Monocyte Chemoattractant Protein 1 (Mcp-1) Gene Expression in Dilated Cardiomyopathy

Lehmann, Michael H.; Kühnert, H; Muller, Sigfrid A.; Sigusch, Holger H.

doi:10.1006/cyto.1998.0354

Cited by 42 publications

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“…CCL2/MCP-1 is known to play an important role in the pathogenesis of severe diseases affecting the brain (Mahad and Ransohoff, 2003), heart (Kolattukudy et al, 1998;Lehmann et al, 1998), kidney (Viedt and Orth, 2002), skeletal muscle (Liprandi et al, 1999;Sell et al, 2006) and lung (Rose et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Amplification of CCL2/MCP-1 and GAPDH cDNAs were performed as described (Lehmann et al, 1998;Lehmann et al, 2002). Accordingly, human CCR2A (MCP-1RA) was amplified using the sense primer 5Ј-GGC TCA CTC TGC TGC AAA TG-3Ј and the antisense primer 5Ј-TCT TTC CTG GTC TCA CTC CTG G-3Ј, and HIV-1 Nef was amplified using the sense primer 5Ј-GGA GCA ATC ACA AGT AGC AA-3Ј and the antisense primer 5Ј-ATC AGG GAA GTA GCC TTG TG-3Ј.…”

Section: Reverse Transcriptase-pcr (Rt-pcr)mentioning

confidence: 99%

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HIV-1 Nef upregulates CCL2/MCP-1 expression in astrocytes in a myristoylation- and calmodulin-dependent manner

Lehmann

Masanetz

Krämer

et al. 2006

Journal of Cell Science

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27 kDa accessory HIV and simian immunodeficiency virus (SIV) protein necessary for efficient virus replication and high viral load, has for several years been considered as a progression factor to AIDS (Greene and Peterlin, 2002). According to several excellent reviews, a variety of diverse functions including downregulation of cell-surface molecules have been assigned to the protein (Das and Jameel, 2005;Piguet and Trono, 1999;Roeth and Collins, 2006). Moreover, HIV-associated dementia (HAD) correlates with infiltration of monocytes into the brain. The accessory HIV-1 negative factor (Nef) protein, which modulates several signaling pathways, is constitutively present in persistently infected astroctyes. We demonstrated that monocytes responded with chemotaxis when subjected to cell culture supernatants of nef-expressing astrocytic U251MG cells. Using a protein array, we identified CC chemokine ligand 2/monocyte chemotactic protein-1 (CCL2/MCP-1) as a potential chemotactic factor mediating this phenomenon. CCL2/MCP-1 upregulation by Nef was further confirmed by ribonuclease protection assay, RT-PCR and ELISA. By applying neutralizing antibodies against CCL2/MCP-1 and using CCR2-deficient monocytes, we confirmed CCL2/MCP-1 as the exclusive factor secreted by nefexpressing astrocytes capable of attracting monocytes. Additionally, we showed that Nef-induced CCL2/MCP-1 expression depends on the myristoylation moiety of Nef and requires functional calmodulin. In summary, we suggest that Nef-induced CCL2/MCP-1 expression in astrocytes contributes to infiltration of monocytes into the brain, and thereby to progression of HAD.

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Section: Discussionmentioning

confidence: 99%

Section: Reverse Transcriptase-pcr (Rt-pcr)mentioning

confidence: 99%

HIV-1 Nef upregulates CCL2/MCP-1 expression in astrocytes in a myristoylation- and calmodulin-dependent manner

Lehmann

Masanetz

Krämer

et al. 2006

Journal of Cell Science

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“…Some clinical studies demonstrated the expression of mRNA of MCP-1 in dilated cardiomyopathy. Seino et al [33] and Lehmann et al [14] have shown the expression of MCP-1 mRNA in endomyocardial biopsy specimens from patients with dilated cardiomyopathy and suggested an important role of this chemokine in the regulation of inflammatory cell infiltration into the myocardium. MCP-1 may act on postmyocarditis ventricular remodeling or on the pathogenesis of chronic ongoing myocarditis.…”

Section: Discussionmentioning

confidence: 99%

Enhanced expression and production of monocyte chemoattractant protein-1 in myocarditis

