Limits...
Axon regeneration impediment: the role of paired immunoglobulin-like receptor B.

Liu J, Wang Y, Fu W - Neural Regen Res (2015)

Bottom Line: Concurrent blocking of NgR and PirB almost completely eliminates the inhibitory effect of myelin-associated inhibitory molecules on axonal regeneration.PirB is an inhibitory receptor similar to NgR, but their effects are not identical.This study summarizes the structure, distribution, relationship with common nervous system diseases, and known mechanisms of PirB, and concludes that PirB is also distributed in cells of the immune and hematopoietic systems.

View Article: PubMed Central - PubMed

Affiliation: Neonatal Intensive Care Center, BAYI Children's Hospital, Beijing Military General Hospital of Chinese PLA, Beijing, China.

ABSTRACT
Regenerative capacity is weak after central nervous system injury because of the absence of an enhancing microenvironment and presence of an inhibitory microenvironment for neuronal and axonal repair. In addition to the Nogo receptor (NgR), the paired immunoglobulin-like receptor B (PirB) is a recently discovered coreceptor of Nogo, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein. Concurrent blocking of NgR and PirB almost completely eliminates the inhibitory effect of myelin-associated inhibitory molecules on axonal regeneration. PirB participates in a key pathological process of the nervous system, specifically axonal regeneration inhibition. PirB is an inhibitory receptor similar to NgR, but their effects are not identical. This study summarizes the structure, distribution, relationship with common nervous system diseases, and known mechanisms of PirB, and concludes that PirB is also distributed in cells of the immune and hematopoietic systems. Further investigations are needed to determine if immunomodulation and blood cell migration involve inhibition of axonal regeneration.

No MeSH data available.


Related in: MedlinePlus

PirB-mediated growth cone collapse and axon growth inhibition.A classical axon inhibition signaling pathway: Nogo on the oligodendrocyte surface binds to the NgR-LINGO1-P75 receptor complex on the neuronal membrane. Cofilin is activated by RHOA-ROCK, resulting in actin depolymerization and axonal inhibition. PirB-mediated signaling pathway: Nogo-66 binds to the PirB receptor on the neuronal membrane. (1) The Shroom3-ROCK-Cofilin and LZK-JNK-Mysoin IIA signaling pathways are activated by the POSH molecule; (2) SHP molecule recruitment leads to TrkB receptor dephosphorylation, PI3K and Akt activation, and finally results in actin depolymerization and axonal inhibition. The figure is modified from Liu et al. (2014).PirB: Paired immunoglobulin-like receptor B; NgR: Nogo receptor; ROCK: Rho-associated coiled coil-forming protein kinase; JNK: c-Jun N-terminal kinase; SHP: Src homology containing protein tyrosine phosphatase; TrkB: tyrosine receptor kinase B; PI3K: phosphatidylinositol 3-kinase.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4590251&req=5

Figure 1: PirB-mediated growth cone collapse and axon growth inhibition.A classical axon inhibition signaling pathway: Nogo on the oligodendrocyte surface binds to the NgR-LINGO1-P75 receptor complex on the neuronal membrane. Cofilin is activated by RHOA-ROCK, resulting in actin depolymerization and axonal inhibition. PirB-mediated signaling pathway: Nogo-66 binds to the PirB receptor on the neuronal membrane. (1) The Shroom3-ROCK-Cofilin and LZK-JNK-Mysoin IIA signaling pathways are activated by the POSH molecule; (2) SHP molecule recruitment leads to TrkB receptor dephosphorylation, PI3K and Akt activation, and finally results in actin depolymerization and axonal inhibition. The figure is modified from Liu et al. (2014).PirB: Paired immunoglobulin-like receptor B; NgR: Nogo receptor; ROCK: Rho-associated coiled coil-forming protein kinase; JNK: c-Jun N-terminal kinase; SHP: Src homology containing protein tyrosine phosphatase; TrkB: tyrosine receptor kinase B; PI3K: phosphatidylinositol 3-kinase.

Mentions: (2) Nogo interaction: PirB binds to different structural domains of the Nogo protein, inhibiting the myelin substrate growth cone, and causing growth cone atrophy and axonal retraction (Thams et al., 2008), a classical pathway of synaptic growth inhibition (Figure 1). The affinities of Nogo inhibitors and PirB are different, therefore the strength of their effects is different in different cell or injury environments (Huebner et al., 2011).


