1,720,983 research outputs found
Trophoblast cell-surface antigen 2 and miR-125b: from normal human placental development to gestational diseases
No full textHuman trophoblastic cell surface antigen 2 (Trop-2) è una glicoproteina di membrana di 35-49 kDa, identificata per la prima volta come marker di superficie nelle cellule di trofoblasto umano.
Trop-2 ha funzioni importanti quali la regolazione dell'adesione cellulare e la crescita e la proliferazione cellulare.
Precedenti studi hanno identificato Trop-2 come target del miR-125b, indicando un possibile ruolo del miR-125b nella modulazione dell'espressione di Trop2.
Lo scopo della tesi è di investigare l'espressione di Trop-2 e del miR-125b durante la gravidanza fisiologica e in condizione di preeclampsia, complicata o no da Restrizione di Crescita Intrauterina (IUGR), così da valutare il possibile ruolo della proteina, e verificare se Trop-2 possa essere il target del miR-125b nella placenta. L'immunofluorescenza in doppio ha mostrato che Trop-2 è localizzato nella membrana basale del sinciziotrofoblasto. Analisi immunoistochimiche e western blotting hanno mostrato un incremento dell'espressione di Trop-2 durante lo sviluppo della normale gravidanza.
In condizioni patologiche, i livelli di Trop-2 sono diminuiti nelle placente PE, mentre sono incrementati nelle PE-IUGR. Il modello in vitro ha confermato quanto osservato con le analisi in vivo.
miR-125b nei tessuti placentari è aumentato durante la normale gravidanza, come Trop-2, suggerendo equilibrio tra le due molecole. In condizioni patologiche, l'espressione del miR-125b è bassa, suggerendo una deregolazione tra Trop-2 e miR-125b nella PE-IUGR.
Nel sangue materno al primo trimestre, miR-125b è più alto nelle donne con PE rispetto a quelle con normale gravidanza, suggerendo che Trop-2 in PE è regolato dal miR-125b circolante nel sangue materno.
Questi risultati supportano la teoria che considera PE e PE-IUGR come due differenti patologie.
Studi futuri possono essere indirizzati sull'approfondimento del ruolo di Trop-2 e sull'uso di miR-125b come biomarker predittivo di PE e PE-IUGR nel sangue materno.Human trophoblastic cell surface antigen 2 (Trop-2) is a 35-49 kDa transmembrane glycoprotein, first identified as a cell surface marker for human trophoblast cells.
Trop-2 has important functions, as the regulation in cell-cell adhesion and in cell growth.
Previous studies identified Trop-2 as a target for miR-125b suggesting a possible role of miR-125b in the modulation of Trop-2 protein expression.
The aim of this study is to investigate the expression of Trop-2 and miR-125b during the physiological pregnancy and in preeclampsia (PE), with or without intrauterine growth restriction (IUGR), in order to evaluate the possible role of the protein, and to verify if Trop-2 could be a target for miR-125b in placenta.
Double-labelling immunofluorescence indicated that Trop-2 is located in the basal membrane of syncytiotrophoblast. Immunohistochemical and western blotting analyses showed an increase of Trop-2 expression during the development of normal pregnancy. In pathological conditions, Trop-2 levels decreased in PE placenta, while increased in PE-IUGR tissues. In vitro model confirmed results obtained by in vivo analyses.
miR-125b in placental tissues increased during the normal pregnancy, as Trop-2 expression, suggesting equilibrium between the two molecules. In pathological conditions the expression of miR-125b was low, suggesting the dysregulation between Trop-2 and miR-125b in PE-IUGR tissues.
In maternal blood at first trimester, miR-125b was higher in women with PE than in women with normal pregnancy, suggesting that Trop-2 in PE is regulated by miR-125b that circulate in maternal blood.