Fuse

Kodama

Hanawa

et al. 2001

Clinical and Experimental Immunology

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SUMMARYMonocyte chemoattractant protein-1 (MCP-1) is a member of the C-C chemokine family that has been shown to play a major role in the migration of monocytes and T cells to an inflammatory focus. To clarify the role of MCP-1 in the pathogenesis of myocarditis, we have examined the expression of MCP-1 in rat hearts with experimental autoimmune myocarditis (EAM), and have also measured serum levels of MCP-1 in patients with histology-proven acute myocarditis. Lewis rats were immunized with cardiac myosin and were killed 9,12,15,18,21,24,27,30,33, 36, 42 and 56 days after immunization. Large mononuclear cells in the myocardial interstitium were stained with an anti-MCP-1 antibody. mRNA of MCP-1 increased in the hearts of EAM rats from days 15±27 as shown by quantitative reverse transcription-polymerase chain reaction. Serum MCP-1 levels of the rats with EAM were significantly elevated from days 15±24. In the clinical study, serum levels of MCP-1 in 24 patients with acute myocarditis at the time of admission (165´2^55´8 pg/ml) were significantly (P 0´0301) elevated compared with those of 20 healthy volunteers (61´8^10´7 pg/ml). Serum MCP-1 levels of 8 fatal cases (371´8^145´2 pg/ml) were significantly (P 0´0058) higher than those of 16 cases who survived (65´5^12´8 pg/ml). In conclusions, MCP-1 may play an important role in the pathogenesis of human acute myocarditis as well as in the progression of rat EAM.

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“…This leads to the hypothesis that non-cardiomyocytes are targets of FGF23. Another heart failure phenotype showing macrophage infiltration and increased MCP-1 levels is dilated cardiomyopathy (DCM) [6,[25][26][27][28]. DCM occurs in the absence of a coronary, valvular, congenital or a pericardial disease and ventricles show dilation and impaired systolic function [26].…”

Section: Fgf23 Is Present In Cardiomyocytes Of Patients With Ischemicmentioning

confidence: 99%

Oncostatin M Induces FGF23 Expression in Cardiomyocytes

Richter¹,

Polyakova²,

Gajawada³

2012

J Clin Exp Cardiolog

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Background: It is well-known that elevated levels of Fibroblast Growth Factor-23 (FGF23), a bone derived hormone, in circulation are associated with renal failure. Recent studies emphasize the correlation between Heart Failure (HF) and FGF23, but the ability of cardiomyocytes themselves to express and secrete this phosphatonin is yet unknown. A further factor involved in HF is the cytokine oncostatin M (OSM). The aims of our study were: 1) to analyze the myocardium of HF patients in terms of FGF23 expression in cardiomyocytes and 2) to assess whether OSM is able to induce FGF23 production in cardiomyocytes. Methods:Cultures of adult cardiomyocytes were treated with OSM and screened for the expression of FGF23 transcripts. FGF23 secretion was determined by Western blot and ELISA of cell culture supernatants. Heart explants of HF patients with Dilated Cardiomyopathy (DCM), Ischemic Cardiomyopathy (ICM) and myocarditis (Myo) were analyzed by immunofluorescence using FGF23 antibodies and compared with healthy controls. FGF23 levels were also determined in mice with a cardiac restricted overexpression of Monocyte Chemotactic Protein-1 (MCP1), which developed an "inflammatory" Heart Failure (iHF) due to macrophage infiltration.Results: OSM massively induced the expression and secretion of FGF23 in cultured adult cardiomyocytes. Confocal microscopy revealed high amounts of FGF23 positive cardiomyocytes in the myocardium of patients with ischemic heart disease (IHD), myocarditis, dilated cardiomyopathy (DCM) and in mice with iHF. Conclusions:The presence of FGF23 in the myocardium of patients with different types of HF and in mice with "inflammatory" HF suggests that macrophages are responsible for the FGF23 expression in cardiomyocytes via OSM. Whether FGF23 acts as a regeneration promoting factor and/or potentially serves as a HF/transplantation marker has to be clarified.

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Monocyte Chemoattractant Protein 1 (Mcp-1) Gene Expression in Dilated Cardiomyopathy

Cited by 42 publications

References 0 publications

HIV-1 Nef upregulates CCL2/MCP-1 expression in astrocytes in a myristoylation- and calmodulin-dependent manner

HIV-1 Nef upregulates CCL2/MCP-1 expression in astrocytes in a myristoylation- and calmodulin-dependent manner

Enhanced expression and production of monocyte chemoattractant protein-1 in myocarditis

Oncostatin M Induces FGF23 Expression in Cardiomyocytes

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