Immunoprecipitation studies of monoclonal antibodies submitted to the Second International Swine CD Workshop

Aasted, Bent; Gori, K.; Dominguez, J.; Ezquerra, Ángel; Bullido, R; Arn, Scott; Bianchi, A.T.J.; Binns, R. M.; Chu, Ruiai; Davis, William C.; Denham, S.; Haverson, Karin; Jensen, Kjeld Truberg; Kim, Y.B; Magyar, Anna; Petersen, K.R; Saalmüller, Armin; Sachs, David H.; Schütt, Christine; Shimizu, Mitsugu; Stokes, C.; Whittall, Trevor; Yang, Huan; Zuckermann, Federico A.

doi:10.1016/s0165-2427(97)00099-8

Cited by 14 publications

(2 citation statements)

References 2 publications

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“…1C, these lesions also have a core of macrophage foam cells, as judged by the positive staining using a porcine macrophage antibody. This antibody recognizes an unknown antigen expressed by porcine macrophages (16). There are many PCNApositive cells that have entered the cell cycle in these lesions (Fig.…”

Section: Resultsmentioning

confidence: 99%

Diabetes Accelerates Smooth Muscle Accumulation in Lesions of Atherosclerosis

et al. 2001

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In combination with other factors, hyperglycemia may cause the accelerated progression of atherosclerosis in people with diabetes. Arterial smooth muscle cell (SMC) proliferation and accumulation contribute to formation of advanced atherosclerotic lesions. Therefore, we investigated the effects of hyperglycemia on SMC proliferation and accumulation in vivo and in isolated arteries and SMCs by taking advantage of a new porcine model of diabetes-accelerated atherosclerosis, in which diabetic animals are hyperglycemic without receiving exogenous insulin. We show that diabetic animals fed a cholesterol-rich diet, like humans, develop severe lesions of atherosclerosis characterized by SMC accumulation and proliferation, whereas lesions in nondiabetic animals contain fewer SMCs after 20 weeks. However, high glucose (25 mmol/l) does not directly stimulate the proliferation of SMCs in isolated arterial tissue from diabetic or nondiabetic animals, or of cultured SMCs from these animals or from humans. Furthermore, the mitogenic actions of platelet-derived growth factor, IGF-I, or serum are not enhanced by high glucose. High glucose increases SMC glucose metabolism through the citric acid cycle and the pentose phosphate pathway by 240 and 90%, respectively, but <10% of consumed glucose is metabolized through these pathways. Instead, most of the consumed glucose is converted into lactate and secreted by the SMCs. Thus, diabetes markedly accelerates SMC proliferation and accumulation in atherosclerotic lesions. The stimulatory effect of diabetes on SMCs is likely to be mediated by effects secondary to the hyperglycemic state. Diabetes 50:851-860, 2001 I t is estimated that 75-80% of adults with diabetes die from complications of atherosclerosis. The progression of atherosclerotic lesions is accelerated by diabetes (1). Thus, stroke, coronary heart disease, and peripheral arterial disease are more common and occur at an earlier age in diabetic people than in the general population (1-2).The cellular mechanisms underlying the accelerated progression of atherosclerotic lesions in diabetic arteries are still largely unknown. Hyperinsulinemia, lipid abnormalities, and hyperglycemia have each been suggested to cause this response. Because smooth muscle cell (SMC) proliferation and accumulation are key events in the development of advanced lesions, a number of studies have investigated the regulation of SMC proliferation. Studies on the effects of hyperinsulinemia show that direct mitogenic effects of insulin on SMCs are weak and that the principal mitogenic response elicited by insulin is mediated through a cross-reaction at high unphysiological insulin concentrations with the IGF-I receptor (3-6). Thus, a direct mitogenic action of hyperinsulinemia on SMCs in vivo is unlikely.It is becoming increasingly clear that many of the complications of diabetes arise from hyperglycemia that cannot be completely prevented using the methods of blood glucose control available today. This is particularly apparent for retinopathy, nephropathy,...

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Section: Resultsmentioning

confidence: 99%

Diabetes Accelerates Smooth Muscle Accumulation in Lesions of Atherosclerosis

et al. 2001

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“…Magyar and Mihalik (1997) characterized the SWC1 antigen as a dimeric protein with a molecular mass of 41 kDa and 15 kDa. Aasted et al (1998) described the molecular mass of SWC1 with either 16 kDa (mAb 76-7-6) or 19 kDa (mAb 335-2). SWC1 expression was found on monocytes, granulocytes and resting T-lymphocytes, while it was absent on erythrocytes, platelets and B-lymphocytes (Pescovitz et al, 1984; Saalmuller et al, 1994a).…”

Section: Resultsmentioning

confidence: 99%

Porcine SWC1 is CD52—Final determination by the use of a retroviral cDNA expression library

Leitner

Reutner

Essler

et al. 2012

Veterinary Immunology and Immunopathology

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During the last decades for several species – e.g. swine – many mAb to leukocyte-specific molecules have been developed and clusters of differentiation corresponding to human CD could be established. However, for a significant amount of the raised mAb the corresponding antigens were not characterized on the molecular level and therefore preliminary clusters – in swine so-called Swine workshop clusters (SWC) – were established. These clusters contain antigens with currently no obvious orthologs to human leukocyte differentiation antigens. In this study, we describe the generation of a eukaryotic cDNA expression library from in vitro activated porcine peripheral blood mononuclear cells. Screening of this library with an antibody recognizing SWC1 enabled isolation and sequencing of cDNAs coding for the porcine SWC1 molecule. A BLAST search of the obtained sequence revealed that SWC1 is the orthologous molecule of human CD52. Therefore, our study provides the basis for comparative studies on the role of CD52 in different mammalian species. In addition, the established cDNA library can be used for investigation of additional SWC-defined molecules.

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Reactivity of monoclonal antibodies to human CD antigens with cells from mink

Aasted

Viuff

2007

Veterinary Immunology and Immunopathology

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Immunoprecipitation studies of monoclonal antibodies submitted to the Second International Swine CD Workshop

Cited by 14 publications

References 2 publications

Diabetes Accelerates Smooth Muscle Accumulation in Lesions of Atherosclerosis

Diabetes Accelerates Smooth Muscle Accumulation in Lesions of Atherosclerosis

Porcine SWC1 is CD52—Final determination by the use of a retroviral cDNA expression library

Reactivity of monoclonal antibodies to human CD antigens with cells from mink

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