Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Yasuyuki Honjo; Chandrasekharam N. Nagineni; Jonas Larsson; Seshagiri R. Nandula; John J. Hooks; Chi Chao Chan; Stefan Karlsson; Ashok B. Kulkarni

doi:10.1016/j.bbrc.2006.11.033

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Yasuyuki Honjo, Chandrasekharam N. Nagineni, Jonas Larsson, Seshagiri R. Nandula, John J. Hooks, Chi Chao Chan, Stefan Karlsson, Ashok B. Kulkarni

Surgery

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

We generated a mouse model (cKO) with a conditional deletion of TGF-β signaling in the retinal neurons by crossing TGF-β receptor I (TGF-β RI) floxed mice with nestin-Cre mice. Almost all of the newborn cKO mice had retinal detachment at the retinal pigment epithelium (RPE)/photoreceptor layer junction of the neurosensory retina (NSR). The immunostaining for chondroitin-6-sulfate showed a very weak reaction in cKO mice in contrast to intense staining in the photoreceptor layer in wild-type mice. Macroscopic cataracts, in one or both eyes, were observed in 50% of the mice by 6 months of age, starting as early as the first month after birth. The cKO mouse model demonstrates that the TGF-β signaling deficiency in retinal cells leads to decreased levels of chondroitin sulfate proteoglycan in the retinal interphotoreceptor matrix. This in turn causes retinal detachment due to the loss of adhesion of the NSR to RPE.

Original language	English (US)
Pages (from-to)	418-422
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	352
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2006.11.033
State	Published - Jan 12 2007

Bibliographical note

Funding Information:
We thank Dr. Ryoichiro Kagayama, Institute of Virus Research, Kyoto University, Japan, for providing nestin-Cre mice. This research was supported [in part] by the Intramural Research Program of the National Institutes of Dental and Craniofacial Research and National Eye Institute, National Institutes of Health. Appendix A

Keywords

Cataracts
Chondroitin-6-sulfate
Cre-lox P system
Extracellular matrix
Retina
Retinal detachment
Retinal pigment epithelium
TGF-β
TGF-β receptor I

Access

10.1016/j.bbrc.2006.11.033

OpenUrl availability

Full text

Cite this

@article{33e6cd0096af42fab6e0d40cc0fc94c7,

title = "Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice",

abstract = "We generated a mouse model (cKO) with a conditional deletion of TGF-β signaling in the retinal neurons by crossing TGF-β receptor I (TGF-β RI) floxed mice with nestin-Cre mice. Almost all of the newborn cKO mice had retinal detachment at the retinal pigment epithelium (RPE)/photoreceptor layer junction of the neurosensory retina (NSR). The immunostaining for chondroitin-6-sulfate showed a very weak reaction in cKO mice in contrast to intense staining in the photoreceptor layer in wild-type mice. Macroscopic cataracts, in one or both eyes, were observed in 50% of the mice by 6 months of age, starting as early as the first month after birth. The cKO mouse model demonstrates that the TGF-β signaling deficiency in retinal cells leads to decreased levels of chondroitin sulfate proteoglycan in the retinal interphotoreceptor matrix. This in turn causes retinal detachment due to the loss of adhesion of the NSR to RPE.",

keywords = "Cataracts, Chondroitin-6-sulfate, Cre-lox P system, Extracellular matrix, Retina, Retinal detachment, Retinal pigment epithelium, TGF-β, TGF-β receptor I",

author = "Yasuyuki Honjo and Nagineni, {Chandrasekharam N.} and Jonas Larsson and Nandula, {Seshagiri R.} and Hooks, {John J.} and Chan, {Chi Chao} and Stefan Karlsson and Kulkarni, {Ashok B.}",

note = "Funding Information: We thank Dr. Ryoichiro Kagayama, Institute of Virus Research, Kyoto University, Japan, for providing nestin-Cre mice. This research was supported [in part] by the Intramural Research Program of the National Institutes of Dental and Craniofacial Research and National Eye Institute, National Institutes of Health. Appendix A ",

year = "2007",

month = jan,

day = "12",

doi = "10.1016/j.bbrc.2006.11.033",

language = "English (US)",

volume = "352",

pages = "418--422",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "2",

}

TY - JOUR

T1 - Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

AU - Honjo, Yasuyuki

AU - Nagineni, Chandrasekharam N.

AU - Larsson, Jonas

AU - Nandula, Seshagiri R.

AU - Hooks, John J.

AU - Chan, Chi Chao

AU - Karlsson, Stefan

AU - Kulkarni, Ashok B.

N1 - Funding Information: We thank Dr. Ryoichiro Kagayama, Institute of Virus Research, Kyoto University, Japan, for providing nestin-Cre mice. This research was supported [in part] by the Intramural Research Program of the National Institutes of Dental and Craniofacial Research and National Eye Institute, National Institutes of Health. Appendix A

PY - 2007/1/12

Y1 - 2007/1/12

N2 - We generated a mouse model (cKO) with a conditional deletion of TGF-β signaling in the retinal neurons by crossing TGF-β receptor I (TGF-β RI) floxed mice with nestin-Cre mice. Almost all of the newborn cKO mice had retinal detachment at the retinal pigment epithelium (RPE)/photoreceptor layer junction of the neurosensory retina (NSR). The immunostaining for chondroitin-6-sulfate showed a very weak reaction in cKO mice in contrast to intense staining in the photoreceptor layer in wild-type mice. Macroscopic cataracts, in one or both eyes, were observed in 50% of the mice by 6 months of age, starting as early as the first month after birth. The cKO mouse model demonstrates that the TGF-β signaling deficiency in retinal cells leads to decreased levels of chondroitin sulfate proteoglycan in the retinal interphotoreceptor matrix. This in turn causes retinal detachment due to the loss of adhesion of the NSR to RPE.

AB - We generated a mouse model (cKO) with a conditional deletion of TGF-β signaling in the retinal neurons by crossing TGF-β receptor I (TGF-β RI) floxed mice with nestin-Cre mice. Almost all of the newborn cKO mice had retinal detachment at the retinal pigment epithelium (RPE)/photoreceptor layer junction of the neurosensory retina (NSR). The immunostaining for chondroitin-6-sulfate showed a very weak reaction in cKO mice in contrast to intense staining in the photoreceptor layer in wild-type mice. Macroscopic cataracts, in one or both eyes, were observed in 50% of the mice by 6 months of age, starting as early as the first month after birth. The cKO mouse model demonstrates that the TGF-β signaling deficiency in retinal cells leads to decreased levels of chondroitin sulfate proteoglycan in the retinal interphotoreceptor matrix. This in turn causes retinal detachment due to the loss of adhesion of the NSR to RPE.

KW - Cataracts

KW - Chondroitin-6-sulfate

KW - Cre-lox P system

KW - Extracellular matrix

KW - Retina

KW - Retinal detachment

KW - Retinal pigment epithelium

KW - TGF-β

KW - TGF-β receptor I

UR - http://www.scopus.com/inward/record.url?scp=33751510956&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33751510956&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2006.11.033

DO - 10.1016/j.bbrc.2006.11.033

M3 - Article

C2 - 17126294

AN - SCOPUS:33751510956

SN - 0006-291X

VL - 352

SP - 418

EP - 422

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 2

ER -

Neuron-specific TGF-β signaling deficiency results in retinal detachment and cataracts in mice

Abstract

Bibliographical note

Keywords

Access

OpenUrl availability

Other files and links

Fingerprint

Cite this