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Characterization of nestin expression in astrocytes in the rat hippocampal CA1 region following transient forebrain ischemia.

Cho JM, Shin YJ, Park JM, Kim J, Lee MY - Anat Cell Biol (2013)

Bottom Line: However, induction of nestin expression did not correlate simply with astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns.Almost all of the nestin-positive cells also expressed a transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67.However, all of the nestin-positive astrocytes expressed the calcium-binding protein S100β, which is known to be expressed in a distinct, post-mitotic astrocyte population.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Cell Death Disease Research Center, The Catholic University of Korea College of Medicine, Seoul, Korea.

ABSTRACT
Recent studies have suggested that nestin facilitates cellular structural remodeling in vasculature-associated cells in response to ischemic injury. The current study was designed to investigate the potential role of post-ischemic nestin expression in parenchymal astrocytes. With this aim, we characterized ischemia-induced nestin expression in the CA1 hippocampal region, an area that undergoes a delayed neuronal death, followed by a lack of neuronal generation after transient forebrain ischemia. Virtually all of the nestin-positive cells in the ischemic CA1 hippocampus were reactive astrocytes. However, induction of nestin expression did not correlate simply with astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns. Nestin induction in astrocytes of the pyramidal cell layer was rapid and transient, while a long-lasting induction of nestin was observed in astrocytes located in the CA1 dendritic subfields, such as the stratum oriens and radiatum, until at least day 28 after ischemia. There was no detectable expression in the stratum lacunosum moleculare despite the evident astroglial reaction. Almost all of the nestin-positive cells also expressed a transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67. However, all of the nestin-positive astrocytes expressed the calcium-binding protein S100β, which is known to be expressed in a distinct, post-mitotic astrocyte population. Thus, our data indicate that in the ischemic CA1 hippocampus, nestin expression was induced in astroglia that were becoming reactive, but not in a progenitor/stem cell population, suggesting that nestin may allow for the structural remodeling of these cells in response to ischemic injury.

No MeSH data available.


Related in: MedlinePlus

Relationship between S100β and nestin (A, B, D, E) or glial fibrillary acidic protein (GFAP) (C, F) in the CA1 hippocampal region after transient forebrain ischemia. All of the nestin-positive cells expressed S100β, corresponding to only a small fraction of all of the S100β-positive cells at all time points examined. Note that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes. Scale bars in (C, F)=100 µm (A-F).
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Figure 5: Relationship between S100β and nestin (A, B, D, E) or glial fibrillary acidic protein (GFAP) (C, F) in the CA1 hippocampal region after transient forebrain ischemia. All of the nestin-positive cells expressed S100β, corresponding to only a small fraction of all of the S100β-positive cells at all time points examined. Note that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes. Scale bars in (C, F)=100 µm (A-F).

Mentions: For the phenotype characterization of nestin-positive astrocytes in the ischemic CA1 hippocampal region, we performed double-labeling with nestin and proliferation marker Ki-67. Consistent with previous data [32], only some nestin-positive cells in the CA1 hippocampus were positive for Ki-67 (Fig. 4A-F). We then characterized these nestin-positive cells by double-labeling using nestin and either Sox-2 or Sox-9, transcription factors for neural/glial progenitors [33-35]. All of the nuclei of nestin-positive cells were immunoreactive for Sox-2 or Sox-9 over 3-28 days following ischemic injury (Fig. 4G-F). However, some cells expressing Sox-2 or Sox-9 were not immunoreactive for nestin in the hippocampal CA1 region of control and ischemic rats, corresponding to GFAP-positive, nestin-negative astrocytes (data not shown). We then clarified whether nestin-positive astrocytes expressed the calcium-binding protein, S100β, which is known to be expressed in a distinct post-mitotic astrocyte population [15, 36, 37]. Nearly all of the nestin-positive astrocytes co-expressed S100β, corresponding to a subpopulation of the S100β-positive cells at all time points examined (Fig. 5A, B, D, E). Considering that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes (Fig. 5C, F), nestin-negative S100β-positive cells may be considered as reactive astrocytes.


Characterization of nestin expression in astrocytes in the rat hippocampal CA1 region following transient forebrain ischemia.

Cho JM, Shin YJ, Park JM, Kim J, Lee MY - Anat Cell Biol (2013)

Relationship between S100β and nestin (A, B, D, E) or glial fibrillary acidic protein (GFAP) (C, F) in the CA1 hippocampal region after transient forebrain ischemia. All of the nestin-positive cells expressed S100β, corresponding to only a small fraction of all of the S100β-positive cells at all time points examined. Note that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes. Scale bars in (C, F)=100 µm (A-F).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3713277&req=5

Figure 5: Relationship between S100β and nestin (A, B, D, E) or glial fibrillary acidic protein (GFAP) (C, F) in the CA1 hippocampal region after transient forebrain ischemia. All of the nestin-positive cells expressed S100β, corresponding to only a small fraction of all of the S100β-positive cells at all time points examined. Note that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes. Scale bars in (C, F)=100 µm (A-F).
Mentions: For the phenotype characterization of nestin-positive astrocytes in the ischemic CA1 hippocampal region, we performed double-labeling with nestin and proliferation marker Ki-67. Consistent with previous data [32], only some nestin-positive cells in the CA1 hippocampus were positive for Ki-67 (Fig. 4A-F). We then characterized these nestin-positive cells by double-labeling using nestin and either Sox-2 or Sox-9, transcription factors for neural/glial progenitors [33-35]. All of the nuclei of nestin-positive cells were immunoreactive for Sox-2 or Sox-9 over 3-28 days following ischemic injury (Fig. 4G-F). However, some cells expressing Sox-2 or Sox-9 were not immunoreactive for nestin in the hippocampal CA1 region of control and ischemic rats, corresponding to GFAP-positive, nestin-negative astrocytes (data not shown). We then clarified whether nestin-positive astrocytes expressed the calcium-binding protein, S100β, which is known to be expressed in a distinct post-mitotic astrocyte population [15, 36, 37]. Nearly all of the nestin-positive astrocytes co-expressed S100β, corresponding to a subpopulation of the S100β-positive cells at all time points examined (Fig. 5A, B, D, E). Considering that virtually all of the S100β-positive cells in the ischemic CA1 region were GFAP-positive astrocytes (Fig. 5C, F), nestin-negative S100β-positive cells may be considered as reactive astrocytes.

Bottom Line: However, induction of nestin expression did not correlate simply with astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns.Almost all of the nestin-positive cells also expressed a transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67.However, all of the nestin-positive astrocytes expressed the calcium-binding protein S100β, which is known to be expressed in a distinct, post-mitotic astrocyte population.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Cell Death Disease Research Center, The Catholic University of Korea College of Medicine, Seoul, Korea.

ABSTRACT
Recent studies have suggested that nestin facilitates cellular structural remodeling in vasculature-associated cells in response to ischemic injury. The current study was designed to investigate the potential role of post-ischemic nestin expression in parenchymal astrocytes. With this aim, we characterized ischemia-induced nestin expression in the CA1 hippocampal region, an area that undergoes a delayed neuronal death, followed by a lack of neuronal generation after transient forebrain ischemia. Virtually all of the nestin-positive cells in the ischemic CA1 hippocampus were reactive astrocytes. However, induction of nestin expression did not correlate simply with astrogliosis, but rather showed characteristic time- and strata-dependent expression patterns. Nestin induction in astrocytes of the pyramidal cell layer was rapid and transient, while a long-lasting induction of nestin was observed in astrocytes located in the CA1 dendritic subfields, such as the stratum oriens and radiatum, until at least day 28 after ischemia. There was no detectable expression in the stratum lacunosum moleculare despite the evident astroglial reaction. Almost all of the nestin-positive cells also expressed a transcription factor for neural/glial progenitors, i.e., Sox-2 or Sox-9, and some cells were also positive for Ki-67. However, all of the nestin-positive astrocytes expressed the calcium-binding protein S100β, which is known to be expressed in a distinct, post-mitotic astrocyte population. Thus, our data indicate that in the ischemic CA1 hippocampus, nestin expression was induced in astroglia that were becoming reactive, but not in a progenitor/stem cell population, suggesting that nestin may allow for the structural remodeling of these cells in response to ischemic injury.

No MeSH data available.


Related in: MedlinePlus