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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Mol Cancer Ther. 2012 Aug 6;11(11):2516–2525. doi: 10.1158/1535-7163.MCT-12-0494

Figure 4. Mouse serum quickly diminishes wtCXCL12 function whereas CXCL122 remains active for at least 24 hours.

Figure 4

(A) Degradation of 10 nM wtCXCL12 and CXCL122 were monitored by ELISA in the presence of mouse serum (n=3). Representative of 2 independent experiments with similar results. (B) WtCXCL12 (initial starting concentration, 10 nM) degradation monitored in the presence of a protease inhibitor cocktail (cOmplete, Mini, EDTA-free (Roche); n=3). (C) Degradation of CXCL122 (initial starting concentration, 10 nM) was monitored in the presence of protease inhibitors. Negative control (labeled “−”) contained no chemokine but contained 1% mouse serum (n=3). (D) WtCXCL12-induced chemotaxis as a function of time the chemokine is incubated with 90% mouse serum (n=3). (E) Inhibition of 10 nM wtCXCL12-induced migration by either 10 nM or 100 nM CXCL122 incubated with 90% mouse serum for indicated time. Chemotaxis assays were performed using THP-1 monocyte cells (n=3). Negative control (labeled “−”) contained no CXCL122 but contained 10 nM wtCXCL12 and 1% mouse serum. As a positive control (labeled “fresh”), the indicated chemokines were incubated only with 1% mouse serum, which did not result in degradation (data not shown).