Protein tyrosine phosphatases expression during development of mouse superior colliculus

Reinhard, Jacqueline; Horvat-Bröcker, Andrea; Illes, Sebastian; Zaremba, Angelika; Knyazev, Piotr; Ullrich, Axel; Faissner, Andréas

doi:10.1007/s00221-009-1963-6

Cited by 8 publications

(3 citation statements)

References 96 publications

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“…Images were taken with a confocal laser‐scanning microscope LSM 510 META (Zeiss). Laser lines and emission filters were optimized with the Zeiss LSM Image Browser software . Tenascin‐C and 473HD immunoreactivity were analyzed using an ImageJ macro .…”

Section: Methodsmentioning

confidence: 99%

Early remodelling of the extracellular matrix proteins tenascin‐C and phosphacan in retina and optic nerve of an experimental autoimmune glaucoma model

Reinehr

Reinhard

Wiemann

et al. 2016

J Cellular Molecular Medi

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Glaucoma is characterized by the loss of retinal ganglion cells (RGCs) and optic nerve fibres. Previous studies noted fewer RGCs after immunization with ocular antigens at 28 days. It is known that changes in extracellular matrix (ECM) components conduct retina and optic nerve degeneration. Here, we focused on the remodelling of tenascin‐C and phosphacan/receptor protein tyrosine phosphatase β/ζ in an autoimmune glaucoma model. Rats were immunized with optic nerve homogenate (ONA) or S100B protein (S100). Controls received sodium chloride (Co). After 14 days, no changes in RGC number were noted in all groups. An increase in GFAP mRNA expression was observed in the S100 group, whereas no alterations were noted via immunohistochemistry in both groups. Extracellular matrix remodelling was analyzed after 3, 7, 14 and 28 days. Tenascin‐C and 473HD immunoreactivity in retinae and optic nerves was unaltered in both immunized groups at 3 days. At 7 days, tenascin‐C staining increased in both tissues in the ONA group. Also, in the optic nerves of the S100 group, an intense tenascin‐C staining could be shown. In the retina, an increased tenascin‐C expression was also observed in ONA animals via Western blot. 473HD immunoreactivity was elevated in the ONA group in both tissues and in the S100 optic nerves at 7 days. At 14 days, tenascin‐C and 473HD immunoreactivity was up‐regulated in the ONA retinae, whereas phosphacan expression was up‐regulated in both groups. We conclude that remodelling of tenascin‐C and phosphacan occurred shortly after immunization, already before RGC loss. We assume that both ECM molecules represent early indicators of neurodegeneration.

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Section: Methodsmentioning

confidence: 99%

Early remodelling of the extracellular matrix proteins tenascin‐C and phosphacan in retina and optic nerve of an experimental autoimmune glaucoma model

Reinehr

Reinhard

Wiemann

et al. 2016

J Cellular Molecular Medi

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“…During development, PTPs exhibit a distinct spatial pattern of expression and are implicated in axon growth and guidance in CNS (Bixby, 2000; Stoker, 2001). A number of PTPs display a distinct spatiotemporal regulation in the pre- and postnatal superior colliculus, which appears to correlate with neuronal proliferation, differentiation, axon innervation and arborization (Reinhard et al, 2009). The LAR subfamily is composed of three vertebrate homologs: LAR, PTPσ, and PTPδ, which share 66% amino acid identity in the full-length proteins and 84% identity in the catalytic domains.…”

Section: Receptor-mediated Inhibition By Cspgsmentioning

confidence: 99%

Molecular mechanisms of scar-sourced axon growth inhibitors

Ohtake

2015

Brain Research

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Astrogliosis is a defense response of the CNS to minimize primary damage and to repair injured tissues, but it ultimately generates harmful effects by upregulating inhibitory molecules to suppress neuronal elongation and forming potent barriers to axon regeneration. Chondroitin sulfate proteoglycans (CSPGs) are highly expressed by reactive scars and are potent contributors to the non-permissive environment in mature CNS. Surmounting strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. Currently, enzymatic digestion of CSPGs with locally applied chondroitinase ABC is the main in vivo approach to overcome scar inhibition, but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of molecular mechanisms underlying CSPG function may facilitate development of new effective therapies to overcome scar-mediated inhibition. Previous studies support that CSPGs act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions, but two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase σ and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibition. CSPGs may also act by binding two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3. Thus, CSPGs inhibit axon growth through multiple mechanisms, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries.

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“…During development, PTPs exhibit a distinct spatial pattern of expression and are implicated in axon growth and guidance in the CNS(Bixby 2000; Stoker 2001). For example, a number of PTPs displayed a distinct spatiotemporal regulation in the pre- and postnatal superior colliculus, which appears to correlate with neuronal proliferation, differentiation, axon innervation and arborisation(Reinhard et al 2009). The LAR subfamily is composed of three vertebrate homologs: LAR, PTPσ, and PTPδ, which share 66% amino acid identity in the full-length proteins and 84% identity in the catalytic domains.…”

Section: Lar Subfamily Of Phosphatases As the Functional Receptors Fomentioning

confidence: 99%

Scar-mediated inhibition and CSPG receptors in the CNS

Sharma

Selzer

2012

Experimental Neurology

162

128

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Severed axons in adult mammals do not regenerate appreciably after central nervous system (CNS) injury due to developmentally determined reductions in neuron-intrinsic growth capacity and extracellular environment for axon elongation. Chondroitin sulfate proteoglycans (CSPGs), which are generated by reactive scar tissues, are particularly potent contributors to the growth-limiting environment in mature CNS. Thus, surmounting the strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. As of now, the main in vivo approach to overcoming inhibition by CSPGs is enzymatic digestion with locally applied chondroitinase ABC (ChABC), but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of the molecular mechanisms underlying CSPG action is needed in order to develop more effective therapies to overcome CSPG-mediated inhibition of axon regeneration and/or sprouting. Because of their large size and dense negative charges, CSPGs were thought to act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions. Although this may be true, recent studies indicate that two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase σ (PTPσ) and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibitory effects. CSPGs also may act by binding to two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3 (NgR1 and NgR3). If confirmed, it would suggest that CSPGs have multiple mechanisms by which they inhibit axon growth, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries, including spinal cord injury (SCI).

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Protein tyrosine phosphatases expression during development of mouse superior colliculus

Cited by 8 publications

References 96 publications

Early remodelling of the extracellular matrix proteins tenascin‐C and phosphacan in retina and optic nerve of an experimental autoimmune glaucoma model

Early remodelling of the extracellular matrix proteins tenascin‐C and phosphacan in retina and optic nerve of an experimental autoimmune glaucoma model

Molecular mechanisms of scar-sourced axon growth inhibitors

Scar-mediated inhibition and CSPG receptors in the CNS

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