Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

Re-establishing the regen… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Kontaktformulär








 


OBS! Vill du ha svar, ange e-post eller telefonnummer!




Re-establishing the regenerative potential of central nervous system axons in postnatal mice.

Artikel i vetenskaplig tidskrift
Författare Kin-Sang Cho
Liu Yang
Bin Lu
Hong Feng Ma
Xizhong Huang
Milos Pekny
Dong Feng Chen
Publicerad i Journal of cell science
Volym 118
Nummer/häfte Pt 5
Sidor 863-72
ISSN 0021-9533
Publiceringsår 2005
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Sidor 863-72
Språk en
Länkar dx.doi.org/10.1242/jcs.01658
Ämnesord Animals, Animals, Newborn, Astrocytes, cytology, metabolism, Axons, metabolism, Blotting, Western, Brain, metabolism, Central Nervous System, physiology, Coculture Techniques, DNA Primers, chemistry, Down-Regulation, Female, Glial Fibrillary Acidic Protein, metabolism, Gliosis, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Models, Anatomic, Nerve Regeneration, Neurons, metabolism, Optic Nerve, anatomy & histology, metabolism, pathology, physiology, Proto-Oncogene Proteins c-bcl-2, metabolism, physiology, Retina, metabolism, Reverse Transcriptase Polymerase Chain Reaction, Transgenes, Vimentin, metabolism
Ämneskategorier Fysiologi, Cellbiologi

Sammanfattning

At a certain point in development, axons in the mammalian central nervous system lose their ability to regenerate after injury. Using the optic nerve model, we show that this growth failure coincides with two developmental events: the loss of Bcl-2 expression by neurons and the maturation of astrocytes. Before postnatal day 4, when astrocytes are immature, overexpression of Bcl-2 alone supported robust and rapid optic nerve regeneration over long distances, leading to innervation of brain targets by day 4 in mice. As astrocytes matured after postnatal day 4, axonal regeneration was inhibited in mice overexpressing Bcl-2. Concurrent induction of Bcl-2 and attenuation of reactive gliosis reversed the failure of CNS axonal re-elongation in postnatal mice and led to rapid axonal regeneration over long distances and reinnervation of the brain targets by a majority of severed optic nerve fibers up to 2 weeks of age. These results suggest that an early postnatal downregulation of Bcl-2 and post-traumatic reactive gliosis are two important elements of axon regenerative failure in the CNS.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?