Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury
J. Clin. Invest. Lixin Sun, et al. 113:1364
doi:10.1172/JCI20001 [Go to this article.]

Figure 1
SCF induced by “freeze” injury to the brain. (A) Schematic illustration of “freeze” injury. Blue arrow indicates the insertion track of the precooled needle. Red lines separate the forebrain into injured and uninjured hemispheres and divide the hemispheres into its dorsal and ventral halves. CX, cortex; CPu, caudate putamen (striatum); CC, corpus callosum; LV, lateral ventricle. (B) Custom microarray confirms increased SCF message in the injured brain at day 5. The cDNA clones from SSH library were loaded individually onto duplicate nitrocellulose filters, one hybridized by the injured brain_derived cDNAs (Injury) and another hybridized by contralateral control (Control). Membranes with the SCF gene are shown, and the SCF spots are marked with red and blue circles. Actin and GAPDH are shown as green and black circles, respectively. SCF images are stronger in the injured brain_derived cDNA_hybridized blot than the control. (C) Quantitative RT-PCR. Fold induction of SCF mRNA in “freeze”-injured forebrain 5 days after injury compared with the uninjured contralateral side (P < 0.05). The SCF mRNAs were individually normalized to levels of 18S RNA. (D) Time-dependent changes in SCF protein induction after “freeze” brain injury, as measured by Western blot, using uninjured forebrain as a control. Two major bands were present, representing the transmembrane form of SCF (33 kDa) and the cleaved, soluble form of SCF (19 kDa). (E) Quantification of SCF expression by computer densitometry. The band intensities of SCF were normalized to those of β-tubulin.