Untitled

Chen, Zhi Jiang; Negra, Micheal; Levine, Angela; Ughrin, Yvonne; Levine, Joel M.

doi:10.1023/a:1025791614468

Cited by 77 publications

(10 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oligodendrocytes inhibit axon growth cones 52-56 , and OPCs are both repulsive and nonpermissive for growing axons 57, 58 . While the effects of changes in oligodendrocyte abundance on synaptic formation and plasticity are unknown, it seems likely that increased abundance would result in suppression of synaptogenesis.…”

Section: Discussionmentioning

confidence: 99%

Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus

et al. 2014

View full text Add to dashboard Cite

Stress can exert long-lasting changes on the brain that contribute to vulnerability to mental illness, yet mechanisms underlying this long-term vulnerability are not well understood. We hypothesized that stress may alter the production of oligodendrocytes in the adult brain, providing a cellular and structural basis for stress-related disorders. We found that immobilization stress decreased neurogenesis and increased oligodendrogenesis in the dentate gyrus (DG) of the adult rat hippocampus, and that injections of the rat glucocorticoid stress hormone corticosterone (cort) were sufficient to replicate this effect. The DG contains a unique population of multipotent neural stem cells (NSCs) that give rise to adult newborn neurons, but oligodendrogenic potential has not been demonstrated in vivo. We used a nestin-CreER/YFP transgenic mouse line for lineage tracing and found that cort induces oligodendrogenesis from nestin-expressing NSCs in vivo. Using hippocampal NSCs cultured in vitro, we further showed that exposure to cort induced a pro-oligodendrogenic transcriptional program and resulted in an increase in oligodendrogenesis and decrease in neurogenesis, which was prevented by genetic blockade of glucocorticoid receptor (GR). Together, these results suggest a novel model in which stress may alter hippocampal function by promoting oligodendrogenesis, thereby altering the cellular composition and white matter structure.

show abstract

Section: Discussionmentioning

confidence: 99%

Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Although the best known aspect of reactive astrogliosis is scar formation the concept of reactive astrogliosis is still incomplete, we are only just starting to understand its molecular and cellular characteristics, as well as its multifaceted functions in disease pathogenesis and in CNS recovery from injury. The scar is composed primarily of astrocytes, however, in severe lesions, interaction with other cell types including oligodendrocyte progenitor cells (OPCs) and fibromeningeal cells also occurs ( 86 , 87 ). Several specific molecular and morphological features have been observed in astrocytes during reactive astrogliosis in both human pathology and animal models ( 88 , 89 ), of which upregulation of GFAP, vimentin, nestin, and the less investigated synemin are hallmarks.…”

Section: Astrocytes In Multiple Sclerosismentioning

confidence: 99%

The Role of Astrocytes in Multiple Sclerosis Progression

2015

View full text Add to dashboard Cite

Multiple sclerosis (MS) is an inflammatory disorder causing central nervous system (CNS) demyelination and axonal injury. Although its etiology remains elusive, several lines of evidence support the concept that autoimmunity plays a major role in disease pathogenesis. The course of MS is highly variable; nevertheless, the majority of patients initially present a relapsing–remitting clinical course. After 10–15 years of disease, this pattern becomes progressive in up to 50% of untreated patients, during which time clinical symptoms slowly cause constant deterioration over a period of many years. In about 15% of MS patients, however, disease progression is relentless from disease onset. Published evidence supports the concept that progressive MS reflects a poorly understood mechanism of insidious axonal degeneration and neuronal loss. Recently, the type of microglial cell and of astrocyte activation and proliferation observed has suggested contribution of resident CNS cells may play a critical role in disease progression. Astrocytes could contribute to this process through several mechanisms: (a) as part of the innate immune system, (b) as a source of cytotoxic factors, (c) inhibiting remyelination and axonal regeneration by forming a glial scar, and (d) contributing to axonal mitochondrial dysfunction. Furthermore, regulatory mechanisms mediated by astrocytes can be affected by aging. Notably, astrocytes might also limit the detrimental effects of pro-inflammatory factors, while providing support and protection for oligodendrocytes and neurons. Because of the dichotomy observed in astrocytic effects, the design of therapeutic strategies targeting astrocytes becomes a challenging endeavor. Better knowledge of molecular and functional properties of astrocytes, therefore, should promote understanding of their specific role in MS pathophysiology, and consequently lead to development of novel and more successful therapeutic approaches.

show abstract

“…In the setting of brain injury, OPC actions are not always beneficial to neurons. At the injured site, OPCs, along with microglia and astrocytes, form a glial scar that inhibit axonal growth and regeneration of neurons (Chen et al, 2002). In a spinal cord injury model, mice with deletion of β-catenin specifically in OPCs had reduced glial scar formation and increased axon regeneration.…”

Section: Cross-talk Between Opc and Other Cell Types In Stroke Injmentioning

confidence: 99%

Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

et al. 2015

View full text Add to dashboard Cite

White matter damage is a clinically important aspect of several central nervous system diseases, including stroke. Cerebral white matter primarily consists of axonal bundles ensheathed with myelin secreted by mature oligodendrocytes, which play an important role in neurotransmission between different areas of gray matter. During the acute phase of stroke, damage to oligodendrocytes leads to white matter dysfunction through the loss of myelin. On the contrary, during the chronic phase, white matter components promote an environment, which is favorable for neural repair, vascular remodeling, and remyelination. For effective remyelination to take place, oligodendrocyte precursor cells (OPCs) play critical roles by proliferating and differentiating into mature oligodendrocytes, which help to decrease the burden of axonal injury. Notably, other types of cells contribute to these OPC responses under the ischemic conditions. This mini-review summarizes the non-cell autonomous mechanisms in oligodendrogenesis and remyelination after white matter damage, focusing on how OPCs receive support from their neighboring cells.

show abstract

Untitled

Cited by 77 publications

References 72 publications

Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus

Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus

The Role of Astrocytes in Multiple Sclerosis Progression

Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

Contact Info

Product

Resources

About