Anti-CFL1 (aa 1-100) Monoclonal Antibody, clone FQS20963©

Sericin peptides have a high proportion of hydrophilic amino acid residues, which are considered to protect cells from freezing stress due to the maintenance of water in the cells. In this paper, the hypothermia protection effect of sericin peptides was studied by reading optical density of cells at 600 nm, which was detailedly optimized to be a direct and practical spectrophotometric method. The survival rate of Lactobacillus bulgaricus after frozen storaged with addition of 0.1 mg/mL sericin peptides was close to that of 10% (v/v) glycerol (p > 0.05). The survival rate of 5 mg/mL sericin peptides was up to 64.17%.

Human stromal stem cells (hMSCs) differentiate into adipocytes that play a role in skeletal tissue homeostasis and whole body energy metabolism. During adipocyte differentiation, hMSCs exhibit significant changes in cell morphology suggesting changes in cytoskeletal organization. Here, we examined the effect of direct modulation of actin microfilament dynamics on adipocyte differentiation. Stabilizing actin filaments in hMSCs by siRNA-mediated knock down of the two main actin depolymerizing factors (ADFs):Cofilin 1 (CFL1) and Destrin (DSTN) or treating the cells by Phalloidin reduced adipocyte differentiation as evidenced by decreased number of mature adipocytes and decreased adipocyte specific gene expression (ADIPOQ, LPL, PPARG, FABP4). In contrast, disruption of actin cytoskeleton by Cytochalasin D enhanced adipocyte differentiation. Follow up studies revealed that the effects of CFL1 on adipocyte differentiation depended on the activity of LIM domain kinase 1 (LIMK1) which is the major upstream kinase of CFL1. Inhibiting LIMK by its specific chemical inhibitor LIMKi inhibited the phosphorylation of CFL1 and actin polymerization, and enhanced the adipocyte differentiation. Moreover, treating hMSCs by Cytochalasin D inhibited ERK and Smad2 signaling and this was associated with enhanced adipocyte differentiation. On the other hand, Phalloidin enhanced ERK and Smad2 signaling, but inhibited adipocyte differentiation which was rescued by ERK specific chemical inhibitor U0126. Our data provide a link between restructuring of hMSCs cytoskeleton and hMSCs lineage commitment and differentiation. (C) 2018 Elsevier B.V. All rights reserved.