Both cell-surface carbohydrates and protein tyrosine phosphatase are involved in the differentiation of astrocytes in vitro

Sasaki, Takaya; Endo, Tamao

doi:10.1002/1098-1136(200010)32:1<60::aid-glia60>3.0.co;2-5

Cited by 13 publications

(14 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This increase in reactive gliosis is particularly intriguing in light of our previous work that demonstrates that the uninjured SHP‐1 deficient mouse brain possesses half the number of GFAP+ astrocytes of wild‐type mice (Wishcamper et al, 2001). Whereas induction of tyrosine phosphatase activity has been shown previously to be required for astrocyte differentiation in vitro (Sasaki and Endo, 2000), our results suggest that induction of SHP‐1 after MCAO in vivo acts to limit astrocyte activation and that loss of SHP‐1 leads to large, early increases in astrocyte activation.…”

Section: Discussioncontrasting

confidence: 59%

Motheaten (me/me) mice deficient in SHP‐1 are less susceptible to focal cerebral ischemia

Beamer

Brooks

Lurie

2006

J of Neuroscience Research

View full text Add to dashboard Cite

We have demonstrated previously that the protein tyrosine phosphatase SHP-1 seems to play a role in glial development and is upregulated in non-dividing astrocytes after injury. The present study examines the effect of loss of SHP-1 on the CNS response to permanent focal ischemia. SHP-1 deficient (me/me) mice and wild-type littermates received a permanent middle cerebral artery occlusion (MCAO). At 1, 3, and 7 days after MCAO, infarct volume, neuronal survival and cell death, gliosis, and inflammatory cytokine levels were quantified. SHP-1 deficient me/me mice display smaller infarct volumes at 7 days post-MCAO, increased neuronal survival within the ischemic penumbra, and decreased numbers of cleaved caspase 3+ cells within the ischemic core compared with wild-type mice. In addition, me/me mice exhibit increases in GFAP+ reactive astrocytes, F4-80+ microglia, and a concomitant increase in the level of interleukin 12 (IL-12) over baseline compared with wild-type. Taken together, these results demonstrate that loss of SHP-1 results in greater healing of the infarct due to less apoptosis and more neuronal survival in the ischemic core and suggests that pharmacologic inactivation of SHP-1 may have potential therapeutic value in limiting CNS degeneration after ischemic stroke.

show abstract

Section: Discussioncontrasting

confidence: 59%

Motheaten (me/me) mice deficient in SHP‐1 are less susceptible to focal cerebral ischemia

Beamer

Brooks

Lurie

2006

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…AICAR-induced stellation was observed to be similar to that induced by AMP, with fewer cells exhibiting complete membrane retraction. In several cases using cultured astrocytes, stellate morphology correlates with increased GFAP expression [5,39,46]. Therefore, we investigated GFAP protein levels over the time course of AICAR-induced stellation.…”

Section: Resultsmentioning

confidence: 99%

A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

Favero

Mandell

2007

Brain Research

View full text Add to dashboard Cite

AMP-activated protein kinase (AMPK) represents a key energy-sensing molecule in many cell types. Because astrocytes are key mediators of metabolic signaling in the brain, we have initiated studies on the expression and activation of AMPK in these cells. Treatment of cultured rat cortical astrocytes with a pharmacological AMPK activator, AICA-riboside (AICAR) resulted in a time-and concentration-dependent increase in phosphorylation of AMPK and acetyl-CoA carboxylase (ACC), a direct substrate. AICAR treatment also induced a transition from epithelioid to stellate morphology in a time-and concentration-dependent manner. As stellation is indicative of actin cytoskeletal reorganization, the formation of stress fibers and focal adhesions in response to AICAR was assessed. AICAR-induced stellation correlated with F-actin disassembly and focal adhesion dispersal. Furthermore, transient transfection of an activated RhoA construct prevented AICAR-induced stellation, indicating a mechanism upstream of RhoA. Use of pharmacological inhibitor compound C prevented AICAR-induced stellation demonstrating necessity of AMPK activity for the response. Our findings suggest that AMPK mediates morphological alterations of astrocytes in response to energy depletion.

show abstract

“…In fact, DSA reacted strongly with many rat astrocyte glycoproteins, but reacted with very few neuronal glycoproteins (Sasaki and Endo, 1999). Actually, DSA did not affect neuronal cell migration or axonal extension and did not induce any morphological change of neurons (Sasaki and Endo, 2000). Taken together, these results suggest that DSA can distinguish between astrocytic and neuronal glycoreceptors.…”

Section: Discussionmentioning

confidence: 74%

“…We previously found that DSA induced astrocyte differentiation through tyrosine dephosphorylation, specifically a decrease in the extent of tyrosine phosphorylation of a 38-kDa protein (Sasaki and Endo, 2000). Further studies are needed to elucidate molecular mechanism by which DSA acts on glioma cells.…”

Section: Discussionmentioning

confidence: 99%

“…It is Datura stramonium agglutinin (DSA) which binds specifically to glycans containing multiantennary and/or N-acetyllactosamine repeat units (Cummings and Kornfeld, 1984;Yamashita et al, 1987). Recently, we found that DSA induced differentiation of astrocytes (Sasaki and Endo, 2000). Addition of DSA caused a morphological change from a polygonal shape to a stellate shape with many long processes, an increase of glial fibrillary acidic protein (GFAP) and suppression of proliferation.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of proliferation and induction of differentiation of glioma cells with Datura stramonium agglutinin

et al. 2002

View full text Add to dashboard Cite

We found that a lectin, Datura stramonium agglutinin, induced irreversible differentiation in C6 glioma cells. The differentiated cells had long processes, a low rate of proliferation and a high content of glial fibrillary acidic protein. When the medium was replaced with Datura stramonium agglutinin-free medium after 1 h, cell proliferation continued to be inhibited. Experiments with several other lectins indicated that both recognition of linear N-acetyllactosamine repeats and recognition of multiantennary units of cell-surface glycans were required for the inhibition of C6 proliferation. Proliferation of four human glial tumour cells was also inhibited by Datura stramonium agglutinin. Further, these differentiated human glial tumour cells had long processes and a high content of glial fibrillary acidic protein similar to differentiated C6 glioma cells. Taken together, these observations suggest that Datura stramonium agglutinin may be useful as a new therapy for treating glioma without side effects.

show abstract

Both cell-surface carbohydrates and protein tyrosine phosphatase are involved in the differentiation of astrocytes in vitro

Cited by 13 publications

References 46 publications

Motheaten (me/me) mice deficient in SHP‐1 are less susceptible to focal cerebral ischemia

Motheaten (me/me) mice deficient in SHP‐1 are less susceptible to focal cerebral ischemia

A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

Inhibition of proliferation and induction of differentiation of glioma cells with Datura stramonium agglutinin

Contact Info

Product

Resources

About