Glomerular Polyanion and Control of Cell Function

1990 ◽  
Vol 10 (1) ◽  
pp. 14-18 ◽  
Author(s):  
Francesco Pugliese ◽  
Paolo Menè ◽  
Giulio A. Cinotti
2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10036-10036
Author(s):  
H. G. Hass ◽  
J. Jobst ◽  
O. Nehls ◽  
A. Frilling ◽  
J. T. Hartmann ◽  
...  

10036 Background: Cholangiocarcinomas (CCC) are the second most common primary hepatic malignancy with a still poor prognosis and arise from biliary epithelia or cholangiocytes. Until now, less is known about the molecular pathways leeding to CCC. Methods: Oligonucleotide arrays were used to analyze gene expression profiles of 8 intrahepatic CCCs. After isolation of tRNA and transcription into cDNA, biotin-labelled cRNA probes were hybridized to GeneArrays (Affymetrix U 133A) containing probes of more than 22.000 genes/ESTs. For two-dimensional cluster analysis we used special software programs (Genexplore, GeneSpring). Dysregulated genes were determined by presence in more than 70% and a 2-fold change in relation to the corresponding non-malignant liver tissue. Lightcycler analysis were performed to validate the expression datas of dysregulated genes. Results: A total of 694 dysregulated genes (330 up-/364 down-regulated, compared with corresponding non-malignant tissue) were detected. As the gene with the highest and most consistent upregulation we were able to identify osteopontin (OPN) with an average 5-fold overexpression in all CCC tissues. OPN is an acidic phosphoprotein that is secreted by osteoblasts, macrophages and many other cell types and binds to a variety of cell surface receptors (integrins/CD44). OPN is multifunctional, with activities in cell migration, regulation of bone metabolism, immune cell function and control of tumor cell phenotype. Elevated OPN levels were seen in different tumors but until now no data exist about the expression in CCCs. As one possible interaction in human carcinogenesis, OPN has recently been shown to be a novel substrate for some MMPs, which play an importand role in tumor invasion and metastasis. Conclusions: This is the first report about an overexpression of OPN in CCC and our data indicate an important role in cholangiocarcinogenesis. Further studies are needed to illucidate the moleculargenetic mechanisms of OPN interactions in CCC. No significant financial relationships to disclose.


2000 ◽  
Vol 99 (4) ◽  
pp. 343-348 ◽  
Author(s):  
Kohichi TAMURA ◽  
Shinzo TAKAMORI ◽  
Hiroharu MIFUNE ◽  
Akihiro HAYASHI ◽  
Kazuo SHIROUZU

Atrial natriuretic peptide (ANP) is a cardiac hormone which affects endothelial cell function through a receptor-mediated process. Pneumonectomy is a common thoracic surgical procedure that can cause pulmonary oedema in the remaining lung. Few reports have investigated the aetiology of this complication. The aim of this study was to determine the changes in ANP concentration and expression of its receptors following pneumonectomy as a possible aetiology for postpneumonectomy pulmonary oedema (PPE). We compared plasma ANP concentrations, cGMP concentrations, and natriuretic peptide receptor (NPR)-A mRNA and NPR-C mRNA expression in rat lung 3 h after pneumonectomy (n = 5) or a sham operation (n = 5). The ANP concentrations in plasma and lung tissue in the pneumonectomy group were significantly higher than in the control group (749.5 versus 202.7 pgċml-1, P < 0.01; 33.1 versus 6.8 ngċg-1 wet tissue, P < 0.01 respectively). The level of ANP mRNA expression in the pneumonectomy group was significantly higher than in the control group (1.44 versus 0.41 relative ANP mRNA expression, P < 0.05). The concentration of cGMP and the level of NPR-A mRNA expression were not significantly different between the pneumonectomy and control groups. The level of NPR-C mRNA expression in the pneumonectomy group was significantly higher than in the control group (4.17 versus 2.19 relative NPR-C mRNA expression, P < 0.01). These findings suggest that changes in pulmonary ANP and NPR-C expression may contribute to the development of PPE in the remaining lung in the acute phase following pneumonectomy.


2011 ◽  
Vol 300 (5) ◽  
pp. C951-C967 ◽  
Author(s):  
Larissa A. Shimoda ◽  
Jan Polak

The ability to sense and respond to oxygen deprivation is required for survival; thus, understanding the mechanisms by which changes in oxygen are linked to cell viability and function is of great importance. Ion channels play a critical role in regulating cell function in a wide variety of biological processes, including neuronal transmission, control of ventilation, cardiac contractility, and control of vasomotor tone. Since the 1988 discovery of oxygen-sensitive potassium channels in chemoreceptors, the effect of hypoxia on an assortment of ion channels has been studied in an array of cell types. In this review, we describe the effects of both acute and sustained hypoxia (continuous and intermittent) on mammalian ion channels in several tissues, the mode of action, and their contribution to diverse cellular processes.


Folia Medica ◽  
2019 ◽  
Vol 61 (3) ◽  
pp. 397-403 ◽  
Author(s):  
Meliha Kasapoğlu Aksoy ◽  
Lale Altan ◽  
İlknur Aykurt Karlıbel

Introduction: Thirty percent of the muscle mass is lost between the third and eighth decades of life. Vitamin D may have different roles in different aspects of the muscle cell function. Aim: To assess the correlation between vitamin 25(OH)D levels, handgrip strength (HGS), and finger pinch strength (FPS) in elderly. Materials and methods: This was a clinical observational study. It included a total of 92 patients of 65 years and over with good general health status and 66 young healthy volunteers. They all underwent HGS and FPS measurements. Study groups were further stratified into those with a serum 25(OH)D levels higher than 30 ng/dl and those with lower than 30 ng/dl. Results: When geriatric patients were divided into two groups based on 25(OH)D levels, no statistically significant intergroup differences were found in FPS (p>0.05) while statistically significant differences were found in HGS (p<0.05). The analysis of the correlations between HGS and 25(OH)D concentrations revealed a positive, statistically significant correlation between these two parameters at r= 0.330 (p<0.05). Conclusions: This study demonstrated that serum vitamin 25(OH)D levels have an impact on HGS in both geriatric group and control group.


