OBJECTIVES: We characterized the transcriptional profiles of GM-CSF- (GM-MØ) and M-CSF-induced macrophages (M-MØ) and investigated in situ a subset of differentially expressed genes in human and mouse atherosclerotic lesions. METHODS AND RESULTS: Using microarrays we identified a number of genes and biological processes differentially regulated in M-MØ vs GM-MØ. By varying in culture the M-CSF/GM-CSF ratio (0-10), a spectrum of macrophage phenotypes was explored by RT-QPCR. M-CSF (10 ng/ml) stimulated expression of several genes, including selenoprotein-1 (SEPP1), stabilin-1 (STAB1) and CD163 molecule-like-1 (CD163L1) which was inhibited by a low dose of GM-CSF (1 ng/ml); M-CSF inhibited the expression of pro-platelet basic protein (PPBP) induced by GM-CSF. Combining tissue microarrays/quantitative immunohistochemistry of human aortic lesions with RT-QPCR expression data either from human carotids vs mammary non-atherosclerotic arteries or from the apoE null mice normal and atherosclerotic aortas showed that, STAB1, SEPP1 and CD163L1 (M-CSF-sensitive genes) and PPBP (GM-CSF-sensitive gene) were expressed in both human arterial and apoE null mice atherosclerotic tissues. CONCLUSION: A balance between M-CSF vs GM-CSF defines macrophage functional polarisation and may contribute to the progression of atherosclerosis.
OBJECTIVES: We characterized the transcriptional profiles of GM-CSF- (GM-MØ) and M-CSF-induced macrophages (M-MØ) and investigated in situ a subset of differentially expressed genes in human and mouseatherosclerotic lesions. METHODS AND RESULTS: Using microarrays we identified a number of genes and biological processes differentially regulated in M-MØ vs GM-MØ. By varying in culture the M-CSF/GM-CSF ratio (0-10), a spectrum of macrophage phenotypes was explored by RT-QPCR. M-CSF (10 ng/ml) stimulated expression of several genes, including selenoprotein-1 (SEPP1), stabilin-1 (STAB1) and CD163 molecule-like-1 (CD163L1) which was inhibited by a low dose of GM-CSF (1 ng/ml); M-CSF inhibited the expression of pro-platelet basic protein (PPBP) induced by GM-CSF. Combining tissue microarrays/quantitative immunohistochemistry of human aortic lesions with RT-QPCR expression data either from human carotids vs mammary non-atherosclerotic arteries or from the apoE null mice normal and atherosclerotic aortas showed that, STAB1, SEPP1 and CD163L1 (M-CSF-sensitive genes) and PPBP (GM-CSF-sensitive gene) were expressed in both human arterial and apoE null miceatherosclerotic tissues. CONCLUSION: A balance between M-CSF vs GM-CSF defines macrophage functional polarisation and may contribute to the progression of atherosclerosis.
Authors: Nikita G Nikiforov; Natalia V Elizova; Michael Bukrinsky; Larisa Dubrovsky; Vsevolod J Makeev; Yoshiyuki Wakabayashi; Poching Liu; Kathy K Foxx; Howard S Kruth; Xueting Jin; Emile R Zakiev; Alexander N Orekhov Journal: Curr Pharm Des Date: 2017 Impact factor: 3.116
Authors: Jian-Da Lin; Hitoo Nishi; Jordan Poles; Xiang Niu; Caroline Mccauley; Karishma Rahman; Emily J Brown; Stephen T Yeung; Nikollaq Vozhilla; Ada Weinstock; Stephen A Ramsey; Edward A Fisher; P'ng Loke Journal: JCI Insight Date: 2019-02-21
Authors: Sina Tavakoli; John D Short; Kevin Downs; Huynh Nga Nguyen; Yanlai Lai; Wei Zhang; Paul Jerabek; Beth Goins; Mehran M Sadeghi; Reto Asmis Journal: Radiology Date: 2016-11-16 Impact factor: 11.105
Authors: Jacklyn N Hellwege; Nicholette D Palmer; Julie T Ziegler; Carl D Langefeld; Carlos Lorenzo; Jill M Norris; Toshinari Takamura; Donald W Bowden Journal: Gene Date: 2013-10-24 Impact factor: 3.688