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Gene Review:

Lrdg1 - light induced retinal degeneration 1

Mus musculus

Donovan, M. et al., Zhang, C. et al., Zhang, C. et al., Torbidoni, V. et al., Carmody, R.J. et al., et al.

Zhang, Shen, Lam, Zeng, Chiang, Yang, Tso, Chen, Chuang, Cheng, Hsu, Chang, Pardue, Grimm, Wenzel, Remé, Grimm, Wenzel, Hafezi, Remé, Grimm, Wenzel, Hafezi, Yu, Redmond, Remé, Zhang, Lei, Lam, Yang, Sinha, Tso,

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High impact information on Lrdg1

Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration [1].
Inhibition of c-fos expression might therefore represent a novel therapeutic strategy to retard the time course of retinal dystrophies and light-induced retinal degeneration [2].
Furthermore, photoreceptor apoptosis cannot be inhibited with the broad range caspase inhibitor zVAD-fmk indicating that light-induced retinal degeneration is caspase-independent [3].
Finally, we show that the calcium-dependent proteases calpains are active during light-induced retinal degeneration and establish that the calcium channel blocker D-cis-diltiazem completely inhibits photoreceptor apoptosis [3].
Previous studies have reported the ability of antioxidants to ameliorate light-induced retinal degeneration, suggesting a role for oxidative stress in photoreceptor cell death [4].

Anatomical context of Lrdg1

This study was conducted to evaluate the neuroprotective effect of minocycline and the role of microglia in light-induced retinal degeneration [5].

Associations of Lrdg1 with chemical compounds

Morphologic, morphometric, immunohistochemical, and electrophysiological studies were performed to evaluate the efficacy of minocycline in the amelioration of light-induced retinal degeneration and the possible involvement of microglial cells [5].
CONCLUSIONS: Retinal chemokines such as MCP-3 and their receptors are involved in the activation and migration of retinal microglia in light-induced retinal degeneration, which in turn modulate the apoptotic loss of photoreceptor cells in the outer retina [6].
Here, we present novel observations about the course of light-induced retinal degeneration in BALB-c mice exposed to 1500 lux during 4 days with or without treatment with tezosentan, a mixed endothelinergic antagonist [7].

Regulatory relationships of Lrdg1

Among the apoptosis-related genes, only caspase-1 expression was upregulated by light exposure and Caspase-1 might therefore be involved in light-induced retinal degeneration [8].

Other interactions of Lrdg1

Endothelin-1 and endothelin receptors in light-induced retinal degeneration [9].
NF-kappaB activation in light-induced retinal degeneration in a mouse model [10].
Here, the potential role of WOX1 in light-induced retinal degeneration in vivo was investigated [11].
Acid-sensing ion channel 2 is important for retinal function and protects against light-induced retinal degeneration [12].
The nob mutation does not protect against light-induced retinal degeneration [13].

Analytical, diagnostic and therapeutic context of Lrdg1

PURPOSE: Apoptosis is the final common death pathway of photoreceptors in light-induced retinal degeneration and in several animal models for retinal dystrophy [14].

References

Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration. Grimm, C., Wenzel, A., Hafezi, F., Yu, S., Redmond, T.M., Remé, C.E. Nat. Genet. (2000) [Pubmed]
The absence of c-fos prevents light-induced apoptotic cell death of photoreceptors in retinal degeneration in vivo. Hafezi, F., Steinbach, J.P., Marti, A., Munz, K., Wang, Z.Q., Wagner, E.F., Aguzzi, A., Remé, C.E. Nat. Med. (1997) [Pubmed]
Caspase-independent photoreceptor apoptosis in vivo and differential expression of apoptotic protease activating factor-1 and caspase-3 during retinal development. Donovan, M., Cotter, T.G. Cell Death Differ. (2002) [Pubmed]
Reactive oxygen species as mediators of photoreceptor apoptosis in vitro. Carmody, R.J., McGowan, A.J., Cotter, T.G. Exp. Cell Res. (1999) [Pubmed]
Neuroprotection of photoreceptors by minocycline in light-induced retinal degeneration. Zhang, C., Lei, B., Lam, T.T., Yang, F., Sinha, D., Tso, M.O. Invest. Ophthalmol. Vis. Sci. (2004) [Pubmed]
Activation of microglia and chemokines in light-induced retinal degeneration. Zhang, C., Shen, J.K., Lam, T.T., Zeng, H.Y., Chiang, S.K., Yang, F., Tso, M.O. Mol. Vis. (2005) [Pubmed]
Endothelin receptors in light-induced retinal degeneration. Torbidoni, V., Iribarne, M., Suburo, A.M. Exp. Biol. Med. (Maywood) (2006) [Pubmed]
Gene expression in the mouse retina: the effect of damaging light. Grimm, C., Wenzel, A., Hafezi, F., Remé, C.E. Mol. Vis. (2000) [Pubmed]
Endothelin-1 and endothelin receptors in light-induced retinal degeneration. Torbidoni, V., Iribarne, M., Ogawa, L., Prasanna, G., Suburo, A.M. Exp. Eye Res. (2005) [Pubmed]
NF-kappaB activation in light-induced retinal degeneration in a mouse model. Wu, T., Chen, Y., Chiang, S.K., Tso, M.O. Invest. Ophthalmol. Vis. Sci. (2002) [Pubmed]
Light-induced retinal damage involves tyrosine 33 phosphorylation, mitochondrial and nuclear translocation of WW domain-containing oxidoreductase in vivo. Chen, S.T., Chuang, J.I., Cheng, C.L., Hsu, L.J., Chang, N.S. Neuroscience (2005) [Pubmed]
Acid-sensing ion channel 2 is important for retinal function and protects against light-induced retinal degeneration. Ettaiche, M., Guy, N., Hofman, P., Lazdunski, M., Waldmann, R. J. Neurosci. (2004) [Pubmed]
The nob mutation does not protect against light-induced retinal degeneration. Pardue, M.T., Grimm, C., Wenzel, A., Remé, C.E. Adv. Exp. Med. Biol. (2003) [Pubmed]
Retinal degeneration in the rd mouse in the absence of c-fos. Hafezi, F., Abegg, M., Grimm, C., Wenzel, A., Munz, K., Stürmer, J., Farber, D.B., Remé, C.E. Invest. Ophthalmol. Vis. Sci. (1998) [Pubmed]

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