The chemokine receptor CXCR2 is differentially regulated on glial cells in vivo but is not required for successful remyelination after cuprizone-induced demyelination

✍ Scribed by Maren Lindner; Corinna Trebst; Sandra Heine; Thomas Skripuletz; Paraskevi N. Koutsoudaki; Martin Stangel

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 29 KB
• Volume: 57
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.20833

✦ Synopsis

After publication of our manuscript, we have been informed that the antibody against the chemokine receptor CXCR2 (sc-683, Santa Cruz Biotechnology) used in our study is of questionable specificity. Although there was clear positive staining of cells in our experiments (as shown in Fig. 2 H) another group was apparently not able to stain CNS tissue specifically for CXCR2 with the same antibody and other available antibodies and proposed that the staining was not specific. We were not aware of this problem when performing the experiments. Nonetheless, our results are quite compatible with other published results showing that CXCR2 is constitutively expressed on oligodendrocytes and upregulated on microglia upon activation in traumatic or ischemic lesions. Although we could demonstrate that there was upregulation of the antigen recognised by the questionable antibody on microglia it is now not clear if this was indeed CXCR2. Therefore, our data in Figure 3 and Table 1, and the conclusion that CXCR2 was upregulated in cuprizone induced lesions on microglial cells might not be correct. However, the main finding in our paper that CXCR2 expression was not required for successful remyelination is not affected by this new information as this was generated in a different set of experiments with CXCR2 knock out mice.