Renal protection from ischemia mediated by A_2A adenosine receptors on bone marrow–derived cells
J. Clin. Invest. Yuan-Ji Day, et al. 112:883 doi:10.1172/JCI15483 [Go to this article.]

Figure 1
Genotyping and phenotyping mice for the A_2AR gene. (a) Ethidium bromide–stained PCR amplification products of tail-clip DNA from WT (A_2A^+/+) and A_2A-KO (A_2A^–/–) mice. The A_2A-KO allele was identified by PCR of the inserted neomycin resistance cassette using oligonucleotide primers (see Methods) NEO-F and NEO-R and yielding a 618-bp product. The A_2A WT allele was identified by PCR of a portion of the WT A_2AR gene that was deleted from the KO construct using primers WT-F and WT-R and yielding a 163-bp band. +/+, WT; +/–, heterozygous; –/–, homozygous A_2A-KO. Each lane represents PCR products from individual mice. (b) Immunohistochemical localization of A_2AR in mouse forebrain sections. In the WT brain sections (top), dense A_2AR-like immunoreactivity is present in the striatum (caudate putamen) and extends through the cell bridges of the striatum (arrow) to the olfactory tubercles on the ventral surface of the brain. In A_2A-KO brain (bottom), specific immunoreactivity is completely absent. Scale bar, 1 mm. CPu, caudate putamen; Tu, tubercles; cc, corpus callosum. (c) Effect of ATL146e in A_2A-KO mice. A_2A-KO mice were subjected to IRI (see Methods). The rise in plasma creatinine after ATL146e was similar to that after vehicle administration (n = 6, not significant). Values are means ± SE.