| First Author | Hutter-Schmid B | Year | 2016 |
| Journal | Pharmacology | Volume | 98 |
| Issue | 5-6 | Pages | 251-260 |
| PubMed ID | 27463512 | Mgi Jnum | J:318374 |
| Mgi Id | MGI:6859412 | Doi | 10.1159/000448007 |
| Citation | Hutter-Schmid B, et al. (2016) Alpha-Smooth Muscle Actin mRNA and Protein Are Increased in Isolated Brain Vessel Extracts of Alzheimer Mice. Pharmacology 98(5-6):251-260 |
| abstractText | Alzheimer's disease (AD) is a severe neurodegenerative disorder of the brain, characterized by extracellular beta-amyloid (Abeta) plaques, intracellular tau pathology, neurodegeneration and inflammation. There is clear evidence that the blood-brain barrier is damaged in AD and that vessel function is impaired. Alpha-smooth muscle actin (alphaSMA) is a prominent protein expressed on brain vessels, especially in cells located closer to the arteriole end of the capillaries, which possibly influences the blood vessel contraction. The aim of the present study was to observe alphaSMA protein and mRNA expression in isolated brain vessel extracts and cortex in an Alzheimer mouse model with strong Abeta plaque deposition. Our data revealed a prominent expression of alphaSMA protein in isolated brain vessel extracts of AD mice by Western blot analysis. Immunostaining showed that these vessels were associated with Abeta plaques. Quantitative real-time PCR analysis confirmed this increase at the mRNA expression level and showed a significant increase of transforming growth factor beta-1 mRNA expression in AD mice. In situ hybridization demonstrated a strong expression pattern of alphaSMA mRNA in the whole cortex and hippocampus. In conclusion, our data provide evidence that alphaSMA protein and mRNA are enhanced in vessels in an AD mouse model, possibly counteracting vessel malfunction in AD. |
