NDLI: Regulation of Rod Photoreceptor Differentiation by STAT3 Is Controlled by a Tyrosine Phosphatase

Content Provider	Springer Nature Link
Author	Pinzon Guzman, Carolina Xing, Tiaosi Zhang, Samuel Shao Min Barnstable, Colin J.
Copyright Year	2014
Abstract	Signal pathways that reduce the levels of tyrosine-phosphorylated STAT3 (pSTAT3) allow late retinal progenitors to exit the cell cycle and enter a terminal differentiation pathway into rod photoreceptors. In the mouse retina, we previously identified PKC-β1 and PKC-γ isoforms as essential components of a key signal pathway and IGF-1 as a major extrinsic factor regulating rod formation. In this manuscript, we demonstrate that PKC decreases phosphotyrosine but not phosphoserine on STAT3 in neonatal mouse retinas. Neither IGF-1 nor PMA induced a significant change in the levels of STAT3 or in the levels of the key proteins regulating STAT3 degradation, SOCS3, and PIAS3. Treatment of neonatal mouse retinal explants with sodium orthovanadate inhibited the PKC-mediated reduction in pSTAT3, indicating a role for a phosphatase. Addition of the PTEN inhibitor bpV(phen) to explant cultures treated with IGF-1 or PMA had no effect on the reduction in pSTAT3 levels, but the effect of both IGF-1 and PMA was blocked by a concentration of the inhibitor NSC87877 that is selective for the phosphatases Shp1 and Shp2. Inhibition of Shp1/2 phosphatases was also sufficient to abolish the IGF1-mediated induction of rod photoreceptor differentiation in the retina explant cultures. We conclude that one or both of these phosphatases are key components regulating the formation of rod photoreceptors in mouse retina.
Starting Page	152
Ending Page	159
Page Count	8
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	55
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2014-08-10
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Rod photoreceptor IGF1 STAT3 PTEN Shp1 Shp2 Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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