Obesity is characterized by low-grade inflammation that originates predominantly from the expanding visceral adipose tissue, in which adipocytes respond to lipid overload with hypertrophy, and consequently die by apoptosis. Recruited adipose tissue macrophages (ATMs) take up the excess lipids and remove the dead cells; however, long-term exposure to high concentrations of lipids alters their phenotype to M1-like ATMs that produce pro-inflammatory cytokines and resistin leading to insulin resistance and other obesity-related pathologies. Mer tyrosine kinase is expressed by macrophages and by being an efferocytosis receptor, and by suppressing inflammation, we hypothesized that it might play a protective role against obesity. To our surprise, however, the loss of Mer protected mice against high-fat diet (HFD)-induced obesity. We report in this paper that Mer is also expressed by adipocytes of both white and brown adipose tissues, and while its activity facilitates adipocyte lipid storage both in vitro and in vivo in mice exposed to HFD, it simultaneously attenuates thermogenesis in the brown adipose tissue contributing to its ‘whitening’. Our data indicate that Mer is one of the adipocyte tyrosine kinase receptors, the activity of which contributes to the metabolic decision about the fate of excess lipids favoring their storage within the body.
Background: Astrocytoma, an IDH-mutant is a common primary brain tumor. Total surgical resection is not feasible due to peritumoral infiltration mediated by extracellular matrix (ECM) molecules. Methods: This study aimed at determining the expression pattern of ECM molecules in different prognostic groups of WHO grade 2 and grade 3 patients and identifying the effect of onco-radiotherapy on tumor cell invasion of grade 3 patients. Gene and protein expression of ECM molecules was determined by qRT-PCR and immunohistochemistry, respectively. Results: In the different prognostic groups of grade 2 tumors HMMR, IDH-1, MKI-67, PDGF-A and versican, in grade 3 tumors integrin α-3, and in both groups integrin α-3 and IDH-1 mRNA expression was significantly different. Regarding protein expression, only integrin αV expression changed significantly in the prognostic groups of grade 2 tumors. Conclusions: Based on the invasion spectrum determined by this joint gene and protein expression analysis, there was a sensitivity of 87.5% and a negative predictive value of 88.9% regarding the different prognostic groups of grade 2 astrocytoma. For grade 3 tumors, the applied standard oncotherapeutic modalities apparently lacked significant anti-invasive effects.