Delayed peripheral nerve regeneration and central nervous system collateral sprouting in leucocyte common antigen-related protein tyrosine phosphatase-deficient mice

2003 ◽  
Vol 17 (5) ◽  
pp. 991-1005 ◽  
Author(s):  
C. E. E. M. Van der Zee ◽  
T. Y. Man ◽  
E. M. M. Van Lieshout ◽  
I. Van der Heijden ◽  
M. Van Bree ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Peripheral Nerve ◽  
Protein Tyrosine Phosphatase ◽  
Peripheral Nerve Regeneration ◽  
Tyrosine Phosphatase ◽  
Common Antigen ◽  
Related Protein ◽  
Collateral Sprouting ◽  
Deficient Mice

scholarly journals Critical Role for Protein Tyrosine Phosphatase SHP-1 in Controlling Infection of Central Nervous System Glia and Demyelination by Theiler's Murine Encephalomyelitis Virus

2002 ◽  
Vol 76 (16) ◽  
pp. 8335-8346 ◽  
Author(s):  
Paul T. Massa ◽  
Stacie L. Ropka ◽  
Sucharita Saha ◽  
Karen L. Fecenko ◽  
Kathryn L. Beuler
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Virus Replication ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine ◽  
Normal Littermate ◽  
Encephalomyelitis Virus ◽  
Deficient Mice

ABSTRACT We previously characterized the expression and function of the protein tyrosine phosphatase SHP-1 in the glia of the central nervous system (CNS). In the present study, we describe the role of SHP-1 in virus infection of glia and virus-induced demyelination in the CNS. For in vivo studies, SHP-1-deficient mice and their normal littermates received an intracerebral inoculation of an attenuated strain of Theiler's murine encephalomyelitis virus (TMEV). At various times after infection, virus replication, TMEV antigen expression, and demyelination were monitored. It was found that the CNS of SHP-1-deficient mice uniquely displayed demyelination and contained substantially higher levels of virus than did that of normal littermate mice. Many infected astrocytes and oligodendrocytes were detected in both brains and spinal cords of SHP-1-deficient but not normal littermate mice, showing that the virus replicated and spread at a much higher rate in the glia of SHP-1-deficient animals. To ascertain whether the lack of SHP-1 in the glia was primarily responsible for these differences, glial samples from these mice were cultured in vitro and infected with TMEV. As in vivo, infected astrocytes and oligodendrocytes of SHP-1-deficient mice were much more numerous and produced more virus than did those of normal littermate mice. These findings indicate that SHP-1 is a critical factor in controlling virus replication in the CNS glia and virus-induced demyelination.

Expression of receptor protein tyrosine phosphatase δ, PTPδ, in mouse central nervous system

2016 ◽  
Vol 1642 ◽  
pp. 244-254 ◽  
Author(s):  
Maria Shishikura ◽  
Fumio Nakamura ◽  
Naoya Yamashita ◽  
Noriko Uetani ◽  
Yoichiro Iwakura ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Receptor Protein ◽  
Protein Tyrosine ◽  
Receptor Protein Tyrosine Phosphatase ◽  
Mouse Central Nervous System

scholarly journals Insight into the Role of the STriatal-Enriched Protein Tyrosine Phosphatase (STEP) in A2A Receptor-Mediated Effects in the Central Nervous System

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria Rosaria Domenici ◽  
Cinzia Mallozzi ◽  
Rita Pepponi ◽  
Ida Casella ◽  
Valentina Chiodi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Tyrosine Phosphatase ◽  
Motor Behavior ◽  
Tyrosine Phosphatase ◽  
Neuroblastoma Cell ◽  
Rat Striatum ◽  
Protein Tyrosine ◽  
Neuropsychiatric Diseases ◽  
The Central Nervous System

The STriatal-Enriched protein tyrosine phosphatase STEP is a brain-specific tyrosine phosphatase that plays a pivotal role in the mechanisms of learning and memory, and it has been demonstrated to be involved in several neuropsychiatric diseases. Recently, we found a functional interaction between STEP and adenosine A2A receptor (A2AR), a subtype of the adenosine receptor family widely expressed in the central nervous system, where it regulates motor behavior and cognition, and plays a role in cell survival and neurodegeneration. Specifically, we demonstrated the involvement of STEP in A2AR-mediated cocaine effects in the striatum and, more recently, we found that in the rat striatum and hippocampus, as well as in a neuroblastoma cell line, the overexpression of the A2AR, or its stimulation, results in an increase in STEP activity. In the present article we will discuss the functional implication of this interaction, trying to examine the possible mechanisms involved in this relation between STEP and A2ARs.

Sign in / Sign up

Export Citation Format

Share Document