Figure 2
Figure 2. CaR stimulation does not alter cell cycle status, or cell survival, but significantly increases HSC adhesion to collagen I. (A) Cell cycle profiles for LKS+F−, LKS+F+, and LKS−F+ subpopulations (n = 4 from 2 independent experiments). (B) Percentage of LKS cells undergoing apoptosis after treatment. The percentage of apoptotic cells was determined as 7-amino-actinomycin (7-AAD) negative and PE Annexin V positive (n = 3 from 3 independent experiments). (C) Adhesion of LKS+F−, LKS+F+, and LKS−F+ cells to fibronectin and collagen I. Cells were allowed to adhere to wells coated with fibronectin and collagen I for 3 hours at 37°C and 5% CO2. Bovine serum albumin (BSA; 1%) was used as a control for nonspecific binding (**P < .01; n = 8 from 3 independent experiments; error bars represent SEMs).

CaR stimulation does not alter cell cycle status, or cell survival, but significantly increases HSC adhesion to collagen I. (A) Cell cycle profiles for LKS+F, LKS+F+, and LKSF+ subpopulations (n = 4 from 2 independent experiments). (B) Percentage of LKS cells undergoing apoptosis after treatment. The percentage of apoptotic cells was determined as 7-amino-actinomycin (7-AAD) negative and PE Annexin V positive (n = 3 from 3 independent experiments). (C) Adhesion of LKS+F, LKS+F+, and LKSF+ cells to fibronectin and collagen I. Cells were allowed to adhere to wells coated with fibronectin and collagen I for 3 hours at 37°C and 5% CO2. Bovine serum albumin (BSA; 1%) was used as a control for nonspecific binding (**P < .01; n = 8 from 3 independent experiments; error bars represent SEMs).

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