Fig 1: P. aeruginosa induces MCT-dependent elevation of lactate and ASL acidification in CFBE.(A) CF HBE ASL pH and G. ASL Lactate concentration after 6 hours in HCO3−-buffered basolateral salt solution containing 5 mM D-glucose in the absence (CF HBE only) or presence of 1 × 106 CFU apical PA01 (+PA01), or 100 nM MCT2 inhibitor AR-C155858 (ARC). *P < 0.05, **P < 0.01, n = 5. Data represent the means ± S.E.M.
Fig 2: Hyperglycaemia increases airway surface liquid (ASL) glucose and monocarboxylate transporter (MCT)-dependent concentrations in primary airway epithelial cultures.(A) Glucose concentration of ASL from non-CF and CF primary HBE cell monolayers after 6 hours in the presence of basolateral 5 mM or 15 mM D-glucose. Lactate concentration of ASL from primary HBE cell (B) H441 (C) and Calu-3 (D) monolayers after 6 hours in the presence of basolateral 5 mM or 15 mM D-glucose in the absence or presence of 100 nM MCT2 inhibitor AR-C15585 (ARC) and 50 μM phloretin (PT). ns P > 0.05, *P < 0.05, **P < 0.01, n = 5–13. Data represent the means ± S.E.M.
Fig 3: Hyperglycaemia induces MCT-dependent ASL acidification in airway epithelial cultures lacking CFTR-dependent bicarbonate secretion.(A) H441 ASL pH after 6 hours in 5 or 15 mM basolateral D-glucose, in the absence or presence of 100 nM MCT2 inhibitor AR-C155858 (ARC) *P < 0.05, **P < 0.01, n = 5. (B) Calu-3 ASL pH after 6 hours in HCO3− or HEPES-buffered basolateral salt solution containing 5 or 15 mM D-glucose, in the absence or presence of 100 nM AR-C155858 (ARC) *P < 0.05, n = 9. (C) HBE or CF HBE ASL pH after 6 hours in 5 or 15 mM basolateral D-glucose, in the absence or presence of 100 nM AR-C155858 (ARC) *P < 0.05, n = 5. Data represent the means ± S.E.M.
Fig 4: Distribution of immunoreactivities for MCT1 (a–c), MCT2 (d–f), MCT4 (g–i), MCT3 (j,k), MCT5 (l,m), MCT8 (n,o), and HCA1-R (p,q), in autopsied human brains. Immunohistochemical findings from cases 1 (g), 3 (a,h,j,k,m,p), 4, (c,f,i), 5 (b,d,l), 6 (e,q), and 8 (n,o) are shown. Immunohistochemical images in microvessels indicated by thin arrows in hippocampal samples are shown in (a,d,f,g,n,p), whereas images in epithelial cells of CP located in lateral ventricles indicated by thick arrows are shown in (b,e,h,k,o,q). Immunohistochemical images in reactive astrocytes in hippocampal samples indicated by short arrows are shown in (c,f,i), whereas MCT2 immunostaining in neurons in hippocampal samples indicated by double arrows is shown in (d). No MCT3 immunostaining in microvessels is shown in (j), whereas no MCT5 immunostaining in microvessels and CPEs is shown in (l,m). Scale bars indicate 20 μm.
Fig 5: Protein expression level of MCT1, MCT2, MCT4, and HIF-1α in normoxia and hypoxia. (A) Western blot analysis of MCT1, MCT2, MCT4, and HIF-1α in normoxia and hypoxia in A549 cells. The protein expression levels of MCT1 (B), MCT2 (C), MCT4 (D), and HIF-1α (E) were visualized, respectively. Data are presented as mean ± standard error of three independent experiments. *p < 0.05 compared with the normoxia using unpaired Student’s t test.
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