Thyroidal hormones restore cell proliferation to the lenses of hypophysectomized adult frogs

Weinsieder, A.; Roberts, Linda G.

doi:10.1016/0016-6480(80)90275-0

Cited by 11 publications

(4 citation statements)

References 37 publications

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“…One eye of postmetamorphic Ram catesbeiana Cottier, 1962;Wainwright et al, 1976 Weinsieder andRoberts, 1980;Weinsieder and Rothstein, 1980] and 4-week-old Columbia-Sherman rats was exposed to an X-ray dose of 25 and 12 Gy, respec tively. Hypophysectomized and intact animals received the irradiation.…”

Section: Methodsmentioning

confidence: 99%

“…The hypothesis mentioned can be conveniently tested now, because hypophysectomy causes all lens mitosis to subside in frogs [ Van Buskirk et al, 1975Rothstein et al, 1976, whereas in rats this effect, if it occurs at all, is minor [Cotlier, 1962], The hypophysectomy-associated arrest of cell proliferation in frogs may be traced to a requirement for insulin-like growth factors probably generated in the liver under the influence of growth hormone, prolactin, triiodothyronine and thyroxin Wainwright et al, 1976;Weinsieder and Roberts, 1980;Wein-sieder and Rothstein, 1980]. Hence, the state of mitotic arrest caused by pituitary ablation is reversed by injection of purified human somatomedin C [Rothstein et al, 1980b) multiplication stimulating activity (MSA) or insulin [Rothstein et al, 1980a], These materials also restore proliferation in organ-cultured lenses from hypophysectomized frogs, whereas the pre viously noted pituitary and thyroidal hormones are only active in vivo [Wainwright et al, 1978].…”

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confidence: 99%

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G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

Rothstein¹,

Worgul²,

Medvedovsky³

et al. 1982

Ophthalmic Res

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

Rothstein¹,

Worgul²,

Medvedovsky³

et al. 1982

Ophthalmic Res

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“…Thyroid hormones also stimulate cell proliferation in lens epithelium of both intact (4) and hypophysectomized adult frogs (5). In chick embryos thyroid hormones accelerate the develop ment of corneal epithelium and endothelium, the two cell layers essential for the maintenance of corneal transparency (6).…”

mentioning

confidence: 99%

Epidermal Growth Factor in Mouse Ocular Tissue: Effects of Thyroxine and Exogenous Epidermal Growth Factor

et al. 1985

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ABSTRACT. Using a specific and sensitive epidermal growth factor (EGF) radioimmunoassay, we identified radioimmunoasayable EGF both in developing and adult mouse ocular tissues. In neonatal animals ocular EGF concentrations increase during the first 4-9 days and then decline between 9 and 15 days. Thyroxine (T4) administration (0.4 pg/g body weightlday from day 0) increased local EGF concentrations in eye and skin of 7-day-old neonatal mouse pups. However, this treatment did not affect submandibular gland EGF concentrations during the 1st wk of life. Both EGF and T4 are known to accelerate eye opening in the neonatal mouse. Exogenous EGF administration (2 pg/g body weightlday) during the first 8 days of life elicited precocious eyelid opening as expected but did not alter the serum T4 concentration, suggesting that EGF does not mediate eye opening by T4 dependent mechanism(~). Tissue EGF measurements revealed that the exogenous EGF was localized in skin and eye; however, other tissues including lung, liver, heart and submandibular gland also contained exogenous EGF. Kidney-EGF concentrations did not rise while brain-EGF levels were significantly decreased after exogenous EGF, suggesting that different EGF uptake and regulatory mechanism(s) exist in different tissues during the neonatal period. T4 administration (0.4 pg/g body weightlday) for 10 days to adult mice also increased ocular-EGF concentrations. However, this increase was abolished by sialoadenectomy, suggesting in contrast to the newborn, that submandibular gland is an important source of ocular-EGF in adult mice. These studies indicate that ocular EGF in the mouse is thyroxine responsive only during the neonatal period. (Pediatr Res 19: 315-319,1985) Abbreviations T4, thyroxine EGF, epidermal growth factor BW, body weight SMG, submandibular glands RIA, radioimmunoassay T3, triiodothyronine

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“…Similarly, the formation of skin glands during metamorphosis in Xenopus seems to involve a thyroxine-triggered change in the mitotic pattern of epidermal cells (McGarry and Vanable, 1969). Thyroid hormone treatment will reinitiate mitoses in previously quiescent lens epithelium of hypophysectomized adult frogs (Weinseider and Roberts, 1980) and stimulate mitotic activity in epidermis of frogs (Wright, 1977;Wright et al, 1981) and newts (Hoffman and Dent, 1977). Postnatal neurogenesis in vertebrate cerebellum is also thyroxine dependent (reviewed in Lauder, 1983).…”

Section: Mode Of Action Of Thyroxinementioning

confidence: 99%

Control of the development of the ipsilateral retinothalamic projection in Xenopus laevis by thyroxine: Results and speculation

Hoskins

1986

J. Neurobiol.

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The ipsilateral retinothalamic projection of the frog Xenopus laevis is formed by the axons of a subset of retinal ganglion cells which are found throughout peripheral and non-nasodorsal retina. Unlike the crossed retinotectal and retinothalamic projections, which begin to form during early embryonic stages, the ipsilateral projection does not begin to develop until late in tadpole life, at stages when thyroxine first becomes detectable in the circulation. Blocking the production of thyroid hormone in tadpoles prevents the development of the ipsilateral projection, in a reversible manner. Intraocular injection of thyroxine can "rescue" the development of the projection in tadpoles which otherwise remain premetamorphic. In addition, the projection from one eye of a metamorphically-blocked tadpole can be induced to form by an intraocular injection of thyroxine at a dose which has no detectable effect on retinal development in the other, untreated eye. These results indicate that the development of the ipsilateral retinothalamic projection is dependent upon thyroxine, and strongly suggest that the hormone acts at the level of the eye, rather than at the optic chiasm or thalamic target, to bring about the development of a new pathway. A number of ways in which thyroxine might act in the system are discussed.

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Thyroidal hormones restore cell proliferation to the lenses of hypophysectomized adult frogs

Cited by 11 publications

References 37 publications

G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

Epidermal Growth Factor in Mouse Ocular Tissue: Effects of Thyroxine and Exogenous Epidermal Growth Factor

Control of the development of the ipsilateral retinothalamic projection in Xenopus laevis by thyroxine: Results and speculation

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Thyroidal hormones restore cell proliferation to the lenses of hypophysectomized adult frogs

Cited by 11 publications

References 37 publications

G0/G1Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

G0/G1Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

Epidermal Growth Factor in Mouse Ocular Tissue: Effects of Thyroxine and Exogenous Epidermal Growth Factor

Control of the development of the ipsilateral retinothalamic projection in Xenopus laevis by thyroxine: Results and speculation

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G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract

G₀/G₁Arrest of Cell Proliferation in the Ocular Lens Prevents Development of Radiation Cataract