Change of body weights of mice in the three groups over whole experiment period of 35 days.

<p>Standard deviations are shown in single direction.</p

Effects of imatinib and nilotinib on proliferation (A) and viability (B) of PNF-derived Schwann cells.

<p>Data are absorbance normalized to that of untreated controls. Significant (<i>P</i><0.05) and highly significant (<i>P</i><0.001) differences were marked with * and **, respectively.</p

Xenograft on sciatic nerve in mouse.

<p>(A) The exposed sciatic nerve (white arrow) for implantation, (B) a PNF xenograft (red arrow) integrated onto the sciatic nerve, (C) images and (D) three-dimensional reconstruction of a xenograft by (red arrow) a Vevo 2100 micro-imaging system.</p

Imatinib significantly (*<i>P</i><0.05) elevated cytotoxicity of mouse spleen cells on cultured PNF Schwann cells.

<p>The elevation by nilotinib was not significant.</p

Change of xenograft size in each mouse over the 4-weeks of treatment period in the untreated (A), nilotinib (B) and imatinib (C) groups.

<p>Group-means (D) differed significantly among the three groups (P<0.05).</p

Overexpression of cyclooxygenase-2 in adipocytes reduces fat accumulation in inguinal white adipose tissue and hepatic steatosis in high-fat fed mice

Cyclooxygenases are known as important regulators of metabolism and immune processes via conversion of C20 fatty acids into various regulatory lipid mediators, and cyclooxygenase activity has been implicated in browning of white adipose tissues. We generated transgenic (TG) C57BL/6 mice expressing the Ptgs2 gene encoding cyclooxygenase-2 (COX-2) in mature adipocytes. TG mice fed a high-fat diet displayed marginally lower weight gain with less hepatic steatosis and a slight improvement in insulin sensitivity, but no difference in glucose tolerance. Compared to littermate wildtype mice, TG mice selectively reduced inguinal white adipose tissue (iWAT) mass and fat cell size, whereas the epididymal (eWAT) fat depot remained unchanged. The changes in iWAT were accompanied by increased levels of specific COX-derived lipid mediators and increased mRNA levels of interleukin-33, interleukin-4 and arginase-1, but not increased expression of uncoupling protein 1 or increased energy expenditure. Epididymal WAT (eWAT) in TG mice exhibited few changes except from increased infiltration with eosinophils. Our findings suggest a role for COX-2-derived lipid mediators from adipocytes in mediating type 2 immunity cues in subcutaneous WAT associated with decreased hepatic steatosis, but with no accompanying induction of browning and increased energy expenditure