Display Settings:

Items per page
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 7

1.
FIG. 5

FIG. 5. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

COX-2 protein localizes to chondroprogenitors and the early chondrocyte population. Immunohistochemical staining for COX-2 was performed on fracture calluses from young (left; Y) and aged mice (right; A) between 5 and 14 days. Consistent with mRNA data, COX-2 protein was most abundantly expressed in chondroprogenitors. In young mice at day 10, the COX-2 signal almost completely disappears from cartilage and is limited to the periosteum and osteoblasts. Aged mice have fewer cartilage cells staining positive on days 5 and 7 but have persistent expression in cartilage through days 10 and 14.

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
2.
FIG. 4

FIG. 4. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Cox-2 mRNA is expressed in chondroprogenitor cells in healing fractures. In situ hybridization was performed on fractures obtained from young mice between 3 and 10 days after fracture using murine specific sense and antisense riboprobes for COX-2 and col2a1. Detection was with Kodak Biomax MR X-ray film. COX-2 expression occurs in regions where early chondrocyte precursors express col2a1. COX-2 expression subsequently declines as chondrocytes mature (Figure 5A). Microscopic expression was determined in histological sections of day 5 fracture callus and confirms the co-expression of COX-2 and col2a1 in early chondroprogenitor cell populations (Figure 5B). S-10d represents use of the sense probe on day 10 tissue sections, which acts as a negative control.

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
3.
FIG. 6

FIG. 6. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Fractures in aged mice have delayed osteoclast formation. High-power images, ×20 and ×40, show immunostaining using anti-COX-2 and anti-RANKL antibodies in chondroprogenitors and immature chondrocytes at 7 days after fracture. Endothelial cells (arrow) also stained for COX-2 and RANKL (A). Tissues were harvested from young and aged mice at 7, 10, 14, or 21 days after fracture, and sections were stained for TRACP (B-I). The sections from young mice show TRACP+ osteoclasts by day 7 along the periosteal surface (B). Osteoclasts increase through day 14 when the entire callus is interspersed with TRACP+ osteoclasts (F). By day 21, remodeling is advanced, and the number of osteoclasts is reduced (H). In contrast, osteoclasts do not appear until day 10 in fractures from aged mice, and resorption area appears maximal at 21 days (C, E, G, and I).

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
4.
FIG. 2

FIG. 2. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Fractures in aged mice have delayed cartilage and bone formation. Histology sections were prepared from young and aged mice harvested at various times after fracture (A-L). By day 10, calluses were composed of abundant mature cartilage in young mice compared with largely immature cartilage in aged mice. By day 14, most callus tissue consisted of new bone in young animals, whereas aged animals showed a persistence of cartilage and delayed completion of endochondral ossification. On days 18, 25, and 35, young mice had more advanced remodeling compared with aged animals. Histomorphometric analysis of total callus, bone, and cartilage areas were completed in n = 4 young and n = 4 aged mice, respectively, with three levels analyzed per sample. Histomorphometry showed delayed formation of cartilage, bone and total callus area in aged mice (M-O). Statistical comparisons were performed using ANOVA and significant differences are denoted by symbols: *p < 0.05 and **p < 0.005.

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
5.
FIG. 1

FIG. 1. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Aged mice have a radiographic delay in fracture healing. Serial radiographs of representative young and aged mice at various times after fracture. Young mice showed evidence of callus mineralization by day 10, which was delayed to day 14 in aged mice (A, *). By day 14 in young mice and day 18 in aged mice, the callus showed union (black arrows). Remodeling was delayed in aged mice compared with young mice (A, white arrows). The delay in fracture repair was consistently observed in day 14 fractures (n = 4) (B). Fractures were harvested, and high-resolution μCT scans were performed on young (n = 5) and aged (n = 5) mice. For vascular analysis, mice were perfused with a lead chromate microfil contrast reagent before decalcification. Representative scans are shown for days 10, 14, and 18 for calcified callus (C) and vascularization (D) for young and aged mice, respectively. Mean calculated mineral (E) and vascular (F) volumes were obtained. Mineral volume analysis showed lower mineral accretion in aged mice, particularly on days 10 and 14 (C and E). On days 10 and 14, aged mice have a significant reduction in the proportion of blood vessels in their calluses compared with young mice (D and F). Statistical comparisons were performed using ANOVA and are denoted by symbols: *p < 0.05 and **p < 0.005.

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
6.
FIG. 7

FIG. 7. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Administration of an EP4 agonist to fractures in aged mice accelerates fracture repair and increase bone formation. Fractures in young mice were injected with vehicle (100 μl twice per day), whereas fractures in aged mice received injection of either vehicle or a selective EP4 agonist (CP73; 20 mg/kg/d). Mice (n = 4 per group) were harvested 14 and 21 days after fracture, and tissues were prepared for histology. Representative sections from day 14 are shown in A. Histomorphometry was used to measure the relative populations of undifferentiated mesenchyme, immature cartilage, hypertrophic cartilage, total cartilage, and new bone at day 14 (B). Total callus and bone area was measured on days 14 and 21 (mm2) (C and D). CP73 accelerated the completion of endochondral bone formation and resulted in reduced cartilage and increased bone formation compared with the vehicle-treated aged fractures. The anabolic effects of CP73 on bone formation persisted to day 21 in aged animals. These changes compensated for the age-related effects on fracture healing (B-D). Statistical comparisons were performed using ANOVA, and significance is denoted by symbols: *p < 0.05 and **p < 0.005.

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.
7.
FIG. 3

FIG. 3. From: Reduced COX-2 Expression in Aged Mice Is Associated With Impaired Fracture Healing.

Fracture in aged mice have altered patterns of gene expression during the chondrogenesis, bone formation, and remodeling phases of repair. Total RNA was harvested and pooled from n = 4 young and aged mice at various points. Real-time RT-PCR was performed and normalized to β-actin expression. Values from young mice are shown in the white bars and aged mice in the black bars. The bars at the top of each figure denote the period of time in which maximal expression of each gene occurred in the fractures from both young (white bar) and aged (black bar) mice. Peak expression of col2a1, COX-2, RANKL, and OPG occur in fractures in young mice during the chondrogenic phase of fracture healing between days 0 and 7 (A, F, G, and H). ColX and BMP-2 are maximal at day 10 during the peak of endochondral bone formation (B and D). Finally, osteocalcin and bmp-4 gene expression (C and E) are maximal at day 14, consistent with the peak of primary bone formation on the cartilage template. In contrast, fractures have mice have an altered pattern of gene expressions. COX-2 gene expression was diminished on days 3, 5, and 7 during the phase of chondrogenesis (H). Other genes were delayed, had reduced or delayed maximal expression, or had a broader duration of expression. Statistical comparisons were performed using ANOVA and significance denoted by symbols: *p < 0.05 and **p < 0.005. Peak expression periods are denoted by the bars at the top of the figure. The maximal value measured in young and old mice for each gene is statistically different (p < 0.05; A, B, E, F, and H) in all cases except for panels in which “ns” appears with the bars (C, D, and G).

Amish A Naik, et al. J Bone Miner Res. 2009 February;24(2):251-264.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk