Collagen II Antibody - BSA Free

Western Blot: Collagen II Antibody - BSA Free [NBP1-77795] -

MiR‐155 promotes chondrocyte apoptosis and catabolic activity through targeting PIK3R1‐mediated PI3K/Akt pathway. A, Primary chondrocytes were transfected with NC inhibitors (NC inh) or miR‐155 inhibitors (miR‐155 inh) along with siNC or siPIK3R1 as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The expression of PIK3R1, p‐Akt and Akt was analysed by Western blot assay. GAPDH is the loading control. B, Primary chondrocytes were transfected with NC mimics or miR‐155 mimics along with pcDNA vector or pcDNA‐PIK3R1 as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The protein expression was analysed as in (A). C and E, Primary chondrocytes were transfected with NC inh or miR‐155 inh along with DMSO or 1 uM Akt inhibitor MK‐2206 as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. C, The protein expression of PIK3R1, p‐Akt and Akt was analysed as in (A). (D‐E) The protein expression of cleaved caspase‐3, collagen Ⅱ, aggrecan, MMP3 and MMP13 was also analysed. The representative images (D) were shown, and the relative protein expression (E) was analysed by ImageJ software. Means +/- SEM ANOVA test (n = 3), **P < 0.01. NS, not significant. F, Primary chondrocytes were treated as in (C). Cell apoptosis was detected by TUNEL staining. The representative images (left, 200 magnification) and quantification of TUNEL positive cells (right) are shown. Means +/- SEM ANOVA test (n = 15), **P < 0.01. NS, not significant Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32562373), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Collagen II Antibody - BSA Free [NBP1-77795] -

The targeted PIK3R1 mediates miR‐155 promotive effects on chondrocyte apoptosis and catabolic activity. A and B, Primary chondrocytes were transfected with NC inhibitors (NC inh) or miR‐155 inhibitors (miR‐155 inh) (A), or NC mimics or miR‐155 mimics (B), and cultured for further 24 hours in the presence or absence of 10 ug/mL IL‐1 beta. PIK3R1 expression was detected by Western blot analysis. Images represent three independent assays. C and D, Primary chondrocytes were transfected with NC inhibitors or miR‐155 inhibitors along with siRNA targeting negative control (siNC) or PIK3R1 (siPIK3R1) as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The expression of PIK3R1, cleaved caspase‐3, collagen Ⅱ, aggrecan, MMP3 and MMP13 was analysed by Western blot assay. GAPDH is the loading control. C, Images represent three independent assays. D, The relative protein expression was analysed by ImageJ software. Means +/- SEM ANOVA test (n = 3), **P < 0.01. NS, not significant. E and F, Primary chondrocytes were transfected with NC mimics or miR‐155 mimics along with pcDNA vector or pcDNA‐PIK3R1 as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The analysis of protein expression was performed as in (C‐D) Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32562373), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Collagen II Antibody - BSA Free [NBP1-77795] -

MiR‐155 is up‐regulated in OA cartilage and IL‐1 beta ‐treated primary chondrocytes in vitro. A, Western blot analysis of cleaved caspase‐3, collagen Ⅱ, aggrecan, MMP3 and MMP13 expression in three representative cartilage tissues from healthy donors (control) and patients with osteoarthritis (OA). GAPDH is the loading control. Images represent three independent assays. Protein expression relative to GAPDH was quantified and noted beneath each band, and lane 1 was set with value 1. B, qRT‐PCR analysis of miR‐155 level in control group (n = 8) and OA group (n = 18). Data were normalized to RNU6B level. Each dot represents the mean value of each patient. Means +/- SEM ANOVA test. C, Pearson's correlation analysis of miR‐155 level and a modified Mankin scale of 18 OA patients. r = 0.523, P < 0.001. D and E, Primary chondrocytes were treated with increasing concentrations of IL‐1 beta as indicated for 24 hours. The protein expression (D) and miR‐155 level (E) were analysed as in (A) and (B), respectively. Data are means +/- SEM from 3 independent assays. ANOVA test, *P < 0.05; **P < 0.01 Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32562373), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Collagen II Antibody - BSA Free [NBP1-77795] -

The targeted PIK3R1 mediates miR‐155 promotive effects on chondrocyte apoptosis and catabolic activity. A and B, Primary chondrocytes were transfected with NC inhibitors (NC inh) or miR‐155 inhibitors (miR‐155 inh) (A), or NC mimics or miR‐155 mimics (B), and cultured for further 24 hours in the presence or absence of 10 ug/mL IL‐1 beta. PIK3R1 expression was detected by Western blot analysis. Images represent three independent assays. C and D, Primary chondrocytes were transfected with NC inhibitors or miR‐155 inhibitors along with siRNA targeting negative control (siNC) or PIK3R1 (siPIK3R1) as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The expression of PIK3R1, cleaved caspase‐3, collagen Ⅱ, aggrecan, MMP3 and MMP13 was analysed by Western blot assay. GAPDH is the loading control. C, Images represent three independent assays. D, The relative protein expression was analysed by ImageJ software. Means +/- SEM ANOVA test (n = 3), **P < 0.01. NS, not significant. E and F, Primary chondrocytes were transfected with NC mimics or miR‐155 mimics along with pcDNA vector or pcDNA‐PIK3R1 as indicated and cultured with 10 ug/mL IL‐1 beta for further 24 hours. The analysis of protein expression was performed as in (C‐D) Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32562373), licensed under a CC-BY license. Not internally tested by Novus Biologicals.