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Br J Ophthalmol. Feb 1999; 83(2): 209–218.
PMCID: PMC1722920

Transforming growth factor β isoforms in human optic nerve heads


AIM—To determine if the isoforms of transforming growth factor β (TGF-β) are present in fetal, normal adult, and glaucomatous optic nerve heads.
METHODS—To localise cells synthesising TGF-β, optic nerve heads were stained using antibodies to TGF-β1, TGF-β2, and TGF-β3. To demonstrate synthesis, human optic nerve heads from fetal, glaucomatous, and normal age matched subjects were explanted, cultured overnight, and the culture supernatant was assayed for the presence of TGF-β1 and TGF-β2 by bioassay. In addition, semiquantitative RT-PCR was performed to determine the gene expression pattern of TGF-β2.
RESULTS—Immunohistochemistry of glaucomatous samples revealed the presence of intense staining for TGF-β2 primarily in astrocytes, whereas TGF-β1 was localised to blood vessels. No TGF-β3 immunoreactivity was observed. There was little or no expression of TGF-β in normal optic nerve heads. Optic nerve heads from glaucomatous eyes released 70-100-fold more TGF-β2 than normal age matched optic nerve heads. Fetal optic nerve heads released 90-100-fold more TGF-β2 than normal adult optic nerve heads. TGF-β1 was undetectable by bioassay in all samples tested. There was no apparent increase in TGF-β2 gene expression in glaucomatous and fetal eyes, suggesting post-transcriptional regulatory mechanisms.
CONCLUSIONS—These results demonstrate that TGF-β2 is produced in high levels in the fetal and glaucomatous optic nerve heads, perhaps by a mechanism of post-transcriptional regulation. TGF-β may be important during development of the optic nerve head and, in glaucoma, TGF-β2 may be a mediator of astrocyte reactivation and extracellular matrix remodelling in the lamina cribrosa.

Keywords: astrocytes; glaucoma; optic nerve head; transforming growth factor β

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Figures and Tables

Figure 1
TGF-β1 and TGF-β2 immunoperoxidase staining in normal optic nerve head, donor age 68 years old. Little or no staining for TGF-β2 is observed. Few blood vessels were stained with TGF-β1 (arrow, E). (A) and (D) Prelaminar ...
Figure 2
TGF-β1 and TGF-β2 immunoperoxidase staining in fetal optic nerve head (gestational age 24 weeks). TGF-β1 immunoreactivity was restricted to blood vessels throughout the optic nerve head (A, D) and TGF-β2 reactivity ...
Figure 3
TGF-β1 immunoperoxidase staining in advanced primary open angle glaucoma, donor age 78 years old. Note staining around blood vessels (arrows). (A) Prelaminar region; (B) lamina cribrosa; (C) negative control. vs = vitreal ...
Figure 4
TGF-β2 immunoperoxidase staining in advanced (A, B, and C) and mild (D, E, and F) primary open angle glaucoma, donor ages 74 years old (advanced glaucoma) and 67 years old (mild glaucoma). Note widespread staining of astrocytes ...
Figure 5
Co-localisation of TGF-β2 and GFAP by immunofluorescence in the lamina cribrosa of a glaucomatous donor (age 92 years old). In (A) immunoreactivity for TGF-β2 is localised to cells inside the cribriform plates (CP) and in the ...
Figure 6
TGF-β2 mRNA levels in fetal, normal adult, and glaucomatous eyes, as determined by relative RT-PCR. Similar levels of TGF-β2 mRNA were observed in all samples tested (upper), when compared with β actin levels (lower). ...

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