽  
Rebecca Anders ◽  
Sabine Nissel ◽  
Jens Grosche ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Age Dependent

Transitional Cell Hyperplasia and Carcinomas in Urinary Bladders of Transgenic Mice with Keratin 5 Promoter-Driven Cyclooxygenase-2 Overexpression

2005 ◽  
Vol 65 (5) ◽  
pp. 1808-1813 ◽  
Author(s):  
Russell D. Klein ◽  
Carolyn S. Van Pelt ◽  
Anita L. Sabichi ◽  
Jorge dela Cerda ◽  
Susan M. Fischer ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Transitional Cell ◽  
Cyclooxygenase 2 ◽  
Cell Hyperplasia ◽  
Keratin 5

Aβ levels in serum, CSF and brain, and cognitive deficits in APP + PS1 transgenic mice

Neuroreport ◽  
2003 ◽  
Vol 14 (1) ◽  
pp. 163-166 ◽  
Author(s):  
Li Liu ◽  
Tero Tapiola ◽  
Sanna-Kaisa Herukka ◽  
Matti Heikkilä ◽  
Heikki Tanila
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits

scholarly journals Transgenic expression of cyclooxygenase-2 in pancreatic acinar cells induces chronic pancreatitis

2019 ◽  
Vol 316 (1) ◽  
pp. G179-G186
Author(s):  
Haojie Huang ◽  
Jiaxiang Chen ◽  
Lisi Peng ◽  
Yao Yao ◽  
Defeng Deng ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Transgenic Mice ◽  
Fibrous Tissue ◽  
Acinar Cells ◽  
Cyclooxygenase 2 ◽  
Therapeutic Interventions ◽  
Pancreatic Stellate Cells ◽  
Pancreatic Acinar Cells ◽  
Transgenic Expression ◽  
Cox 2

Replacement of the exocrine parenchyma by fibrous tissue is a main characteristic of chronic pancreatitis. Understanding the mechanisms of pancreatic fibrogenesis is critical for the development of preventive and therapeutic interventions. Cyclooxygenase-2 (COX-2), a rate-limiting enzyme for prostaglandin synthesis, is expressed in patients with chronic pancreatitis. However, it is unknown whether COX-2 can cause chronic pancreatitis. To investigate the roles of pancreatic acinar COX-2 in fibrogenesis and the development of chronic pancreatitis, COX-2 was ectopically expressed specifically in pancreatic acinar cells in transgenic mice. Histopathological changes and expression levels of several profibrogenic factors related to chronic pancreatitis were evaluated. COX-2 was expressed in the pancreas of the transgenic mice, as detected by Western blot analysis. Immunohistochemical staining showed COX-2 was specifically expressed in pancreatic acinar cells. COX-2 expression led to progressive changes in the pancreas, including pancreas megaly, persistent inflammation, collagen deposition, and acinar-to-ductal metaplasia. Quantitative RT-PCR and immunostaining showed that profibrogenic factors were upregulated and pancreatic stellate cells were activated in the COX-2 transgenic mice. Expression of COX-2 in pancreatic acinar cells is sufficient to induce chronic pancreatitis. Targeting this pathway may be valuable in the prevention of chronic pancreatitis. NEW & NOTEWORTHY COX-2 expression is observed in pancreatic tissues of human chronic pancreatitis. In this study, we showed that COX-2 expression caused the development of chronic pancreatitis in transgenic mice, supporting the idea that COX-2 inhibition may be an effective preventive and therapeutic strategy.

Cyclooxygenase 2 inhibits SAPK activation in neuronal apoptosis

2003 ◽  
Vol 300 (4) ◽  
pp. 884-888 ◽  
Author(s):  
Bradley Miller ◽  
Yu-Wen E Chang ◽  
Andrey Sorokin
Keyword(s):  
Neuronal Apoptosis ◽  
Cyclooxygenase 2

The beneficial effects of dietary grape supplementation on improving cognitive deficits in APP/PS1 double transgenic mice

2018 ◽  
Vol 49 ◽  
pp. 224-234 ◽  
Author(s):  
Kangliang Sheng ◽  
Shanshan Shui ◽  
Ling Yan ◽  
Junjie Yu ◽  
Guang Hao ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Beneficial Effects ◽  
Double Transgenic Mice
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