Limits...
Fgf-2 in astroglial cells during vertebrate spinal cord recovery.

Fahmy GH, Moftah MZ - Front Cell Neurosci (2010)

Bottom Line: Our results show that spinal cord injury triggers a significant increase in FGF-2 immunoreactivity in reactive astrocytes at sites of insult.In addition, these results were time-dependent.Therefore, we suggest that FGF-2 may be involved in cell proliferation and/or astroglial cells differentiation after body spinal cord transection, and could thus play an important role in locomotion recovery.

View Article: PubMed Central - PubMed

Affiliation: Zoology Department, Faculty of Science, Alexandria University Alexandria, Egypt.

ABSTRACT
Fibroblast growth factor-2 is a pleiotrophic cytokine with neurotrophic and gliogenic properties. It is known to regulate CNS injury responses, which include transformation of reactive astrocytes, neurogenesis, and promotion of neurotrophic activities. In the brain, it is localized in astrocytes and discrete neuronal populations. Following both central and peripheral nervous system injury, astrocytes become reactive. These activated cells undergo hypertrophy. A key indicator of astrocyte activation is the increased accumulation of intermediate filaments composed of glial fibrillary acidic protein (GFAP). Following physical insult of brain or spinal cord, reactive astrocytes show increased FGF-2 immunoreactivity. Thus, FGF-2 appears to participate in astrocytic differentiation and proliferation and a good candidate for astrocytic function regulation in healthy, injured, or diseased CNS. To further investigate the cellular mechanisms underlying FGF-2 restorative actions and to analyze the changes within astroglial cells, we studied the localization of GFAP and FGF-2 in adult intact and injured Pleurodeles CNS. Our results show that spinal cord injury triggers a significant increase in FGF-2 immunoreactivity in reactive astrocytes at sites of insult. In addition, these results were time-dependent. Increase in FGF-2 immunoreactivity along the CNS axis, starting 1-week post-injury, was long-lasting extending to 6 weeks. This increase was accompanied by an increase in GFAP immunoreactivity in the same spatial pattern except in SC3 where its level was almost similar to sham-operated animals. Therefore, we suggest that FGF-2 may be involved in cell proliferation and/or astroglial cells differentiation after body spinal cord transection, and could thus play an important role in locomotion recovery.

No MeSH data available.


Related in: MedlinePlus

Double labeling of FGF-2 and GFAP in brain stem after 1 week of lesion. (A) Sham operated (B) Lesioned cases. Intense FGF-2 and GFAP immunoreactivity is obvious in cells lining the fourth ventricle and cells surrounding them compared to sham-operated animals. The blue color in upper panel is a nuclear marker and orange color in lower panel (arrow) shows the colocalization between FGF-2 and GFAP showing the presence of FGF-2 in glial cells ×63. (C) Percentages of labeling intensity of FGF-2 and GFAP immunoreactivity compared to sham-operated cases in Brain Stem. The graph shows significant increase in FGF-2.ocalization, which was time-dependent within 1, 2, and 6 weeks after spinal cord lesion. GFAP slightly increased in week 6.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2990542&req=5

Figure 1: Double labeling of FGF-2 and GFAP in brain stem after 1 week of lesion. (A) Sham operated (B) Lesioned cases. Intense FGF-2 and GFAP immunoreactivity is obvious in cells lining the fourth ventricle and cells surrounding them compared to sham-operated animals. The blue color in upper panel is a nuclear marker and orange color in lower panel (arrow) shows the colocalization between FGF-2 and GFAP showing the presence of FGF-2 in glial cells ×63. (C) Percentages of labeling intensity of FGF-2 and GFAP immunoreactivity compared to sham-operated cases in Brain Stem. The graph shows significant increase in FGF-2.ocalization, which was time-dependent within 1, 2, and 6 weeks after spinal cord lesion. GFAP slightly increased in week 6.

Mentions: By the first week after spinal cord injury, large quantities of FGF-2 were prominent in cells lining the fourth ventricle (195.3 ± 0.3%) (Figures 1A–C; Table 1). The intense amount of FGF-2 decreased gradually in cells flanking the neuroglial cells lining the fourth ventricle. GFAP immunoreactivity was also found in large amounts in the fourth ventricle lining cells and less farther from the lumen (105.9 ± 0.3%) (Figures 1A–C, Table 2). The colocalization of FGF-2 and GFAP in the same cells (shown in orange, Figures 1A, B) suggests that the neuroglial cells lining the fourth ventricle are a major source of FGF-2 starting 1 week after spinal cord lesion. We used sham-operated animals as an immunoreactivity threshold (100%) and variations in intensity were proportional to shams level.


