Influences of thrombin, factor XIII and fibronectin on the growth of tumor cells and leukemic cells in vitro

Bruhn, H. D.; Bernsmeier, R.; Lück, Paul Christian; Zurborn, K.-H.; Christophers, Enno

doi:10.1007/bf01488977

Cited by 7 publications

(6 citation statements)

References 7 publications

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“…enzymes. In addition, the well documented mitogenic activity of thrombin on fibroblasts (Chen and Buchanan, 1975;Carney et al, 1978) and epithelial cells (Reddan et al, 1982;Bruhn et al, 1983;Medrano et al, 1987) prompted us to investigate the mitogenic potential of factors II and Ila on differentiated Adl2 HER 10 cells.…”

Section: Introductionmentioning

confidence: 99%

Modulation of morphological differentiation of human neuroepithelial cells by serine proteases: independence from blood coagulation.

et al. 1989

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We have previously shown that a serum protein, termed differentiation reversal factor (DRF), is responsible for neurite retraction in differentiated cultures of an adenovirus 12 (Ad12) transformed human retinoblast cell line. Data is presented here to show that DRF is identical to the serine protease prothrombin. Both proteins have been immunoprecipitated using an antibody raised against purified prothrombin and have been shown to hydrolyse a specific thrombin substrate only after activation by the snake venom ecarin. Following addition to Ad12 HER 10 cells, which had previously been differentiated by culture in the presence of 2 mM dibutyryl cAMP in serum‐free medium, thrombin and prothrombin caused half‐maximal retraction of neurites at concentrations of 0.5 ng/ml and 20 ng/ml respectively. Interestingly, activation of prothrombin was shown to be unnecessary for biological activity. Using the inhibitor di‐isopropylfluorophosphate (DIP), we have shown that abrogation of the proteolytic activity of thrombin also results in a loss (greater than 2000 fold) of differentiation reversal activity. Thrombin and its zymogen both stimulated the mitosis of differentiated Ad12 HER 10 cells to a similar extent. In addition, differentiation reversal was highly specific since, at physiologically significant concentrations, closely related serine proteases did not cause neurite retraction. Prothrombin and thrombin also reversed morphological differentiation in the SK‐N‐SH neuroblastoma cell line and in heterogeneous cultures of cells from various regions in the human foetal brain.

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Section: Introductionmentioning

confidence: 99%

Modulation of morphological differentiation of human neuroepithelial cells by serine proteases: independence from blood coagulation.

et al. 1989

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“…Factor XIII has been found in connective tissue stroma (7), where it may cross-link fibrin to the surface of neoplastic cells without decreasing their viability (8), and provide striu> türal integrity and vascularization support to the tumour mass (9). It has been reported that thrombin and factor XIII show mitogenic activity towards some malignant cell types in vitro (10), There are, to our knowledge, no reports on the behaviour of plasmatic factor XIII in gynaecological oiieology. Therefore, it was the aim of this study to investigate factor XIII in pläsma of patients with benign and malignant gynaecological tumours.…”

Section: Introductionmentioning

confidence: 83%

“…Consumption during locäl activation of the clotting system promotes tumour mainte·nance and perpetuation by conversion of fibrinogen to fibrin (9). The presenee of thrombin and factor XIII on the tumour site may therefore contribute to tumour progression (10). The presenee of thrombin and factor XIII on the tumour site may therefore contribute to tumour progression (10).…”

Section: Discussionmentioning

confidence: 99%

Coagulation Factor XIII in Plasma of Patients with Benign and Malignant Gynaecological Tumours

Wersch¹,

Peters²,

Ubachs³

1994

CCLM

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Fibrinogen and factor XIII were measured in sixty-four women with recently detected gynaecological tumours. Twenty-six of these tumours were benign and 32 were malignant: of the last group, nine patients had metastases. No patient showed clinical signs of bleeding or thrombosis. A reference group consisted of 31 agematched healthy women. For fibrinogen, no significant deviation between the patient groups and the control group was found. The median values of factor XIII were higher in the benign tumour group than in the control group. In patients with a gynaecological tumour and metastases, factor XIII was significantly lower than in the non-metastasized malignancy group or in the benign tumour group.From a clinical point of view, the determination of the factor XIII activity might be helpful in diagnosing metastases in patients with a gynaecological tumour.

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“…Malignancy is aberrant repair-cell hyperactivity caused by positive feedback that induces abnormal thrombin elevations [68,129,130,223,[569][570][571][572][573][574][575][576][577][578][579][580][581]. It may represent reactivated embryological thrombin receptor configurations [45,570,[581][582][583].…”

Section: Malignancymentioning

confidence: 99%

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

Coleman

2010

CHDDT

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Based on Capillary Gate Theory and Tissue Repair Theory, this paper describes the "Stress Repair Mechanism" (SRM) that maintains and repairs vertebrate tissues. It accounts for most of the mysterious manifestations of allostasis that remain unexplained by Hypothalamic-Pituitary-Axis (HPA) hormones and thereby enables the Universal Theory of Medicine predicted by Hans Selye. SRM activity explains hemodynamic physiology, capillary hemostasis, infarction, Korotkoff sounds, blood pressure, hypertension, diabetes, allostasis, allostatic load, anesthesia, analgesia, atherosclerosis, apoptosis, malignancy, eclampsia, sepsis, Multi-System Organ Failure (MSOF), the surgical stress syndrome, the fight or flight response, and numerous other manifestations of physiology and pathology. SRM function comprises the autonomic nervous system, the vascular endothelium, and the dynamic enzymatic interaction of blood-borne hepatic Factors VII, VIIIC, IX and X that produces thrombin, soluble fibrin and insoluble fibrin, whose combined effects account for all SRM manifestations. The vascular endothelium is a diaphanous neuroendocrine organ that lines all blood vessels and is the sole constituent of capillary walls. It secretes tissue factor into extravascular tissues, and insulates those tissues from the hepatic enzymes, so that tissue disruption exposes tissue factor to the enzymatic interaction and activates tissue repair. The vascular endothelium also releases nitric oxide and von Willebrand Factor into blood in accord with autonomic balance to regulate the enzymatic interaction to govern tissue perfusion and organ function. Therefore, continuously fluctuating combinations of nervous stimuli that affect autonomic balance and forces that disrupt tissues determine SRM activity.

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Influences of thrombin, factor XIII and fibronectin on the growth of tumor cells and leukemic cells in vitro

Cited by 7 publications

References 7 publications

Modulation of morphological differentiation of human neuroepithelial cells by serine proteases: independence from blood coagulation.

Modulation of morphological differentiation of human neuroepithelial cells by serine proteases: independence from blood coagulation.

Coagulation Factor XIII in Plasma of Patients with Benign and Malignant Gynaecological Tumours

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

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