endothelium

Growing evidence supports the hypothesis that endothelial cell-derived microparticles (MPs) might contribute to the pathogenesis of cardiovascular (CV) disease. Endothelial cell-derived MPs play a pivotal role in the regulation of the endogenous repair system, thrombosis, coagulation, inflammation, immunity and metabolic memory phenomenon. There is evidence that the MPs are secreted actively accompanied to other regulatory molecules. All these actively synthetizing and secreting factors include proteins, adhesion and intercellular signal molecules, peptides, lipids, free DNAs, microRNAs, and even microparticles (MPs) are defined as cellular secretome. The proteomic profile of secretome is under tightly control of genetic and epigenetic mechanisms, which may altered a secretion of the proteins involved into MPs’ organization. Finally, this may contribute the modification of MP’s after their secretion and throughout transfer to the target cells. As a result, communicative ability of endothelial cell-derived MPs may sufficiently worse. Subsequently, cross talk between some components of secretome might modulate delivering cargos of MPs and their regenerative and proliferative capabilities via intercellular signaling networks. The aim of the review is to discuss the effect of various components of secretome on MP-dependent effects on endothelium.

Previous clinical, observation and epidemiologic studies have demonstrated strong association between serum uric acid (SUA) and cardiovascular disease (hypertension, heart failure, and asymptomatic atherosclerosis), metabolic states (abdominal obesity, diabetes mellitus, metabolic syndrome, insulin resistance) and kidney disease. There is a large body of evidence regarding the role of SUA as predictor of CV events and CV mortality in general population and individuals with established CV disease and metabolic diseases. However, SUA may exhibit protective effects on endothelium and vasculature as well as attenuate endogenous repair system through mobbing and differentiation of cell precursors. Although SUA lowering drugs are widely used in patients with symptomatic hyperuricemia and gout beyond their etiologies, there is no agreement of SUA below target level 6.0 mg/dL in asymptomatic individuals with kidney injury and CV disease and data of ones are sufficiently limited. The short communication is depicted on the controversial role of SUA as primary cell toxicity agent and secondary cell protector against hypoxia, ischemia and apoptosis

Background: Leiomyomas beyond the uterus are defined by benign smooth muscle cell tumors outside of the uterus. Intravenous leiomyomatosis is a rare type of uterine leiomyoma and is characterized by the formation and growth of benign leiomyoma tissue within the vascular wall. Herein, we present a case of Intravenous leiomyomatosis successfully treated by surgical removal and a review of actual medical recommendations.Case presentation: A 49 - year-old woman, maghrébin, G3 P2, no family history of uterine myomas mentioned, having systemic arterial hypertension, presented to our department with hypogastric pain and abnormal uterine bleeding in the prior five months resulting in anemia which required iron supplementation. On physical examination the vital signs were normal. A palpable mass in the hypogastrium was noted. The rest of the exam was unremarkable. Pelvic ultrasound showed a huge uterus with multiple heterogeneous leiomyomas, including at least one intracavity. Computed tomography scans and magnetic resonance imaging were not done initially due to the unaffordability of the patient. The initial diagnosis was leiomyoma. The decision to perform a total abdominal hysterectomy and bilateral salpingo-oophorectomy was taken. The abdomen was opened by a midline vertical incision. During surgery, multiple subserosal, intramural and submucosal fibroids ranging from 2 cm × 3 cm to 10 cm × 10 cm were seen. On pathological examination, the uterus measured 19 cm in the largest diameter and weighed 1.3 kg. The cut section showed white nodular myometrial masses. Microscopically, intravascular growth of benign smooth muscle cells is found within venous channels lined by endothelium. The diagnosis of Intravenous leiomyomatosis of the uterus without malignant transformation was retained. The patient was monitored for 14 months and subsequent computed tomography did not reveal any evidence of tumor recurrence. The follow-up will be performed annually till the age of menopause.Conclusion: Intravenous leiomyomatosis is a benign, rare and potentially lethal pathology. It especially affects premenopausal women with a history of uterine myoma, whether operated on or not. They require close and prolonged follow-up because of the high risk of recurrence.

Background: CPTs are rare intraventricular papillary neoplasms derived from the choroid plexus epithelium. Anti-collagenase and extracellular matrix which have not been expressed in brain tumors. Objective: The purpose of this study was to investigate the expression levels of collagen type VI, anti-collagenase, laminin, MM9, claudins 1 and 5, N and E cadherins, and collagen VII, tejido, and collagen degradation enzyme complexes in choroid plexus tumors.Materials and methods: We studied the expression of adhesion molecules, extracellular matrix, and anticollagenase with an immunohistochemistry approach and electron microscopy analysis in 42 choroid plexus tumors. Results: 28(67%) were choroid plexus papillomas, 8 (19%) were atypical choroid plexus papillomas and 6 (14%) were choroid plexus carcinomas. The Ki67-li and MVD increased from CPC to ACPP, being the highest in malignant tumors as well as a strong immunoexpression of anti-collagenase and were inverse correlation with claudin 5, E, and N cadherin and collagen IV immunoexpressions which added further significant information to the prognosis and varied according to the histologic classification. By ultrastructure, the loss of basal membrane and cilia, disorganization, and proliferation of ECM were observed in CPC. Cerebral homeostasis largely results from the ability of both the Blood–Brain Barrier (BBB) at the brain microvascular endothelium and the Blood–Cerebrospinal Fluid Barrier (BCSFB) at the epithelium of the Choroid Plexuses (CPs), to control the composition of the CSF and cerebral extracellular fluid. Under expression of the tight junction proteins occludin, claudin-1 and claudin-5 are key molecular abnormalities responsible for the increased permeability of tumor endothelial tight junctions. Conclusion: The loss of basement membrane and ECM overexpression could be considered as a poor prognosis predictor in CPT. Anti-collagenase and MMP9 overexpression could be related to basal membrane and BBB plasticity in CPTs.