Axon regeneration impediment: the role of paired immunoglobulin-like receptor B.

Liu J, Wang Y, Fu W - Neural Regen Res (2015)

PirB-mediated growth cone collapse and axon growth inhibition.A classical axon inhibition signaling pathway: Nogo on the oligodendrocyte surface binds to the NgR-LINGO1-P75 receptor complex on the neuronal membrane. Cofilin is activated by RHOA-ROCK, resulting in actin depolymerization and axonal inhibition. PirB-mediated signaling pathway: Nogo-66 binds to the PirB receptor on the neuronal membrane. (1) The Shroom3-ROCK-Cofilin and LZK-JNK-Mysoin IIA signaling pathways are activated by the POSH molecule; (2) SHP molecule recruitment leads to TrkB receptor dephosphorylation, PI3K and Akt activation, and finally results in actin depolymerization and axonal inhibition. The figure is modified from Liu et al. (2014).PirB: Paired immunoglobulin-like receptor B; NgR: Nogo receptor; ROCK: Rho-associated coiled coil-forming protein kinase; JNK: c-Jun N-terminal kinase; SHP: Src homology containing protein tyrosine phosphatase; TrkB: tyrosine receptor kinase B; PI3K: phosphatidylinositol 3-kinase.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590251&req=5

Figure 1: PirB-mediated growth cone collapse and axon growth inhibition.A classical axon inhibition signaling pathway: Nogo on the oligodendrocyte surface binds to the NgR-LINGO1-P75 receptor complex on the neuronal membrane. Cofilin is activated by RHOA-ROCK, resulting in actin depolymerization and axonal inhibition. PirB-mediated signaling pathway: Nogo-66 binds to the PirB receptor on the neuronal membrane. (1) The Shroom3-ROCK-Cofilin and LZK-JNK-Mysoin IIA signaling pathways are activated by the POSH molecule; (2) SHP molecule recruitment leads to TrkB receptor dephosphorylation, PI3K and Akt activation, and finally results in actin depolymerization and axonal inhibition. The figure is modified from Liu et al. (2014).PirB: Paired immunoglobulin-like receptor B; NgR: Nogo receptor; ROCK: Rho-associated coiled coil-forming protein kinase; JNK: c-Jun N-terminal kinase; SHP: Src homology containing protein tyrosine phosphatase; TrkB: tyrosine receptor kinase B; PI3K: phosphatidylinositol 3-kinase.
Mentions: (2) Nogo interaction: PirB binds to different structural domains of the Nogo protein, inhibiting the myelin substrate growth cone, and causing growth cone atrophy and axonal retraction (Thams et al., 2008), a classical pathway of synaptic growth inhibition (Figure 1). The affinities of Nogo inhibitors and PirB are different, therefore the strength of their effects is different in different cell or injury environments (Huebner et al., 2011).

Bottom Line: Concurrent blocking of NgR and PirB almost completely eliminates the inhibitory effect of myelin-associated inhibitory molecules on axonal regeneration.PirB is an inhibitory receptor similar to NgR, but their effects are not identical.This study summarizes the structure, distribution, relationship with common nervous system diseases, and known mechanisms of PirB, and concludes that PirB is also distributed in cells of the immune and hematopoietic systems.

View Article: PubMed Central - PubMed

Affiliation: Neonatal Intensive Care Center, BAYI Children's Hospital, Beijing Military General Hospital of Chinese PLA, Beijing, China.

ABSTRACT
Regenerative capacity is weak after central nervous system injury because of the absence of an enhancing microenvironment and presence of an inhibitory microenvironment for neuronal and axonal repair. In addition to the Nogo receptor (NgR), the paired immunoglobulin-like receptor B (PirB) is a recently discovered coreceptor of Nogo, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein. Concurrent blocking of NgR and PirB almost completely eliminates the inhibitory effect of myelin-associated inhibitory molecules on axonal regeneration. PirB participates in a key pathological process of the nervous system, specifically axonal regeneration inhibition. PirB is an inhibitory receptor similar to NgR, but their effects are not identical. This study summarizes the structure, distribution, relationship with common nervous system diseases, and known mechanisms of PirB, and concludes that PirB is also distributed in cells of the immune and hematopoietic systems. Further investigations are needed to determine if immunomodulation and blood cell migration involve inhibition of axonal regeneration.

No MeSH data available.


Related in: MedlinePlus