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Lack of the protein tyrosine phosphatase SHP‐1 results in decreased numbers of glia within the motheaten (me/me) mouse brain
Author(s) -
Wishcamper Celine A.,
Coffin J. Douglas,
Lurie Diana I.
Publication year - 2001
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.1401
Subject(s) - biology , microglia , immunostaining , protein tyrosine phosphatase , myelin , myelin basic protein , neuroglia , central nervous system , phosphatase , microbiology and biotechnology , endocrinology , neuroscience , immunology , immunohistochemistry , signal transduction , inflammation , phosphorylation
Mice that are homozygous for the autosomal recessive motheaten allele (me/me) lack the protein tyrosine phosphatase SHP‐1. Loss of SHP‐1 leads to many hematopoietic abnormalities, as well as defects such as infertility and low body weight. However, little is known regarding the role SHP‐1 plays in the development of the central nervous system (CNS). To define the role of SHP‐1 in CNS development and differentiation, we examined the brains of me/me mice at various times after birth for neuronal and glial abnormalities. Although the brains of me/me mice are slightly smaller than age‐matched wild‐type littermates, both me/me and wild‐type brains are similar in weight, possess an intact blood‐brain barrier, and have largely normal neuronal architecture. Significantly, the current study reveals that me/me brain shows decreases in the number of glial fibriallary acidic protein (GFAP)+ astrocytes and F480+ microglia compared with wild‐type mice. In addition, decreased immunostaining for the myelin‐synthesizing enzyme CNPase was observed in me/me mice, confirming the loss of myelin in these animals, as reported (Massa et al. [2000] Glia 29:376–385). It is particularly significant that there is a decreased number of immunolabeled glia of all subtypes and that this deficit in glial number is not restricted to a particular class of glia. This suggests that SHP‐1 is necessary for the normal differentiation and distribution of astrocytes, microglia, and oligendrocytes within the murine CNS. J. Comp. Neurol. 441:118–133, 2001. © 2001 Wiley‐Liss, Inc.