Biomedical subjects

P Albertsson

Publications and source records attributed to P Albertsson.

42 records · Page 3Linked to original sources

PubMedDate not supplied

Short- and long-term prognosis after coronary artery bypass grafting in relation to smoking habits.

We describe the 2- and 5-year prognoses following coronary artery bypass grafting (CABG) in relation to smoking habits among consecutive patients being operated on in western Sweden during a 3-year period. Among the 2,121 patients, 10.2% admitted smoking at coronary angiography as compared with 7.5% 2 years after CABG (NS). Among smokers, the mortality during the subsequent 2 years was 8.9% as compared with 6.5% for exsmokers and 7.3% for never smokers (NS). During the 5-year follow-up, smokers had a mortality of 18.8% as compared with 13.6% for exsmokers and 12.5% for never smokers (p = 0.03). When correcting for dissimilarities in previous history, smoking was a strongly significant independent (p < 0.0001) predictor of 5-year mortality.

Aged↗

PubMedDate not supplied

Matrix metalloproteinases of human NK cells.

We have previously reported that MMP-2 and MMP-9 are present in rat A-NK cells, and have recently documented that additional MMPs are present in rodent A-NK cells. To our knowledge only proMMP-9 has previously been reported for human NK and A-NK cells. Herein, we report for the first time the presence of MMP-2 and MT1-MMP in human NK cells. The importance of these enzymes for the migration of A-NK cells into tumor metastases is of great potential relevance. MMPs may be rate limiting in A-NK cells, following their adoptive transfer, to traverse basement membrane and accumulate within established cancer metastases, a likely pre-requisite to their cytolytic function. Human NK cells express and produce MMP-2, MMP-9, MT1-MMP and the inhibitor TIMP-1. Moreover, human A-NK cells degrade the extracellular matrix equivalent (Matrigel) in a seemingly IL-2 dependent manner. It is therefore likely that A-NK cell MMPs play crucial roles in contributing to A-NK cell localisation and positioning the cells in vivo to allow for triggering their cytolytic potential.

Blotting, Western↗

PubMedDate not supplied

Expression of matrix metalloproteinases and their inhibitors by rat NK cells: inhibition of their expression by genistein.

In this study, we describe rat NK cell-derived MMPs including membrane-type MMPs (MT-MMPs) and tissue inhibitors of MMP (TIMPs). RT-PCR analysis from cDNA of rat A-NK cells revealed mRNA for MMP-2, MMP-9, MMP-7, MMP-10, MMP-11, MMP-13, MT1-MMP, MT2-MMP, TIMP-1, and TIMP-2. The RNK-16 cells expressed mRNA for MMP-7, MMP-10, MMP-11, MT1-MMP, MT2-MMP, TIMP-1, and TIMP-2, in addition to MMP-3 and MMP-13. Western blot analysis confirmed proteins for MT1-MMP and MT2-MMP in RNK-16 cells. TIMP-1 in rat A-NK cells was present at molecular mass of 34-kDa protein which may represent a highly glycosylated form. Genistein, a natural isoflavone found in soybeans, inhibited proliferation of RNK-16 cells in dosage dependent manner. In addition, it down-regulated the expression of MMP-13, MT1-MMP, TIMP-1 and TIMP-2. Moreover, genistein greatly impaired the ability of RNK-16 cells to invade through a model basement membrane. This effect might be mediated by the observed down-regulation of MMP-13 and MT1-MMP.

Animals↗

PubMedDate not supplied

Expression of neutrophil collagenase (MMP-8) in Jurkat T leukemia cells and its role in invasion.

BACKGROUND: Previous studies have shown that MMP-8, the neutrophil collagenase, was expressed in neutrophils, chondrocytes and rheumatoid synovial fibroblasts. MATERIALS AND METHODS: We used semi-quantitative RT-PCR analysis, Western blotting, and immunofluorescence assays to determine the expression of MMP-8 in Jurkat T cells. RESULTS: We have determined the expression of MMP-8 from Jurkat cells and the down-regulation of its expression by genistein, a principal soy isoflavone. Genistein inhibited the invasion of Jurkat cells through a model basement membrane by about 75%, similar to the inhibition by BB-94, a synthetic MMP inhibitor. Genistein also down-regulated the expression of MMP-13, but slightly up-regulated the expression of TIMP-1 and TIMP-2. CONCLUSIONS: Our findings documented for the first time the expression of the neutrophil collagenase by a T-cell line. We also determined the inhibition of Jurkat cell invasion by genistein, which was in part mediated through the regulation of the expression of MMPs and TIMPs.

Antineoplastic Agents↗

PubMedDate not supplied

Infiltration and lysis of tumour cell aggregates by adherent interleukin-2-activated natural killer cells is distinct from specific cytolysis.

Adoptively transferred activated natural killer (A-NK) cells infiltrate tumours in vivo. Two in vitro B16-F10 melanoma tumour models were used to study with fluorescence and electron microscopy the infiltration of adherent interleukin 2 (IL-2) A-NK cells: (1) substratum-bound sessile microtumours (MTs), and (2) three-dimensional cell growth on macroporous gelatinous microcarriers (Cultispheres). From 2 h and on increasing numbers of A-NK cells infiltrated the MTs regularly surrounded by a widened intercellular space. An IL-2-dependent disintegration of MTs began at 6-8 h resulting in a release of vital and dead cells. A-NK cell invasion into Cultispheres effectively displaced the melanoma cells from the highly convoluted substratum. Thus, A-NK cell infiltration had a protease-like effect on the tumour cell aggregates which might have a bearing on the interpretation of their cytolytic effect on target cells. Ultrastructural evidence was not obtained of specific A-NK/target conjugate formation or of granule-mediated target cell destruction in either model tumour.

Adoptive Transfer↗

PubMedDate not supplied

Cytolytic activities of IL-2 activated NK cells from MMTV/v-Ha-ras transgenic oncomice during tumor progression.

IL-2 activated natural killer (A-NK) cells have the capacity to infiltrate metastatic tumors and lyse tumor cells. Nevertheless, adoptive immunotherapy with lymphokine-activated killer cells has been only modestly effective in the clinic and has not routinely provided long-term survival in patients with established cancer metastases. This may indicate the need for more carefully investigating the role of effector cells of the immune response, including A-NK cells, in models of tumor progression. Herein we describe the use of the MMTV/v-Ha-ras transgenic mouse model as a system for exploring the role of NK cells during tumor progression. We have examined the lytic capacity of A-NK cells generated from tumor-free and tumor-bearing transgenic oncomice against standard A-NK cell targets (YAC-1 and P815) in addition to tumor cells isolated from these animals. A-NK cells generated from mice without obvious tumor burden show higher lytic activity than A-NK cells generated from mice with evident tumors, i.e., those at a more advanced stage of tumor progression. Only long term (8-day) cultures of late passage A-NK cells generated from tumor-bearing mice showed significant increases in lytic activity over those generated from tumor-free mice. These results suggest that experimental protocols using transgenic oncomice at various stages of tumor growth may constitute a novel model for testing the role of A-NK cells for their capacity to interfere with cancer progression.

Animals↗