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Results: 9

1.
Figure 4

Figure 4. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 promotes expression of genes involved in glycosaminoglycan synthesis. Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide or the Src inhibitor PP2 (10 μmol/l), and transcript levels of genes involved in glycosaminoglycan synthesis were determined by real-time PCR. Expression levels of (a) Xylt1, (b) Xylt2, (c) Chst3 and (d) Chst11 were significantly increased upon Src inhibition (n = 3; *P < 0.05).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
2.
Figure 6

Figure 6. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 represses expression of Src kinase genes. Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide (DMSO) or the Src inhibitor PP2 (10 μmol/l), and transcript levels of Src kinase genes were determined by real-time PCR. Expression levels of (a) Lyn, (b) Frk and (c) Hck were significantly decreased upon Src inhibition (n = 3; ***P < 0.001).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
3.
Figure 7

Figure 7. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 promotes cell rounding and cortical actin formation. Primary mouse chondrocytes were incubated for 24 hours with (a) dimethyl sulphoxide or (b) the Src inhibitor PP2 (10 μmol/l), and cells were stained with rhodamine-phalloidin (red) for polymerized actin and with DAPI for nuclei (blue). PP2 induced cell rounding, loss of stress fibre, and cortical organization of actin (scale bar: 2 μm).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
4.
Figure 5

Figure 5. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 promotes expression of late chondrocyte marker genes. Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide (DMSO) or the Src inhibitor PP2 (10 μmol/l), and transcript levels of late chondrocyte marker genes were determined by real-time PCR. Expression levels of (a) Col10a1, (b) Ihh, (c) Cdkn1c and (d) Atf3 were significantly increased upon Src inhibition (n = 3; *P < 0.05, **P < 0.01, ***P < 0.001).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
5.
Figure 3

Figure 3. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 promotes expression of early chondrocyte marker genes. Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide (DMSO) or the Src inhibitor PP2 (10 μmol/l), and transcript levels of early chondrocyte marker genes were determined by real-time PCR. Expression levels of (a) Sox9, (b) Sox5, (c) Sox6, (d) Col2a1 and (e) Acan (aggrecan) were significantly increased upon Src inhibition (n = 3; **P < 0.01, ***P < 0.001).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
6.
Figure 2

Figure 2. From: Src kinase inhibition promotes the chondrocyte phenotype.

Src kinase activity regulates chondrocyte cell numbers. Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide (DMSO), (a) the general tyrosine kinase inhibitors Tyr A23, Tyr A25 and Tyr A47, or (b) the Src inhibitor PP2 (1 and 10 μmol/l each). Cell numbers were determined by MTT assay. All inhibitors reduced cell numbers at the 10 μmol/l concentration, but the effects of PP2 were more pronounced (n = 4; *P < 0.01, ***P < 0.001).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
7.
Figure 1

Figure 1. From: Src kinase inhibition promotes the chondrocyte phenotype.

Expression of Src kinases in chondrogenic cells. Expression of (a) Lyn, (b) Frk and (c) Hck Src kinase genes during chondrogenic differentiation of ATDC5 cells (days 3 to 18) was analyzed using Taqman real-time PCR analyses. Lyn mRNA levels increased strongly during differentiation, whereas the other two kinase genes exhibited more subtle changes in gene expression. (d) Western blotting confirmed expression of Lyn protein in primary mouse chondrocytes in monolayer culture for 1 to 3 days.

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
8.
Figure 8

Figure 8. From: Src kinase inhibition promotes the chondrocyte phenotype.

PP2 promotes cell rounding and cortical actin formation. Primary mouse chondrocytes were incubated for 24 hours with dimethyl sulphoxide (DMSO) or the Src inhibitor PP2 (10 μmol/l), and cells were stained with antibodies against total focal adhesion kinase (FAK) or FAK phosphorylated on residue tyrosine 397 (green), rhodamine-phalloidin (red) and DAPI (blue). In the presence of DMSO, total and phosphorylated actin localized to focal adhesions at the end of stress fibres. In cells treated with PP2, total FAK acquired a diffuse cytosolic staining, whereas the signal for phosphorylated FAK was greatly reduced (scale bar: 2 μm).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.
9.
Figure 9

Figure 9. From: Src kinase inhibition promotes the chondrocyte phenotype.

Interplay between RhoA/ROCK and Src kinase signalling. (a) Primary mouse chondrocytes were incubated for 1 to 3 days with dimethyl sulphoxide (DMSO) or the Src inhibitor PP2 (10 μmol/l), and Ras homology A (RhoA) activity was measured using the G-LISA™ kit (Cytoskeleton). No significant differences in RhoA activity were observed upon Src inhibition (n = 3). (b) Primary mouse chondrocytes were incubated for 1 or 2 days with DMSO or the Rho-associated, coiled-coil containing protein kinase (ROCK) inhibitor Y27632 (10 μmol/l) or the actin-modifying drugs cytochalasin D (1 μmol/l) and jasplakinolide (50 nmol/l). Expression levels of (b) Lyn, (c) Frk and (d) Hck genes were determined using real-time PCR, which demonstrated regulation of all three genes by the employed drugs (n = 3, *P < 0.001).

Laura Bursell, et al. Arthritis Res Ther. 2007;9(5):R105-R105.

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