Fgf-2 in astroglial cells during vertebrate spinal cord recovery.

Fahmy GH, Moftah MZ - Front Cell Neurosci (2010)

Double labeling of FGF-2 and GFAP in brain stem after 1 week of lesion. (A) Sham operated (B) Lesioned cases. Intense FGF-2 and GFAP immunoreactivity is obvious in cells lining the fourth ventricle and cells surrounding them compared to sham-operated animals. The blue color in upper panel is a nuclear marker and orange color in lower panel (arrow) shows the colocalization between FGF-2 and GFAP showing the presence of FGF-2 in glial cells ×63. (C) Percentages of labeling intensity of FGF-2 and GFAP immunoreactivity compared to sham-operated cases in Brain Stem. The graph shows significant increase in FGF-2.ocalization, which was time-dependent within 1, 2, and 6 weeks after spinal cord lesion. GFAP slightly increased in week 6.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2990542&req=5

Figure 1: Double labeling of FGF-2 and GFAP in brain stem after 1 week of lesion. (A) Sham operated (B) Lesioned cases. Intense FGF-2 and GFAP immunoreactivity is obvious in cells lining the fourth ventricle and cells surrounding them compared to sham-operated animals. The blue color in upper panel is a nuclear marker and orange color in lower panel (arrow) shows the colocalization between FGF-2 and GFAP showing the presence of FGF-2 in glial cells ×63. (C) Percentages of labeling intensity of FGF-2 and GFAP immunoreactivity compared to sham-operated cases in Brain Stem. The graph shows significant increase in FGF-2.ocalization, which was time-dependent within 1, 2, and 6 weeks after spinal cord lesion. GFAP slightly increased in week 6.
Mentions: By the first week after spinal cord injury, large quantities of FGF-2 were prominent in cells lining the fourth ventricle (195.3 ± 0.3%) (Figures 1A–C; Table 1). The intense amount of FGF-2 decreased gradually in cells flanking the neuroglial cells lining the fourth ventricle. GFAP immunoreactivity was also found in large amounts in the fourth ventricle lining cells and less farther from the lumen (105.9 ± 0.3%) (Figures 1A–C, Table 2). The colocalization of FGF-2 and GFAP in the same cells (shown in orange, Figures 1A, B) suggests that the neuroglial cells lining the fourth ventricle are a major source of FGF-2 starting 1 week after spinal cord lesion. We used sham-operated animals as an immunoreactivity threshold (100%) and variations in intensity were proportional to shams level.

Bottom Line: Our results show that spinal cord injury triggers a significant increase in FGF-2 immunoreactivity in reactive astrocytes at sites of insult.In addition, these results were time-dependent.Therefore, we suggest that FGF-2 may be involved in cell proliferation and/or astroglial cells differentiation after body spinal cord transection, and could thus play an important role in locomotion recovery.

View Article: PubMed Central - PubMed

Affiliation: Zoology Department, Faculty of Science, Alexandria University Alexandria, Egypt.

ABSTRACT
Fibroblast growth factor-2 is a pleiotrophic cytokine with neurotrophic and gliogenic properties. It is known to regulate CNS injury responses, which include transformation of reactive astrocytes, neurogenesis, and promotion of neurotrophic activities. In the brain, it is localized in astrocytes and discrete neuronal populations. Following both central and peripheral nervous system injury, astrocytes become reactive. These activated cells undergo hypertrophy. A key indicator of astrocyte activation is the increased accumulation of intermediate filaments composed of glial fibrillary acidic protein (GFAP). Following physical insult of brain or spinal cord, reactive astrocytes show increased FGF-2 immunoreactivity. Thus, FGF-2 appears to participate in astrocytic differentiation and proliferation and a good candidate for astrocytic function regulation in healthy, injured, or diseased CNS. To further investigate the cellular mechanisms underlying FGF-2 restorative actions and to analyze the changes within astroglial cells, we studied the localization of GFAP and FGF-2 in adult intact and injured Pleurodeles CNS. Our results show that spinal cord injury triggers a significant increase in FGF-2 immunoreactivity in reactive astrocytes at sites of insult. In addition, these results were time-dependent. Increase in FGF-2 immunoreactivity along the CNS axis, starting 1-week post-injury, was long-lasting extending to 6 weeks. This increase was accompanied by an increase in GFAP immunoreactivity in the same spatial pattern except in SC3 where its level was almost similar to sham-operated animals. Therefore, we suggest that FGF-2 may be involved in cell proliferation and/or astroglial cells differentiation after body spinal cord transection, and could thus play an important role in locomotion recovery.

No MeSH data available.


Related in: MedlinePlus