These results support the theory proposed in previous studies that consider PE and PE-IUGR as two different pathologies. Future studies that can be focused on the role of Trop-2 protein and the use of miR-125b as predictive biomarker of PE and PE-IUGR using maternal plasma
A New Surgical Protocol For Horizontal Ridge Augmentation: Simplified Apposition Technique. Human Histologic and Radiographic Analysis After 2.5 Years of Follow-Up, A Case Report
Get PDFHigh temperature requirement A1 and fibronectin: two possible players in placental tissue remodelling
No full textCollagen and non-collagenous proteins molecular crosstalk in the pathophysiology of osteoporosis
Get PDFCollagenous and non-collagenous proteins (NCPs) in the extracellular matrix, as well as the coupling mechanisms between osteoclasts and osteoblasts, work together to ensure normal bone metabolism. Each protein plays one or more critical roles in bone metabolism, sometimes even contradictory, thus affecting the final mechanical, physical and chemical properties of bone tissue. Anomalies in the amount and structure of one or more of these proteins can cause abnormalities in bone formation and resorption, which consequently leads to malformations and defects, such as osteoporosis (OP). The connections between key proteins involved in matrix formation and resorption are far from being elucidated. In this review, we resume knowledge on the crosstalk between collagen type I and selected NCPs (Transforming Growth Factor-β, Insulin-like Growth Factor-1, Decorin, Osteonectin, Osteopontin, Bone Sialoprotein and Osteocalcin) of bone matrix, focusing on their possible involvement and role in OP. The different elements of this network can be pharmacologically targeted or used for the design/development of innovative regenerative strategies to modulate a feedback loop in bone remodelling
Heterotopic ossification in a patient with diffuse idiopathic skeletal hyperostosis: Input from histological findings
No full textA high incidence of heterotopic ossification (HO) has been reported in patients with diffuse idiopathic skeletal hyperostosis (DISH), a metabolic disease characterized by calcifications of entheses at spine and peripheral sites. We performed histological and immunohistochemical analyses in five different HO sites in a patient with DISH to study a possible mutual interaction of bone morphogenetic protein 2 (BMP-2), transforming growth factor beta (TGF-β), and decorin, crucial for bone mass increasing, matrix calcification, and endochondral bone formation. We speculated that the surgical trauma triggered HO, inducing TGF-β release at the lesion site. TGF-β recruits osteoblast precursor cells and determines the overexpression of BMP-2 in the surrounding skeletal muscle, inducing a further osteogenic differentiation, contributing to HO onset
Analysis of cytosolic mtDNA release during Staphylococcus aureus infection
No full textMethicillin-resistant Staphylococcus aureus (MRSA) is one of the principal human pathogens, causing severe infections in skin wounds. MRSA infection triggers a cell response mainly by mitochondrial-mediated pathway, resulting in mitochondrial outer membrane permeabilization, extrusion of the mitochondrial inner membrane into the cytoplasm, and then spillage of mitochondrial DNA (mtDNA) into the cytoplasm. The cell recognizes the discharged cytosolic mtDNA (cmtDNA) as “not-itself” because of mtDNA properties and triggers cascade events, such as the activation of inflammasomes. Here, we detail a method to detect and measure the mtDNA release into the cytoplasm in immortalized keratinocytes (HaCaT cells), after the infection with MRSA at different time points after the infection
Use of Hydrosurgical Debridement System for Silicone Gel Removal after Breast Implant Rupture
No full textBreast implant rupture is one of the most common complications in aesthetic and reconstructive surgery. Furthermore, this problem is closely linked to capsular contracture. It is therefore crucially important to effectively and promptly remove silicone leakage from breast pockets. Several techniques are described in the literature and have been typically used for this procedure. Hydrosurgical debridement (HD), which is usually applied in wound care to treat wounds, could be useful for the removal of the silicone leaked from prosthesis pockets after breast implant rupture. An entire periprosthetic capsule that contained a ruptured implant with silicone leakage was removed from a left breast. Half of the capsule was treated with HD, whereas the other half was left untreated as a control. Samples were processed by light microscopy and scanning electron microscopy for morphological analyses. light microscopy demonstrated that the nontreated tissues had a typical synovial-like structure with a middle layer of connective tissue in which there were numerous rounded empty spaces which contained silicone. In contrast, the superficial connective region of the treated tissues (T) had fewer and flattened spaces where the silicone was detected. Scanning electron microscopic analysis showed that in the T samples, the capsule thickness was compact compared with that of the nontreated tissues. Furthermore, the fibrous components appeared well organized with few and smaller silicone lacunae. HD is useful for the removal of silicone (ex vivo) from capsular surfaces after implant rupture. Because of its safety characteristics, this technique could be successfully used in vivo
Mesenchymal Stem Cells Exposed to Persistently High Glucocorticoid Levels Develop Insulin-Resistance and Altered Lipolysis: A Promising In Vitro Model to Study Cushing’s Syndrome
Get PDFBackground: In Cushing’s syndrome (CS), chronic glucocorticoid excess (GC) and disrupted circadian rhythm lead to insulin resistance (IR), diabetes mellitus, dyslipidaemia and cardiovascular comorbidities. As undifferentiated, self-renewing progenitors of adipocytes, mesenchymal stem cells (MSCs) may display the detrimental effects of excess GC, thus revealing a promising model to study the molecular mechanisms underlying the metabolic complications of CS. Methods: MSCs isolated from the abdominal skin of healthy subjects were treated thrice daily with GCs according to two different regimens: lower, circadian-decreasing (Lower, Decreasing Exposure, LDE) versus persistently higher doses (Higher, Constant Exposure, HCE), aimed at mimicking either the physiological condition or CS, respectively. Subsequently, MSCs were stimulated with insulin and glucose thrice daily, resembling food uptake and both glucose uptake/GLUT-4 translocation and the expression of LIPE, ATGL, IL-6 and TNF-α genes were analyzed at predefined timepoints over three days. Results: LDE to GCs did not impair glucose uptake by MSCs, whereas HCE significantly decreased glucose uptake by MSCs only when prolonged. Persistent signs of IR occurred after 30 hours of HCE to GCs. Compared to LDE, MSCs experiencing HCE to GCs showed a downregulation of lipolysis-related genes in the acute period, followed by overexpression once IR was established. Conclusions: Preserving circadian GC rhythmicity is crucial to prevent the occurrence of metabolic alterations. Similar to mature adipocytes, MSCs suffer from IR and impaired lipolysis due to chronic GC excess: MSCs could represent a reliable model to track the mechanisms involved in GC-induced IR throughout cellular differentiatio
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
- …
