Myelin alterations in absence of lysophosphatidic acid receptor LPA1

被引：0

作者：

Estivill-Torrus, G. G. ^{[1
]}

Garcia-Diaz, B. ^{[1
]}

Matas Rico, E. ^{[1
]}

Gomez Conde, A. I. ^{[1
]}

Riquelme, R. ^{[2
]}

Varela Nieto, I. ^{[2
]}

Jimenez, A. J. ^{[3
]}

Leyva, L. ^{[1
]}

Fernandez, O. ^{[4
]}

Chin, J. ^{[5
]}

Rodriguez de Fonseca, F. ^{[1
]}

机构：

[1] Hosp Carlos Haya, Fdn IMABIS, Malaga, Spain

[2] Univ Autonoma Madrid, CSIC, Inst Invest Biomed Alberto Sols, Madrid, Spain

[3] Univ Malaga, Fac Ciencias, Malaga, Spain

[4] Hosp Carlos Haya, Inst Neurociencias Clin, Malaga, Spain

[5] Scripps Res Inst, Dept Mol Biol, Helen L Dorris Child & Adolescent Neuropsychiat D, La Jolla, CA USA

来源：

9TH EUROPEAN MEETING ON GLIAL CELLS IN HEALTH AND DISEASE | 2009年

关键词：

OLIGODENDROCYTES;

D O I：

暂无

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Because of the identified influence of lysophosphatidic acid (LPA) in the differentiation of myclinating cells, maLPA(1)-null mice, lacking the LPA(1) receptor, were analyzed as a new highly attractive model for the study of demyelinating diseases. LPA(1)-null animals show cortical myelin deficit configuring a jumbled spaced myelin fiber pattern and a reduction of oligodendrocytes number. As a possible mechanism involving cell survival we demonstrated an anomalous intracellular transport of PLP myelin protein that showed intracellular accretion to the detriment of its membrane emplacement.

引用

页码：93 / 96

页数：4

共 7 条

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