Figure 1.
Posttraumatic production of CCL2 by the lateral ventricle choroid plexus (CP). (A) Temporal changes in CCL2 mRNA in the ipsilateral CP (Ipsi CP) compared with the contralateral CP (Contr CP) and the CP from sham-injured rats (Sham) (n=9 to 10 rats per time point). These data were obtained by real-time reverse transcriptase polymerase chain reaction (RT-PCR). The number of copies of transcripts for CCL2 relative to the message for cyclophilin A (Cycl-A) is shown. Data represent mean values±s.e.m. **P<0.01 for the ipsilateral versus contralateral CP (Newman–Keuls test). ††P<0.01 for the ipsilateral CP versus the CP from sham-injured rats (Newman–Keuls test). (B) Western blot analysis of choroidal synthesis of CCL2. The CPs were collected at 6 hours after sham injury or traumatic brain injury (TBI) (n=4 rats per group). Data from two independent groups of injured rats, group 1 and group 2 (Grp 1 and Grp 2, respectively), are shown. Consistent with RT-PCR analysis, a band (arrow) with the same apparent molecular weight as recombinant rat CCL2 (St; 1 ng) was detected in the ipsilateral CP. This band was not present in protein extracts from the contralateral CP or the CP collected from sham-injured animals (30 μg per lane). The recombinant rat CCL2 was run on the same gel, but was detected with five times lower concentration of anti-CCL2 antibody. α-Tub is α-tubulin (10 μg of total protein was loaded per lane to be probed with anti-α-tubulin antibody). C, I, and S are contralateral and ipsilateral CPs, and the CPs collected from sham-injured rats, respectively. (C) The levels of CCL2 in the cerebrospinal fluid (CSF) from injured (TBI) versus sham-injured rats (Sham) (n=8 to 11 per group). The samples of CSF were collected from the cisterna magna at 6 hours after TBI. Data represent mean values±s.e.m. ††P<0.01 for injured versus sham-injured rats (Student's t-test).