Differential Akt activation in the photoreceptors of normal and rd1 mice.

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Differential Akt activation in the photoreceptors of normal and rd1 mice. / Johnson, Leif; van Veen, Theo; Ekström, Per.

In: Cell and Tissue Research, Vol. 320, No. 2, 2005, p. 213-222.

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Johnson, Leif ; van Veen, Theo ; Ekström, Per. / Differential Akt activation in the photoreceptors of normal and rd1 mice. In: Cell and Tissue Research. 2005 ; Vol. 320, No. 2. pp. 213-222.

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TY - JOUR

T1 - Differential Akt activation in the photoreceptors of normal and rd1 mice.

AU - Johnson, Leif

AU - van Veen, Theo

AU - Ekström, Per

PY - 2005

Y1 - 2005

N2 - Retinitis pigmentosa is a blinding disease in which unknown mechanisms cause the degeneration of retinal photoreceptors. The retinal degeneration (rd1) mouse is a relevant model for this condition, since it carries a mutation also found in some forms of retinitis pigmentosa. To understand the degenerative process in the rd1 mouse, we must identify the survival and apoptosis-related signaling pathways in its photoreceptors and determine whether signaling differs from that in normal mice. The phosphatidylinositol 3-kinase/Akt kinase pathway promotes survival in several different cell types. The purpose of the present study has been to compare Akt activity in retinal cells of normal and rd1 mice. We have found that, in normal mice, Akt becomes activated in the retina in a developmentally regulated and cell-type-specific fashion, encompassing essentially all retinal cells. In most cell types, once Akt activation has begun, it remains in this state throughout life. An exception is seen in the rod photoreceptors, in which Akt is activated only transiently during their development. The rd1 retina behaves identically in all but one respect, namely that the activation of Akt in rod photoreceptors persists until these cells undergo apoptosis. Thus, Akt may participate in constitutive survival processes in retinal neurons, except in rod photoreceptors in which the role of this pathway may be restricted to the developmental period. However, Akt activation in the rods may be part of a defense mechanism initiated in response to insults, such as the retinal degeneration seen in the rd1 mouse.

AB - Retinitis pigmentosa is a blinding disease in which unknown mechanisms cause the degeneration of retinal photoreceptors. The retinal degeneration (rd1) mouse is a relevant model for this condition, since it carries a mutation also found in some forms of retinitis pigmentosa. To understand the degenerative process in the rd1 mouse, we must identify the survival and apoptosis-related signaling pathways in its photoreceptors and determine whether signaling differs from that in normal mice. The phosphatidylinositol 3-kinase/Akt kinase pathway promotes survival in several different cell types. The purpose of the present study has been to compare Akt activity in retinal cells of normal and rd1 mice. We have found that, in normal mice, Akt becomes activated in the retina in a developmentally regulated and cell-type-specific fashion, encompassing essentially all retinal cells. In most cell types, once Akt activation has begun, it remains in this state throughout life. An exception is seen in the rod photoreceptors, in which Akt is activated only transiently during their development. The rd1 retina behaves identically in all but one respect, namely that the activation of Akt in rod photoreceptors persists until these cells undergo apoptosis. Thus, Akt may participate in constitutive survival processes in retinal neurons, except in rod photoreceptors in which the role of this pathway may be restricted to the developmental period. However, Akt activation in the rods may be part of a defense mechanism initiated in response to insults, such as the retinal degeneration seen in the rd1 mouse.

KW - photoreceptor

KW - apoptosis

KW - retinal degeneration

KW - mouse (CH3)

KW - Akt

U2 - 10.1007/s00441-004-1046-8

DO - 10.1007/s00441-004-1046-8

M3 - Article

VL - 320

SP - 213

EP - 222

JO - Cell and Tissue Research

JF - Cell and Tissue Research

SN - 1432-0878

IS - 2

ER -