Skip to main content
. 2016 Aug 31;9:79. doi: 10.3389/fnmol.2016.00079

Figure 1.

Figure 1

Middle cerebral artery occlusion (MCAO) induces Enolase-phosphatase 1 (ENOPH1) upregulation in ischemic cerebral microvessels. Rats were subjected to 3 h MCAO before isolating hemispheric cerebral microvessels. The mRNA and protein levels of ENOPH1 in cerebral microvessels from nonischemic (Non-I) and ischemic (I) hemispheric tissue were analyzed by real-time RT-PCR and western blot. (A) Representative photographs of triphenyltetrazolium chloride (TTC) stained 1 mm-thick brain sections showing tissue infarction (pale white region) in the ischemic hemispheres (right). (B) Real-time RT-PCR analysis showed that ENOPH1 mRNA expression was significantly increased in ischemic hemispheric microvessels. *P < 0.05 vs. Non-I; n = 6. (C) Western blot analysis revealed increased levels of ENOPH1 protein in ischemic hemispheric microvessels. Upper panel: representative immunoblots of ENOPH1 and the loading control β-actin; bottom panel: quantitative data of protein band intensity after normalization to β-actin. *P < 0.05 vs. Non-I; n = 6.