Anti-CSF1 (aa 33-132) polyclonal antibody

Macrophage colony stimulating factor (M-CSF), commonly known as CSF1, is a cytokine produced by osteoblast cells, and is well known for its important role in differentiation of osteoclasts and white adipocyte hyperplasia. However, the role of M-CSF in lipid metabolic activity is lacking insight. In the current study, we explore unidentified actions of M-CSF in adipocytes. Levels of M-CSF were determined for white and brown adipose tissues and cells, and the expression levels of the important protein markers in lipid metabolism were evaluated through immunoblot analysis, subsequent to blocking M-CSF in fat cells by silencing its receptor Csf1r. Interestingly, we observed presence of M-CSF in brown fat cells. In addition, the lack of M-CSF in HIB1B cells attenuated the expressions of protein markers responsible for lipid metabolism in the brown adipocytes. Further, deficiency of M-CSF resulted in decreased adipogenesis along with reduced expression of lipogenic markers for both white and brown adipocytes. Moreover, lipid metabolism was balanced by M-CSF via the PPAR gamma-mediated LPL activity in white adipocytes. Taken together, the results from this study indicate that MCSF is an important regulatory protein in both white and brown adipocytes.

Current data have shown that punicalagin (PUN), an ellagitannin isolated from pomegranate, possesses antiinflammatory and anti-oxidant properties; however, its direct targets have not yet been reported. This is the first report that PTP1B serves as a direct target of PUN, with IC50 value of 1.04 mu M. Results from NPOI further showed that the K-on and K-off of PUN-PTP1B complex were 3.38e2 M-1 s(-1) and 4.13e-3 s(-1), respectively. The active site Arg24 of PTP1B was identified as a key binding site of PUN by computation simulation and point mutation. Moreover, inhibition of PTP1B by PUN promoted an M2c-like macrophage polarization and enhanced antiinflammatory cytokines expression, including IL-10 and M-CSF. Based on gene expression profile, we elucidated that PUN treatment significantly up-regulated 275 genes and down-regulated 1059 genes. M1-like macrophage marker genes, such as Tlr4, Irf1/2, Hmgb1, and Stat1 were down-regulated, while M2 marker genes, including Tmem171, Gpr35, Csf1, Il1rn, Cebpb, Fos, Vegfa, Slc11a1, and Bhlhe40 were up-regulated in PUN-treated macrophages. Hmox-1, a gene encoding HO-1 protein, was preferentially expressed with 16-fold change. Inhibition of HO-1 obviously restored PUN-induced M2 polarization and IL-10 secretion. In addition, phosphorylation of both Akt and STAT3 contributed to PUN-induced HO-1 expression. This study provided new insights into the mechanisms of PUN-mediated anti-inflammatory and anti-oxidant activities and provided new therapeutic strategies for inflammatory diseases.