Interspecies reactivities of anti-human macrophage monoclonal antibodies to various animal species.

Zeng, Li; Takeya, Motohiro; Ling, Xinsheng; Nagasaki, Akitoshi; Takahashi, Kiyoshi

doi:10.1177/44.8.8756757

Cited by 36 publications

(34 citation statements)

References 3 publications

(6 reference statements)

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“…Slides were counterstained with eosin. The following primary antibodies were used for immunohistochemistry: goat anti-human polyclonal antibody to MCSF (Santa Cruz Biotechnology, Santa Cruz, CA), polyclonal antibody to c-Fms (Santa Cruz), mouse monoclonal antibody to proliferating cell nuclear antigen (PCNA; clone PC10, Dako; Carpinteria, CA) (13,14), monoclonal macrophage 387 (Mac387) antibody (Dako) (15), mouse anti-CD31 antibody (Dako) (13) anti-human antibody to collagen type III clone IV-4h12 (IGN Biomedicals; Aurora, OH) and monoclonal anti-macrophage antibody PM-2K (Biogenesis; Kingston, NH) (44). The Mac387 antibody detects an epitope on the calcium-binding protein MRP14 (17), which is highly expressed in monocytes and rapidly downregulated in mature macrophages (19).…”

Section: Methodsmentioning

confidence: 99%

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MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype

Frangogiannis

Mendoza

Ren

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Myocardial infarction is associated with the rapid induction of mononuclear cell chemoattractants that promote monocyte infiltration into the injured area. Monocyte-to-macrophage differentiation and macrophage proliferation allow a long survival of monocytic cells, critical for effective healing of the infarct. In a canine infarction-reperfusion model, newly recruited myeloid leukocytes were markedly augmented during early reperfusion (5-72 h). By 7 days, the number of newly recruited myeloid cells was reduced, and the majority of the inflammatory cells remaining in the infarct were mature macrophages. Macrophage colony-stimulating factor (MCSF) is known to facilitate monocyte survival, monocyte-to-macrophage conversion, and macrophage proliferation. We demonstrated marked induction of MCSF mRNA in ischemic segments persisting for at least 5 days after reperfusion. MCSF expression was predominantly localized to mature macrophages infiltrating the infarcted myocardium; the expression of the MCSF receptor, c-Fms, a protein with tyrosine kinase activity, was found in these macrophages but was also observed in a subset of microvessels within the infarct. Many infarct macrophages expressed proliferating cell nuclear antigen, a marker of proliferative activity. In vitro MCSF induced monocyte chemoattractant protein-1 synthesis in canine venous endothelial cells. MCSF-induced endothelial monocyte chemoattractant protein-1 upregulation was inhibited by herbimycin A, a tyrosine kinase inhibitor, and by LY-294002, a phosphatidylinositol 3Ј-kinase inhibitor. We suggest that upregulation of MCSF in the infarcted myocardium may have an active role in healing not only through its effects on cells of monocyte/ macrophage lineage, but also by regulating endothelial cell chemokine expression.inflammation; reperfusion; chemokine; growth factors; macrophage colony-stimulating factor REPERFUSED MYOCARDIAL INFARCTION is associated with an intense inflammatory response (7,21,27) leading to healing and scar formation (16). Mononuclear cell chemoattractants are rapidly induced in the infarcted area and mediate monocyte and lymphocyte recruitment (4, 11, 23). Differentiation of monocytes into macrophages is important for their survival, allowing them to actively participate in the repair process through the production of cytokines and growth factors. We hypothesized that monocytes in reperfused infarctions undergo a maturation process, regulated by the local expression of macrophage colony-stimulating factor (MCSF) (8, 38), a hematopoietic growth factor that induces survival, proliferation, differentiation, and activation of mononuclear phagocytes (40,41). Our experiments demonstrated a marked induction of MCSF mRNA in the infarcted areas, associated with evidence of macrophage proliferation in the healing infarct. We present evidence suggesting direct effects of MCSF on endothelial cell phenotype and activity, possibly mediated through c-Fms, resulting in upregulation of monocyte chemoattractant protein-1 (MCP-1). We suggest that local...

