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10.1161/ATVBAHA.114.304454 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.114.304454 25614279!ä!25614279 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25614279.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Arterioscler+Thromb+Vasc+Biol 2015 ; 35 (3): 547-57 Nephropedia Template TP {{tp|p=25614279|t=2015. Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascular inflammation and atherogenesis |pdf=|usr=}}{{25614279}} gab.com Text Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascular inflammation and atherogenesis JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25614279 #FOAvip OBJECTIVE: Atherosclerosis, an inflammatory disease of arterial vessel walls, requires migration and matrix metalloproteinase (MMP)-9-dependent invasion of monocytes/macrophages into the vascular wall. MMP-9 expression is stimulated by transcription factor nuclear factor-kappaB, which is regulated by inhibitor kappaB (IkappaB) and thus IkappaB kinase. Regulators of nuclear factor-kappaB include serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored involvement of SGK1 in vascular inflammation and atherogenesis. APPROACH AND RESULTS: Gene-targeted apolipoprotein E (ApoE)-deficient mice without (apoe(-/-)sgk1(+/+)) or with (apoe(-/-)sgk1(-/-)) additional SGK1 knockout received 16-week cholesterol-rich diet. According to immunohistochemistry atherosclerotic lesions in aorta and carotid artery, vascular CD45(+) leukocyte infiltration, Mac-3(+) macrophage infiltration, vascular smooth muscle cell content, MMP-2, and MMP-9 positive areas in atherosclerotic tissue were significantly less in apoe(-/-)sgk1(-/-)mice than in apoe(-/-)sgk1(+/+)mice. As determined by Boyden chamber, thioglycollate-induced peritonitis and air pouch model, migration of SGK1-deficient CD11b(+)F4/80(+) macrophages was significantly diminished in vitro and in vivo. Zymographic MMP-2 and MMP-9 production, MMP-9 activity and invasion through matrigel in vitro were significantly less in sgk1(-/-) than in sgk1(+/+)macrophages and in control plasmid-transfected or inactive (K127N)SGK1-transfected than in constitutively active (S422D)SGK1-transfected THP-1 cells. Confocal microscopy revealed reduced macrophage number and macrophage MMP-9 content in plaques of apoe(-/-)sgk1(-/-) mice. In THP-1 cells, MMP-inhibitor GM6001 (25 mumol/L) abrogated (S422D)SGK1-induced MMP-9 production and invasion. According to reverse transcription polymerase chain reaction, MMP-9 transcript levels were significantly reduced in sgk1(-/-)macrophages and strongly upregulated in (S422D)SGK1-transfected THP-1 cells compared with control plasmid-transfected or (K127N)SGK1-transfected THP-1 cells. According to immunoblotting and confocal microscopy, phosphorylation of IkappaB kinase and inhibitor kappaB and nuclear translocation of p50 were significantly lower in sgk1(-/-)macrophages than in sgk1(+/+)macrophages and significantly higher in (S422D)SGK1-transfected THP-1 cells than in control plasmid-transfected or (K127N)SGK1-transfected THP-1 cells. Treatment of (S422D)SGK1-transfected THP-1 cells with IkappaB kinase-inhibitor BMS-345541 (10 mumol/L) abolished (S422D)SGK1-induced increase of MMP-9 transcription and gelatinase activity. CONCLUSIONS: SGK1 plays a pivotal role in vascular inflammation during atherogenesis. SGK1 participates in the regulation of monocyte/macrophage migration and MMP-9 transcription via regulation of nuclear factor-kappaB. Twit Text FOAVip Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascular inflammation and atherogenesis ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25614279 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25614279 #FOAvip English Wikipedia <ref>{{Cite pmid|25614279}}</ref> Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascular inflammation and atherogenesis #MMPMID25614279 Borst O; Schaub M; Walker B; Schmid E; Munzer P; Voelkl J; Alesutan I; Rodriguez JM; Vogel S; Schoenberger T; Metzger K; Rath D; Umbach A; Kuhl D; Muller II; Seizer P; Geisler T; Gawaz M; Lang F Arterioscler Thromb Vasc Biol 2015[Mar]; 35 (3): 547-57 PMID25614279show ga OBJECTIVE: Atherosclerosis, an inflammatory disease of arterial vessel walls, requires migration and matrix metalloproteinase (MMP)-9-dependent invasion of monocytes/macrophages into the vascular wall. MMP-9 expression is stimulated by transcription factor nuclear factor-kappaB, which is regulated by inhibitor kappaB (IkappaB) and thus IkappaB kinase. Regulators of nuclear factor-kappaB include serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored involvement of SGK1 in vascular inflammation and atherogenesis. APPROACH AND RESULTS: Gene-targeted apolipoprotein E (ApoE)-deficient mice without (apoe(-/-)sgk1(+/+)) or with (apoe(-/-)sgk1(-/-)) additional SGK1 knockout received 16-week cholesterol-rich diet. According to immunohistochemistry atherosclerotic lesions in aorta and carotid artery, vascular CD45(+) leukocyte infiltration, Mac-3(+) macrophage infiltration, vascular smooth muscle cell content, MMP-2, and MMP-9 positive areas in atherosclerotic tissue were significantly less in apoe(-/-)sgk1(-/-)mice than in apoe(-/-)sgk1(+/+)mice. As determined by Boyden chamber, thioglycollate-induced peritonitis and air pouch model, migration of SGK1-deficient CD11b(+)F4/80(+) macrophages was significantly diminished in vitro and in vivo. Zymographic MMP-2 and MMP-9 production, MMP-9 activity and invasion through matrigel in vitro were significantly less in sgk1(-/-) than in sgk1(+/+)macrophages and in control plasmid-transfected or inactive (K127N)SGK1-transfected than in constitutively active (S422D)SGK1-transfected THP-1 cells. Confocal microscopy revealed reduced macrophage number and macrophage MMP-9 content in plaques of apoe(-/-)sgk1(-/-) mice. In THP-1 cells, MMP-inhibitor GM6001 (25 mumol/L) abrogated (S422D)SGK1-induced MMP-9 production and invasion. According to reverse transcription polymerase chain reaction, MMP-9 transcript levels were significantly reduced in sgk1(-/-)macrophages and strongly upregulated in (S422D)SGK1-transfected THP-1 cells compared with control plasmid-transfected or (K127N)SGK1-transfected THP-1 cells. According to immunoblotting and confocal microscopy, phosphorylation of IkappaB kinase and inhibitor kappaB and nuclear translocation of p50 were significantly lower in sgk1(-/-)macrophages than in sgk1(+/+)macrophages and significantly higher in (S422D)SGK1-transfected THP-1 cells than in control plasmid-transfected or (K127N)SGK1-transfected THP-1 cells. Treatment of (S422D)SGK1-transfected THP-1 cells with IkappaB kinase-inhibitor BMS-345541 (10 mumol/L) abolished (S422D)SGK1-induced increase of MMP-9 transcription and gelatinase activity. CONCLUSIONS: SGK1 plays a pivotal role in vascular inflammation during atherogenesis. SGK1 participates in the regulation of monocyte/macrophage migration and MMP-9 transcription via regulation of nuclear factor-kappaB. |*Chemotaxis[MESH] |Active Transport, Cell Nucleus[MESH] |Animals[MESH] |Aorta/enzymology/pathology[MESH] |Aortic Diseases/*enzymology/genetics/pathology[MESH] |Apolipoproteins E/deficiency/genetics[MESH] |Atherosclerosis/*enzymology/genetics/pathology[MESH] |Carotid Arteries/enzymology/pathology[MESH] |Carotid Artery Diseases/*enzymology/genetics/pathology[MESH] |Cell Line[MESH] |Disease Models, Animal[MESH] |Gene Expression Regulation, Enzymologic[MESH] |Humans[MESH] |I-kappa B Kinase/metabolism[MESH] |I-kappa B Proteins/metabolism[MESH] |Immediate-Early Proteins/deficiency/genetics/*metabolism[MESH] |Inflammation/*enzymology/genetics/pathology[MESH] |Macrophages/enzymology/pathology[MESH] |Male[MESH] |Matrix Metalloproteinase 2/metabolism[MESH] |Matrix Metalloproteinase 9/genetics/metabolism[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Mutation[MESH] |NF-kappa B p50 Subunit/metabolism[MESH] |Peritonitis/chemically induced/enzymology/genetics[MESH] |Plaque, Atherosclerotic[MESH] |Protein Serine-Threonine Kinases/deficiency/genetics/*metabolism[MESH] |Signal Transduction[MESH] |Thioglycolates[MESH] |Transcription, Genetic[MESH] |Transfection[MESH]Pivotal role of serum- and glucocorticoid-inducible kinase 1 in vascul(epmc).pdf DeepDyve Pubget Overpricing