Sections were stained for NF-kB using a p65 antibody

selves [19�21], but also controls the activity of regulatory factors like the Arp2/3 protein complex [22,23], or upstream signaling such as the ROCK/Rho-GTPase pathway [24]. The idea that actin remodeling is a major cellular energy drain is corroborated by the observation that actin filaments are stabilized under conditions of global ATP-depletion in order to prevent ATP-hydrolysis within the filament and, thereby, ATP-consumption [25,26]. Besides ATP availability [27,28], intracellular pH and NAD(P)+/NAD(P)H ratio are other key metabolic parameters that influence actin network dynamics and cell motility [29], either by modifying actin itself [30�32] or by regulating the activity of proteins such as the actin depolymerizing factor cofilin, mical, and the actin severing protein gelsolin [33�35]. In most mammalian cells, production of ATP, NAD+/NADH, and H+ is dominated by carbohydrate catabolism via glycolysis and mitochondrial TCA cycle/oxidative phosphorylation (OXPHOS) pathways. Importantly, various glycolytic pathway enzymes that handle these metabolites/cofactors appear compartmentalized and are found associated with the actin cytoskeleton and with actin dependent cellular structures, such as pseudopodia, membrane ruffles, and lamellipodia [36�39]. Indeed, this coupling helps to explain the dependency of cell motility on glycolysis [40,41]. Also phagocytosis by macrophages depends on glycolysis [42�44], but not much MedChemExpress 518303-20-3 PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19653627 work has been done to study this association in detail. Seeing their vital role in host defense and maintenance of tissue homeostasis and their surprising versatility in adaptation of functioning in many different tissue environments, we wondered whether there is a link between the activation of glucose met