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1.
Fig. 7.

Fig. 7. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

In vivo inhibition of caspase-3 or caspase-9 leads to expansion of the hypertrophic chondrocyte layer. Shown are hematoxylin/eosin-stained sections from 24-day-old mice injected at days 18–23 with DMSO, caspase-3 inhibitor (Z-DEVD-FMK), or caspase-9 inhibitor (Z-LEHD-FMK). Brackets indicate the hypertrophic chondrocyte layer.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
2.
Fig. 4.

Fig. 4. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Growth-plate mineralization in 24-day-old mice. von Kossa staining was performed on sections from 24-day-old wild-type mice fed a regular diet, Hyp mice fed a regular diet, and wild-type mice fed a high-calcium/low-phosphate diet from 18 to 24 days of age. Insets show a magnification of the hypertrophic chondrocytes. Brackets indicate the hypertrophic chondrocyte layer. Data are representative of sections from five mice for each condition.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
3.
Fig. 5.

Fig. 5. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Cleaved caspase-3 immunohistochemistry. Sections from 24-day-old wild-type (WT) mice fed a regular diet, Hyp mice fed a regular diet, and mice fed a high-calcium/low-phosphate diet from 18 to 24 days of age were immunostained with antibody to cleaved caspase-3. Brackets indicate the hypertrophic chondrocyte layer. Data are representative of experiments performed on sections from three or more mice for each condition.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
4.
Fig. 3.

Fig. 3. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Histological analysis and evaluation of hypertrophic chondrocyte apoptosis in Hyp mice. Hematoxylin/eosin staining (A and C) and TUNEL assays (B and D) were performed on sections from wild-type (WT) and Hyp mice at 0.5 day (A and B) and 10 days of age (C and D). Brackets indicate the hypertrophic chondrocyte layer. Data are representative of experiments performed on sections from three or more mice for each condition. EV, Evans blue; T, TUNEL.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
5.
Fig. 2.

Fig. 2. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Biochemical parameters. Serum phosphate (A), serum calcium (B), and immunoreactive PTH (C) were measured in 24-day-old wild-type mice fed a regular diet (black bars), Hyp mice fed a regular diet (white bars), and wild-type mice fed a high-calcium/low-phosphate diet (gray bars). (D) Serum phosphate levels at 18.5 days postcoitum and at 0.5, 10, and 24 days of age in wild-type (♦) and Hyp (○) mice fed a regular diet. Data represent the mean ± SD of values from five mice for each assay. *, P ≤ 0.05.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
6.
Fig. 6.

Fig. 6. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Phosphate induces hypertrophic chondrocyte apoptosis in vitro. Hypertrophic chondrocytes were treated with 7 mM NaCl or 7 mM NaH2PO4 for 18 h in the presence or absence of 1 μM cyclosporin A (CsA). Cell lysates were subjected to Western blot analysis using anti-caspase-9. Lysates of 3T3 fibroblasts and proliferating chondrocytes (PC) treated with 7 mM NaH2PO4 were similarly analyzed. Data are representative of those obtained from three independent cell preparations.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.
7.
Fig. 1.

Fig. 1. From: Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.

Histological analysis and evaluation of hypertrophic chondrocyte apoptosis in 24-day-old mice. Shown are hematoxylin/eosin-stained sections (A and C) and TUNEL assay (B and D). (A and B) Wild-type (WT) and VDR knockout (KO) mice fed a regular diet (Left) or a rescue diet (Right) that normalizes mineral ion homeostasis. (C and D) Wild-type mice fed a regular diet, Hyp mice fed a regular diet, and wild-type mice fed a high-calcium/low-phosphate diet from 18 to 24 days of age. Brackets indicate the hypertrophic chondrocyte layer. Data are representative of experiments performed on sections from three or more mice for each condition. EV, Evans blue; T, TUNEL.

Yves Sabbagh, et al. Proc Natl Acad Sci U S A. 2005 July 5;102(27):9637-9642.

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