胶质瘢痕和胶质细胞(英文)

A pericyte origin of spinal cord scar tissue.

Göritz C, Dias DO, Tomilin N, Barbacid M, Shupliakov O, Frisén J.

Source

Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.

Abstract

There is limited regeneration of lost tissue after central nervous system injury, and the lesion is sealed with a scar. The role of the scar, which often is referred to as the glial scar because of its abundance of astrocytes, is complex and has been discussed for more than a century. Here we show that a specific pericyte subtype gives rise to scar-forming stromal cells, which outnumber astrocytes, in the injured spinal cord. Blocking the generation of progeny by this pericyte subtype results in failure to seal the injured tissue. The formation of connective tissue is common to many injuries and pathologies, and here we demonstrate a cellular origin of fibrosis.

Hepatic stellate cells and astrocytes: Stars of scar formation and tissue repair.

Schachtrup C, Le Moan N, Passino MA, Akassoglou K.

Source

University of California at San Francisco, San Francisco, CA, USA.

Abstract

Scar formation inhibits tissue repair and regeneration in the liver and central nervous system. Activation of hepatic stellate cells (HSCs) after liver injury or of astrocytes after nervous system damage is considered to drive scar formation. HSCs are the fibrotic cells of the liver, as they undergo activation and acquire fibrogenic properties after liver injury. HSC activation has been compared to reactive gliosis of astrocytes, which acquire a reactive phenotype and contribute to scar formation after nervous system injury, much like HSCs after liver injury. It is intriguing that a wide range of neuroglia-related molecules are expressed by HSCs. We identified an unexpected role for the p75 neurotrophin receptor in regulating HSC activation and liver repair.

Here we discuss the molecular mechanisms that regulate HSC activation and reactive gliosis and their contributions to scar formation and tissue repair. Juxtaposing key mechanistic and functional similarities in HSC and astrocyte activation might provide novel insight into liver regeneration and nervous system repair.

PMID:

21555919

[PubMed - in process]

PMCID: PMC3142460

[Available on 2012/6/1]

The unusual response of serotonergic neurons after CNS Injury: lack of axonal dieback and enhanced sprouting within the inhibitory environment of the glial scar.

Hawthorne AL, Hu H, Kundu B, Steinmetz MP, Wylie CJ, Deneris ES, Silver J.

Source

Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106, and Department of Neurosurgery, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. Abstract

Serotonergic neurons possess an enhanced ability to regenerate or sprout after many types of injury. To understand the mechanisms that underlie their unusual properties, we used a combinatorial approach comparing the behavior of serotonergic and cortical axon tips over time in the same injury environment in vivo and to growth-promoting or growth-inhibitory substrates in vitro. After a thermocoagulatory lesion in the rat frontoparietal cortex, callosal axons become dystrophic and die back. Serotonergic axons, however, persist within the lesion edge. At the third week

post-injury, 5-HT+ axons sprout robustly. The lesion environment contains both growth-inhibitory chondroitin sulfate proteoglycans (CSPGs) and growth-promoting laminin. Transgenic mouse