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Section: Methodsmentioning

confidence: 99%

“…It is known to cross-react with canine species (15). The monoclonal antibody PM-2K identifies mature macrophages and has been previously used in canine tissues (44). Appropriate positive and negative controls were used for each antibody.…”

Section: Methodsmentioning

confidence: 99%

MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype

Frangogiannis

Mendoza

Ren

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…26 To detect the BM-derived cells labeled with green fluorescence, samples were snap-frozen and cut with a cryostat. These were incubated with anti-desmin (clone DE-R-11, Dako), anti-vimentin (clone V9, Dako), anti-macrophage (PM-2K), 27 and anti-factor VIII antibody, followed by incubation with FITC-or TRITC-conjugated secondary antisera. The infarction area was evaluated by tetrazolium red staining.…”

Section: Immunohistochemistry and Analyses Of Vessel Numbersmentioning

confidence: 99%

Implantation of Bone Marrow Mononuclear Cells Into Ischemic Myocardium Enhances Collateral Perfusion and Regional Function via Side Supply of Angioblasts, Angiogenic Ligands, and Cytokines

et al. 2001

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Background-Bone marrow implantation (BMI) was shown to enhance angiogenesis in a rat ischemic heart model. This preclinical study using a swine model was designed to test the safety and therapeutic effectiveness of BMI. Methods and Results-BM-derived mononuclear cells (BM-MNCs) were injected into a zone made ischemic by coronary artery ligation. Three weeks after BMI, regional blood flow and capillary densities were significantly higher (4.6-and 2.8-fold, respectively), and cardiac function was improved. Angiography revealed that there was a marked increase (5.7-fold) in number of visible collateral vessels. Implantation of porcine coronary microvascular endothelial cells (CMECs) did not cause any significant increase in capillary densities. Labeled BM-MNCs were incorporated into Ϸ31% of neocapillaries and corresponded to Ϸ8.7% of macrophages but did not actively survive as myoblasts or fibroblasts.There was no bone formation by osteoblasts or malignant ventricular arrhythmia. Time-dependent changes in plasma levels for cardiac enzymes (troponin I and creatine kinase-MB) did not differ between the BMI, CMEC, and medium-alone implantation groups. BM-MNCs contained 16% of endothelial-lineage cells and expressed basic fibroblast growth factorӷvascular endothelial growth factorϾangiopoietin 1 mRNAs, and their cardiac levels were significantly upregulated by BMI. Cardiac interleukin-1␤ and tumor necrosis factor-␣ mRNA expression were also induced by BMI but not by CMEC implantation. BM-MNCs were actively differentiated to endothelial cells in vitro and formed network structure with human umbilical vein endothelial cells. Conclusions-BMI may constitute a novel safety strategy for achieving optimal therapeutic angiogenesis by the natural ability of the BM cells to secrete potent angiogenic ligands and cytokines as well as to be incorporated into foci of neovascularization.

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“…For immunostaining, these segments were immediately embedded in OCT compound without fixation, frozen, and cut into 5-m-thick slices. Serial cryosections were stained with an antibody to human macrophages (PM-2K) 28 or to rat MCP-1 (clone C4) 29 or nonimmune mouse IgG (Zymed Laboratory). In a preliminary study, we confirmed that those antibodies cross-react well with porcine macrophages and MCP-1, respectively.…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

Rho-Kinase Is Involved in Macrophage-Mediated Formation of Coronary Vascular Lesions in Pigs In Vivo

Miyata

Shimokawa

Kimura

et al. 2000

ATVB

182

153

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Abstract-We have previously shown that long-term treatment with an inflammatory cytokine from the adventitia causes the development of coronary vascular lesions, with the accumulation of macrophages. Recent studies in vitro have suggested that small G-protein Rho and its effector, Rho-kinase/ROK/ROCK, may be the key molecules for various cellular functions, including cell adhesion and movement. In this study, we examined whether adventitia-derived macrophages cause the formation of coronary vascular lesions in vivo and, if so, whether Rho-kinase is involved in the process. Porcine coronary segments from the adventitia were chronically treated with monocyte chemoattractant protein-1 alone, oxidized low density lipoprotein alone, or both. Vascular lesion formation (neointimal formation and development of vascular remodeling) was mostly enhanced at the coronary segment cotreated with monocyte chemoattractant protein-1 and oxidized low density lipoprotein, where the phosphorylation of myosin binding subunit of myosin phosphatase was increased, indicating an increased activity of Rho-kinase in vivo. Histological examination demonstrated that macrophages were accumulated at the adventitia and thereafter migrated into the vascular wall. Long-term oral treatment with fasudil, which is metabolized to a specific Rho-kinase inhibitor (hydroxyfasudil) after oral absorption, markedly inhibited the myosin binding subunit phosphorylation, the macrophage accumulation and migration, and the coronary lesion formation in vivo. These results indicate that Rho-kinase is involved in macrophage-mediated formation of coronary vascular lesions in our porcine model in vivo. (Arterioscler Thromb Vasc

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Interspecies reactivities of anti-human macrophage monoclonal antibodies to various animal species.

Cited by 36 publications

References 3 publications

MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype

MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype

Implantation of Bone Marrow Mononuclear Cells Into Ischemic Myocardium Enhances Collateral Perfusion and Regional Function via Side Supply of Angioblasts, Angiogenic Ligands, and Cytokines

Rho-Kinase Is Involved in Macrophage-Mediated Formation of Coronary Vascular Lesions in Pigs In Vivo

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