Skip to main content
. 2022 Apr 4;12(7):3196–3216. doi: 10.7150/thno.71029

Figure 5.

Figure 5

Overexpression of neuronal PTRF reprograms phospholipid metabolism and regulates mitochondrial respiration via PLA2G4A. (A-B) The relative level of PC and LPC were determined by using ELISA kits in HT22 and primary neuronal cells after overexpression of PTRF and/or treated with AACOCF3 (HT22: 0.050 mM, primary neuronal cells: 0.010 mM, n = 5). (C) The relative levels of PC and LPC were determined by using ELISA kits in the ipsilateral penumbra of AAV-shRNA transfected mice co-treated with AACOCF3 (25 mg/kg body weight) after I/R injury. (D) OCR measurements of HT22 cells after overexpression of PTRF and/or treated with AACOCF3 (0.050 mM) using a Seahorse Analyzer. n = 3-5 replicates per group. (E) OCR measurements of basal respiration, proton leakage, and maximal respiration in HT22 cells. (F) Time series for OCR measurements of primary neuronal cells after overexpression of PTRF and/or treated with AACOCF3 (0.010 mM) using a Seahorse Analyzer. n = 3-5 replicates per group. (G) OCR measurements of basal respiration, proton leakage, and maximal respiration in primary neuronal cells. (H-I) The intracellular ATP concentration was determined by using an ATP determination kit in HT22 and primary neuronal cells after overexpression of PTRF and/or treated with AACOCF3, and the ATP levels were expressed as nmol/mg protein. (J) The ATP concentration was determined in the ipsilateral penumbra of AAV-shRNA transfected the I/R mice co-treated with AACOCF3 (25 mg/kg body weight) after I/R injury.