Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Myelination transition zone astrocytes are constitutively phagocytic and have synuclein dependent reactivity in glaucoma.

http://www.ncbi.nlm.nih.gov/pubmed/21199938

Optic nerve head (ONH) astrocytes have been proposed to play both protective and deleterious roles in glaucoma. We now show that, within the postlaminar ONH myelination transition zone (MTZ), there are astrocytes that normally express Mac-2 (also known as Lgals3 or galectin-3), a gene typically expressed only in phagocytic cells. Surprisingly, even in healthy mice, MTZ and other ONH astrocytes constitutive internalize large axonal evulsions that contain whole organelles. In mouse glaucoma models, MTZ astrocytes further up-regulate Mac-2 expression. During glaucomatous degeneration, there are dystrophic processes in the retina and optic nerve, including the MTZ, which contain protease resistant γ-synuclein. The increased Mac-2 expression by MTZ astrocytes during glaucoma likely depends on this γ-synuclein, as mice lacking γ-synuclein fail to up-regulate Mac-2 at the MTZ after elevation of intraocular pressure. These results suggest the possibility that a newly discovered normal degradative pathway for axons might contribute to glaucomatous neurodegeneration.

Pubmed ID: 21199938 RIS Download

Mesh terms: Animals | Astrocytes | Axons | Galectin 3 | Glaucoma | Immunohistochemistry | In Situ Hybridization | Mice | Microscopy, Electron, Scanning | Nerve Fibers, Myelinated | Optic Nerve | Phagocytosis | gamma-Synuclein

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: Wellcome Trust, Id: 075615
  • Agency: Wellcome Trust, Id: 075615/Z/04/z
  • Agency: NCRR NIH HHS, Id: 5P41RR004050
  • Agency: NEI NIH HHS, Id: 5R01EY019305
  • Agency: NIGMS NIH HHS, Id: 5R01GM82949
  • Agency: NEI NIH HHS, Id: 5R21EY019737
  • Agency: NEI NIH HHS, Id: 5T32 EY07143-12
  • Agency: NIDA NIH HHS, Id: DA016602
  • Agency: NEI NIH HHS, Id: T32 EY017203

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.