Programmed cell death (PCD) or apoptosis is a naturally occurring cell suicide pathway induced in a variety of cell types. In many cases, PCD is induced by the withdrawal of specific hormones or growth factors that function as survival factors. In this study, we have investigated the potential role of the extracellular matrix (ECM) as a cell survival factor. Our results indicate that in the absence of any ECM interactions, human endothelial cells rapidly undergo PCD, as determined by cell morphology, nuclei fragmentation, DNA degradation, protein cross-linking, and the expression of the PCD-specific gene TRPM-2. PCD was blocked by plating cells on an immobilized integrin beta 1 antibody but not by antibodies to either the class I histocompatibility antigen (HLA) or vascular cell adhesion molecule-1 (VCAM-1), suggesting that integrin-mediated signals were required for maintaining cell viability. Treatment of the cells in suspension with the tyrosine phosphatase inhibitor sodium orthovanadate also blocked PCD. When other cell types were examined, some, but not all, underwent rapid cell death when deprived of adhesion to the ECM. These results suggest that in addition to regulating cell growth and differentiation, the ECM also functions as a survival factor for many cell types.
COVID-19 is also manifested with hypercoagulability, pulmonary intravascular coagulation, microangiopathy, and venous thromboembolism (VTE) or arterial thrombosis. Predisposing risk factors to severe COVID-19 are male sex, underlying cardiovascular disease, or cardiovascular risk factors including noncontrolled diabetes mellitus or arterial hypertension, obesity, and advanced age. The VAS-European Independent Foundation in Angiology/Vascular Medicine draws attention to patients with vascular disease (VD) and presents an integral strategy for the management of patients with VD or cardiovascular risk factors (VD-CVR) and COVID-19. VAS recommends (1) a COVID-19-oriented primary health care network for patients with VD-CVR for identification of patients with VD-CVR in the community and patients' education for disease symptoms, use of eHealth technology, adherence to the antithrombotic and vascular regulating treatments, and (2) close medical follow-up for efficacious control of VD progression and prompt application of physical and social distancing measures in case of new epidemic waves. For patients with VD-CVR who receive home treatment for COVID-19, VAS recommends assessment for (1) disease worsening risk and prioritized hospitalization of those at high risk and (2) VTE risk assessment and thromboprophylaxis with rivaroxaban, betrixaban, or low-molecular-weight heparin (LMWH) for those at high risk. For hospitalized patients with VD-CVR and COVID-19, VAS recommends (1) routine thromboprophylaxis with weight-adjusted intermediate doses of LMWH (unless contraindication); (2) LMWH as the drug of choice over unfractionated heparin or direct oral anticoagulants for the treatment of VTE or hypercoagulability; (3) careful evaluation of the risk for disease worsening and prompt application of targeted antiviral or convalescence treatments; (4) monitoring of D-dimer for optimization of the antithrombotic treatment; and (5) evaluation of the risk of VTE before hospital discharge using the IMPROVE-D-dimer score and prolonged post-discharge thromboprophylaxis with rivaroxaban, betrixaban, or LMWH.
A century has passed since thromboangiitis obliterans (TAO), or Buerger's disease, was first described, but the etiology remains unclear. It is still uncertain as to whether thrombosis or vascular inflammation is the first event. TAO is an episodic inflammatory and thrombotic-occlusive vascular disease of unknown origin. The involvement of the distal vessels and nerves within the neuro-vascular bundles occurs almost always in legs and occasionally in arms. The cumulative data demonstrate that at the cellular and molecular levels, at least four main components of inflammatory reactions, including endothelial cells, platelets, leukocytes and sensory neurons, might be involved in TAO pathogenesis. The interactions among these cells in an altered microenvironment of small- and medium-sized vessels may also orchestrate the onset of TAO events. In this review, the factors that may promote thrombosis and angiitis are reconsidered at three levels: (1) host characteristics such as male gender and genetic background; (2) probable triggers including cigarette smoking and infectious agents; and (3) environmental factors such as chronic anxiety and mental stress as a consequence of low socioeconomic status. At each level, the interactions among vascular endothelium, platelets, leukocytes and sensory neurons are discussed.
IntroductionNowadays, Buerger's disease (BD) is more common in the developing countries of Asia. Although its prevalence is going to decrease in the developed countries, its decline rate is not in parallel with that for smoking in these countries. Since the number of BD patients reported to MVasRc is increasing annually and its pathogenesis is unknown, the aim of the study was to investigate the smoking habits and socioeconomic status of the patients corresponding with Shionoya's criteria.Material and methodsPoverty line was the key factor of economic condition. Hygiene, education, professional occupation, long-term unemployment and healthy work were considered as social indices. Patients under the poverty line in addition to weakness in more than two social indices were included in low socioeconomic classification.ResultsFrom the total of 86 patients who reported to MVasRc during the 22-month study period, 71.6% and > 95% were new cases of BD and in low socioeconomic status respectively. Smoking ranged from 2 to 80 cigarettes/day. The duration of smoking before the onset of BD varied from 2 months to 35 years.ConclusionsThere is a lack of correspondence between BD and decline in the prevalence of smoking in developed countries. Also, duration and smoking habit varied in the studied patients. On the other hand, the strong dependence of BD on low socioeconomic conditions, as revealed in this research, implies that socioeconomic status may be a risk factor for initiation of BD. Moreover, the prevalence of BD might be an indicator of socioeconomic development in different societies.
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