Cell Kinetics of Growth Cartilage in the Rat Tibia I. Measurements in Young Male Rats

Walker, K. V. R.; Kember, N. F.

doi:10.1111/j.1365-2184.1972.tb00378.x

Cited by 37 publications

(34 citation statements)

References 5 publications

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“…We speculate that the decrease in resting zone chondrocyte numbers might lead to a decrease in PTHrP production and consequently may explain why, in older animals, proliferative chondrocytes stop replicating and undergo hypertrophic differentiation at a point closer to the resting zone than occurs in the young animal. Therefore, diminished production of PTHrP in a dwindling resting zone might explain why the length of the proliferative columns decreases with age, a prominent feature of growth plate senescence (Walker & Kember 1972, Nilsson & Baron 2004.…”

Section: E16mentioning

confidence: 99%

Organization of the Indian hedgehog – parathyroid hormone-related protein system in the postnatal growth plate

Chau¹,

Forcinito²,

Andrade³

et al. 2011

Journal of Molecular Endocrinology

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In embryonic growth cartilage, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP) participate in a negative feedback loop that regulates chondrocyte differentiation. Postnatally, this region undergoes major structural and functional changes. To explore the organization of the Ihh-PTHrP system in postnatal growth plate, we microdissected growth plates of 7-day-old rats into their constituent zones and assessed expression of genes participating in the Ihh-PTHrP feedback loop. Ihh, Patched 1, Smoothened, Gli1, Gli2, Gli3, and Pthr1 were expressed in regions analogous to the expression domains in embryonic growth cartilage. However, PTHrP was expressed in resting zone cartilage, a site that differs from the embryonic source, the periarticular cells. We then used mice in which lacZ has replaced coding sequences of Gli1 and thus serves as a marker for active hedgehog signaling. At 1, 4, 8, and 12 weeks of age, lacZ expression was detected in a pattern analogous to that of embryonic cartilage. The findings support the hypothesis that the embryonic Ihh-PTHrP feedback loop is maintained in the postnatal growth plate except that the source of PTHrP has shifted to a more proximal location in the resting zone.

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Section: E16mentioning

confidence: 99%

Organization of the Indian hedgehog – parathyroid hormone-related protein system in the postnatal growth plate

Chau¹,

Forcinito²,

Andrade³

et al. 2011

Journal of Molecular Endocrinology

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“…These functional senescent changes are accompanied by structural senescent changes. There is a gradual decline in the overall growth plate height, proliferative zone height, hypertrophic zone height, size of hypertrophic chondrocytes, and column density (Kember & Walker 1971, Kember 1973, Masoud et al 1986a, Masoud et al 1986b, Walker & Kember 1972a, Walker & Kember 1972b, Hunziker & Schenk 1989, Farquharson & Loveridge 1990. The growth plate undergoes ossification as the final step in the senescence program .…”

Section: Introductionmentioning

confidence: 99%

Depletion of resting zone chondrocytes during growth plate senescence

Schrier

Ferns²,

Barnes³

et al. 2006

Journal of Endocrinology

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With age, the growth plate undergoes senescent changes that cause linear bone growth to slow and finally cease. Based on previous indirect evidence, we hypothesized that this senescent decline occurs because growth plate stem-like cells, located in the resting zone, have a finite proliferative capacity that is gradually depleted. Consistent with this hypothesis, we found that the proliferation rate in rabbit resting zone chondrocytes (assessed by continuous 5-bromo-2 -deoxy-uridine labeling) decreases with age, as does the number of resting zone chondrocytes per area of growth plate.Glucocorticoid excess slows growth plate senescence. To explain this effect, we hypothesized that glucocorticoid inhibits resting zone chondrocyte proliferation, thus conserving their proliferative capacity. Consistent with this hypothesis, we found that dexamethasone treatment decreased the proliferation rate of rabbit resting zone chondrocytes and slowed the numerical depletion of these cells. Estrogen is known to accelerate growth plate senescence. However, we found that estradiol cypionate treatment slowed resting zone chondrocyte proliferation.Our findings support the hypotheses that growth plate senescence is caused by qualitative and quantitative depletion of stem-like cells in the resting zone and that growth-inhibiting conditions, such as glucocorticoid excess, slow senescence by slowing resting zone chondrocyte proliferation and slowing the numerical depletion of these cells, thereby conserving the proliferative capacity of the growth plate. We speculate that estrogen might accelerate senescence by a proliferation-independent mechanism, or by increasing the loss of proliferative capacity per cell cycle.

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“…At the onset of sexual maturation, the growth plate undergoes structural and functional changes. There is a gradual decline in the overall growth plate height (Masoud et al 1986), proliferative zone height (Walker & Kember 1972), hypertropic zone height (Kember & Walker 1971), size of hypertropic chondrocytes (Kember & Walker 1971, Hunziker & Schenk 1989, Breur et al 1991, and column density (Kember 1971).…”

Section: Introductionmentioning

confidence: 99%

The aromatase inhibitor letrozole increases epiphyseal growth plate height and tibial length in peripubertal male mice

Eshet

Maor²,

Ari³

et al. 2004

Journal of Endocrinology

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Sex hormones may influence longitudinal growth, either indirectly, by affecting the growth-hormone-insulin-like growth factor I (IGF-I) axis, or directly, by affecting changes within the epiphyseal growth plate (EGP). The aim of the present study was to investigate the effects of letrozole, an aromatase inhibitor, on longitudinal growth and changes in the EGP in vivo. Eighteen peripubertal male mice were divided into three groups. The first group was killed at baseline, the second was injected with letrozole (Femara) s.c., 2 mg/kg body weight/day, for 10 days, and the third was injected with the vehicle alone. Serum testosterone levels were found to be significantly higher in the treated group than in the controls. Letrozole induced a significant increase in body weight, tail length and serum growth hormone level, but had no significant effect on the level of serum IGF-I. On histomorphometric study, there was a significant increase (12%) in EGP height in the treated animals compared with controls. Immunohistochemistry showed a 3·4-fold letrozole-induced increase in the proliferation of the EGP chondrocytes, as estimated by the number of proliferation cell nuclear antigen-stained cells, and a decrease in the differentiation of the EGP chondrocytes, as estimated by type X collagen staining. Letrozole did not interfere with type II collagen levels. The study group also showed a twofold increase in the number of IGF-I receptor-positive cells compared with controls. In conclusion, the aromatase inhibitor, letrozole, appears to increase the linear growth potential of the EGP in mice.

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Cell Kinetics of Growth Cartilage in the Rat Tibia I. Measurements in Young Male Rats

Cited by 37 publications

References 5 publications

Organization of the Indian hedgehog – parathyroid hormone-related protein system in the postnatal growth plate

Organization of the Indian hedgehog – parathyroid hormone-related protein system in the postnatal growth plate

Depletion of resting zone chondrocytes during growth plate senescence

The aromatase inhibitor letrozole increases epiphyseal growth plate height and tibial length in peripubertal male mice

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