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NF‐κB‐inducing kinase is a key regulator of inflammation‐induced and tumour‐associated angiogenesis
Abstract Angiogenesis is essential during development and in pathological conditions such as chronic inflammation and cancer progression. Inhibition of angiogenesis by targeting vascular endothelial growth factor (VEGF) blocks disease progression, but most patients eventually develop resistance which may result from compensatory signalling pathways. In endothelial cells (ECs), expression of the pro‐angiogenic chemokine CXCL12 is regulated by non‐canonical nuclear factor (NF)‐κB signalling. Here, we report that NF‐κB‐inducing kinase (NIK) and subsequent non‐canonical NF‐κB signalling regulate both inflammat...
Source: The Journal of Pathology - August 28, 2014 Category: Pathology Authors: Ae R Noort, Katinka PM van Zoest, Ester M Weijers, Pieter Koolwijk, Chrissta X Maracle, Deborah V Novack, Martin J Siemerink, Reinier O Schlingemann, Paul P Tak, Sander W Tas Tags: Original Paper Source Type: research

NF‐κB inducing kinase is a key regulator of inflammation‐induced and tumor‐associated angiogenesis
Abstract Angiogenesis is essential during development and in pathological conditions such as chronic inflammation and cancer progression. Inhibition of angiogenesis by targeting vascular endothelial growth factor (VEGF) blocks disease progression, but most patients eventually develop resistance which may result from compensatory signaling pathways. In endothelial cells (EC) expression of the pro‐angiogenic chemokine CXCL12 is regulated by non‐canonical nuclear factor (NF)‐κB signaling. Here, we report that NF‐κB‐inducing kinase (NIK) and subsequent non‐canonical NF‐κB signaling regulates both inflammation�...
Source: The Journal of Pathology - July 9, 2014 Category: Pathology Authors: A.R. Noort, K.P.M. van Zoest, E.M. Weijers, P. Koolwijk, C.X. Maracle, D.V. Novack, M.J. Siemerink, R.O. Schlingemann, P.P. Tak, S.W. Tas Tags: Original Article Source Type: research

Differential regulation of HIF‐mediated pathways increases mitochondrial metabolism and ATP production in hypoxic osteoclasts.
Abstract Inappropriate osteoclast activity instigates pathological bone loss in rheumatoid arthritis. We have investigated how osteoclasts generate sufficient ATP for the energy‐intensive process of bone resorption in the hypoxic microenvironment associated with this rheumatic condition. We show that in human osteoclasts differentiated from CD14+ monocytes hypoxia (24h, 2% O2) (i) increases ATP production and mitochondrial electron transport chain activity (Alamar Blue, O2 consumption); (ii) increases glycolytic flux (glucose consumption, lactate production) and (iii) increases glutamine consumption. We demonstrate that ...
Source: The Journal of Pathology - January 1, 2013 Category: Pathology Authors: Karl J Morten, Luned Badder, Helen J Knowles Tags: Original Paper Source Type: research