Ciliary neurotrophic factor (CNTF) induces reactive gliosis and gfap expression in müller cells

V. Sarthy, S. J. Brodjian, Sylvia B Smith

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Purpose. The glial fibrillary acidic protein (GFAP) gene is induced in Müller cells in response to retinal injury, detachment or photoreceptor degeneration. The inductive signal responsible for de novo GFAP synthesis is not currently known. There is growing evidence that CNTF might be involved in regulating gliosis in conical astrocytes. The aim of the present study was to examine whether CNTF could induce GFAP expression in Müller cells in the normal mouse retina. Methods. CNTF (0.5 ul) was injected intravitreally into one eye of adult B6 mice at a concentration of 1 u,g/ul. Die fellow eye was injected with physiological saline. Following survival times of 3, 7, 14 and 21 days, animals were killed, and the eyes were processed for immunocytochemistry. A polyclonal antibody to GFAP was used to immunostain cryostat sections of the retina. In some experiments, mouse eyes were injected with bFGF instead of CNTF. Results. In animals injected with CNTF, there was strong immunostaining of radial fibers throughout the retina with the most intense staining at the Müller cell endfeet. Although CNTF was injected at a single site in the eye, GFAP immunostaining was noted throughout the retina. Müller cell staining was seen three days after injection and the intensity of staining remained unchanged at 21 days. In eyes injected with saline, a few Müller cells were immunoreactive in the vicinity of the injection site but the rest of the retina contained no stained Müller cells. In eyes injected with bFGF, there was some GFAP expression in Müller cells; the intensity of the response was, however, considerably weaker than that noted in CNTF-injected eyes. Conclusions. Exogenous CNTF is a potent inducer of GFAP expression in mouse retinal Müller cells. Since retina is known to upregulate CNTF in response to injury, it is likely that CNTF is a major inductive signal for GFAP expression and reactive gliosis in the mammalian retina.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number4
StatePublished - Dec 1 1997

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Ciliary Neurotrophic Factor
Gliosis
Glial Fibrillary Acidic Protein
Retina
Staining and Labeling
Vertebrate Photoreceptor Cells
Injections
Wounds and Injuries
Retinal Detachment
Astrocytes
Up-Regulation
Immunohistochemistry

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Ciliary neurotrophic factor (CNTF) induces reactive gliosis and gfap expression in müller cells. / Sarthy, V.; Brodjian, S. J.; Smith, Sylvia B.

In: Investigative Ophthalmology and Visual Science, Vol. 38, No. 4, 01.12.1997.

Research output: Contribution to journalArticle

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title = "Ciliary neurotrophic factor (CNTF) induces reactive gliosis and gfap expression in m{\"u}ller cells",
abstract = "Purpose. The glial fibrillary acidic protein (GFAP) gene is induced in M{\"u}ller cells in response to retinal injury, detachment or photoreceptor degeneration. The inductive signal responsible for de novo GFAP synthesis is not currently known. There is growing evidence that CNTF might be involved in regulating gliosis in conical astrocytes. The aim of the present study was to examine whether CNTF could induce GFAP expression in M{\"u}ller cells in the normal mouse retina. Methods. CNTF (0.5 ul) was injected intravitreally into one eye of adult B6 mice at a concentration of 1 u,g/ul. Die fellow eye was injected with physiological saline. Following survival times of 3, 7, 14 and 21 days, animals were killed, and the eyes were processed for immunocytochemistry. A polyclonal antibody to GFAP was used to immunostain cryostat sections of the retina. In some experiments, mouse eyes were injected with bFGF instead of CNTF. Results. In animals injected with CNTF, there was strong immunostaining of radial fibers throughout the retina with the most intense staining at the M{\"u}ller cell endfeet. Although CNTF was injected at a single site in the eye, GFAP immunostaining was noted throughout the retina. M{\"u}ller cell staining was seen three days after injection and the intensity of staining remained unchanged at 21 days. In eyes injected with saline, a few M{\"u}ller cells were immunoreactive in the vicinity of the injection site but the rest of the retina contained no stained M{\"u}ller cells. In eyes injected with bFGF, there was some GFAP expression in M{\"u}ller cells; the intensity of the response was, however, considerably weaker than that noted in CNTF-injected eyes. Conclusions. Exogenous CNTF is a potent inducer of GFAP expression in mouse retinal M{\"u}ller cells. Since retina is known to upregulate CNTF in response to injury, it is likely that CNTF is a major inductive signal for GFAP expression and reactive gliosis in the mammalian retina.",
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N2 - Purpose. The glial fibrillary acidic protein (GFAP) gene is induced in Müller cells in response to retinal injury, detachment or photoreceptor degeneration. The inductive signal responsible for de novo GFAP synthesis is not currently known. There is growing evidence that CNTF might be involved in regulating gliosis in conical astrocytes. The aim of the present study was to examine whether CNTF could induce GFAP expression in Müller cells in the normal mouse retina. Methods. CNTF (0.5 ul) was injected intravitreally into one eye of adult B6 mice at a concentration of 1 u,g/ul. Die fellow eye was injected with physiological saline. Following survival times of 3, 7, 14 and 21 days, animals were killed, and the eyes were processed for immunocytochemistry. A polyclonal antibody to GFAP was used to immunostain cryostat sections of the retina. In some experiments, mouse eyes were injected with bFGF instead of CNTF. Results. In animals injected with CNTF, there was strong immunostaining of radial fibers throughout the retina with the most intense staining at the Müller cell endfeet. Although CNTF was injected at a single site in the eye, GFAP immunostaining was noted throughout the retina. Müller cell staining was seen three days after injection and the intensity of staining remained unchanged at 21 days. In eyes injected with saline, a few Müller cells were immunoreactive in the vicinity of the injection site but the rest of the retina contained no stained Müller cells. In eyes injected with bFGF, there was some GFAP expression in Müller cells; the intensity of the response was, however, considerably weaker than that noted in CNTF-injected eyes. Conclusions. Exogenous CNTF is a potent inducer of GFAP expression in mouse retinal Müller cells. Since retina is known to upregulate CNTF in response to injury, it is likely that CNTF is a major inductive signal for GFAP expression and reactive gliosis in the mammalian retina.

AB - Purpose. The glial fibrillary acidic protein (GFAP) gene is induced in Müller cells in response to retinal injury, detachment or photoreceptor degeneration. The inductive signal responsible for de novo GFAP synthesis is not currently known. There is growing evidence that CNTF might be involved in regulating gliosis in conical astrocytes. The aim of the present study was to examine whether CNTF could induce GFAP expression in Müller cells in the normal mouse retina. Methods. CNTF (0.5 ul) was injected intravitreally into one eye of adult B6 mice at a concentration of 1 u,g/ul. Die fellow eye was injected with physiological saline. Following survival times of 3, 7, 14 and 21 days, animals were killed, and the eyes were processed for immunocytochemistry. A polyclonal antibody to GFAP was used to immunostain cryostat sections of the retina. In some experiments, mouse eyes were injected with bFGF instead of CNTF. Results. In animals injected with CNTF, there was strong immunostaining of radial fibers throughout the retina with the most intense staining at the Müller cell endfeet. Although CNTF was injected at a single site in the eye, GFAP immunostaining was noted throughout the retina. Müller cell staining was seen three days after injection and the intensity of staining remained unchanged at 21 days. In eyes injected with saline, a few Müller cells were immunoreactive in the vicinity of the injection site but the rest of the retina contained no stained Müller cells. In eyes injected with bFGF, there was some GFAP expression in Müller cells; the intensity of the response was, however, considerably weaker than that noted in CNTF-injected eyes. Conclusions. Exogenous CNTF is a potent inducer of GFAP expression in mouse retinal Müller cells. Since retina is known to upregulate CNTF in response to injury, it is likely that CNTF is a major inductive signal for GFAP expression and reactive gliosis in the mammalian retina.

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