2017 ◽  
Vol 199 (8) ◽  
pp. 2815-2822 ◽  
Author(s):  
Satyanarayana Swamy Cheekatla ◽  
Deepak Tripathi ◽  
Sambasivan Venkatasubramanian ◽  
Padmaja Paidipally ◽  
Elwyn Welch ◽  
...  

2018 ◽  
Vol 293 (43) ◽  
pp. 16951-16952 ◽  
Author(s):  
Davide Vigetti ◽  
Ilaria Caon ◽  
Alberto Passi

Nutrient sensing is a critical cell function that regulates survival and growth by adjusting metabolism. During nutrient shortage, autophagy enables the recycling of major cellular components to prevent cell death. Understanding the mechanisms that trigger and control autophagy is of fundamental importance, as this degradative pathway plays a pivotal role in many diseases. Gubbiotti et al. report the identification of a new player, the proteoglycan decorin, which functions as a nutrient sensor in the extracellular matrix and controls autophagy in the heart.


Blood ◽  
1984 ◽  
Vol 63 (3) ◽  
pp. 714-720 ◽  
Author(s):  
BS van Asbeck ◽  
JJ Marx ◽  
A Struyvenberg ◽  
JH van Kats ◽  
J Verhoef

Abstract Inhibition of the iron-mediated generation of toxic oxygen species by polymorphonuclear leukocytes (PMN) might prevent oxidative damage and thus enhance phagocytic function of PMN. To investigate this point, we studied the effect of the specific iron chelator, deferoxamine, on the antibacterial function of PMN. PMN were incubated for 20 hr with various concentrations of deferoxamine at 37 degrees C in medium containing 0.54 microM endogenous iron. The cells were then washed, and the phagocytic cell function was assessed. The results were compared with those for control PMN preincubated for 20 hr without deferoxamine, and those of nonincubated PMN. Compared with that of control PMN, the uptake of radiolabeled Staphylococcus aureus by PMN treated with 1 microM-1 mM deferoxamine was, on average, 10%-20% higher. This effect was not observed when iron-saturated deferoxamine (DFO) was used. Bacterial uptake was similarly increased in nonpreincubated PMN or PMN preincubated for 20 hr at 4 degrees C instead of 37 degrees C. The intracellular killing capacity of both deferoxamine-treated and control PMN exceeded 90%. PMN incubated for 20 hr at 37 degrees C with DFO not only phagocytosed more bacteria than control cells, but were also capable of killing the greater number of bacteria ingested. This increased activity of deferoxamine-treated PMN was accompanied by enhanced generation of chemiluminescence and production of superoxide during phagocytosis of S. aureus. These findings indicate that deferoxamine may enhance the antibacterial activity of PMN by protecting the cells against damage by iron-mediated generation of toxic oxygen metabolites in resting PMN.


2006 ◽  
Vol 27 (3) ◽  
pp. 983-992 ◽  
Author(s):  
Simone Meuter ◽  
Patrick Schaerli ◽  
Regula Stuber Roos ◽  
Oliver Brandau ◽  
Michael R. Bösl ◽  
...  

ABSTRACT Dendritic cells (DCs) have long been recognized as key regulators of immune responses. However, the process of their recruitment to peripheral tissues and turnover during homeostasis remains largely unknown. The chemokine CXCL14 (BRAK) is constitutively expressed in skin and other epithelial tissues. Recently, the human chemokine was proposed to play a role in the homeostatic recruitment of macrophage and/or DC precursors toward the periphery, such as skin. Although so far no physiological function could be demonstrated for the murine CXCL14, it shows a remarkable homology to the human chemokine. In order to elucidate the in vivo role of CXCL14, we generated a mouse defective for this chemokine. We studied various components of the immune system with emphasis on monocytes/macrophages and DC/Langerhans cell (LC) populations in different tissues during steady state but did not find a significant difference between knockout (CXCL14 − / −) and control mice. Functionally, LCs were able to become activated, to migrate out of skin, and to elicit a delayed type of hypersensitivity reaction. Overall, our data indicate that murine CXCL14 is dispensable for the homeostatic recruitment of antigen-presenting cells toward the periphery and for LC functionality.


2021 ◽  
Author(s):  
Xuangjie Guo ◽  
Yiping Xu ◽  
Wei Luo ◽  
Li Cai ◽  
Ping Wang ◽  
...  

Abstract Background: Biliary atresia (BA) is a severe cholangiopathy resulting from virus-induced and immune-mediated injury of the biliary system. IFN-g, secreted from CD4+ Th1 cells and CD8+ cytotoxic T cells, is a major mediator of liver pathology. Programmed death 1 (PD-1) signaling suppresses T cell function. However, how PD-1 modify T cell function in BA remains incompletely understood. Methods: Frequencies of PD-1 expressing CD4+ and CD8+ T cells were analyzed in the liver and blood from BA and control subjects. Associations of PD-1+CD4+/CD8+T cell abundances with liver function indices were measured. Function of PD-1 was measured by administration of an anti-PD-1 antibody in a Rhesus Rotavirus (RRV)-induced BA model. Survival, histology, direct bilirubin, liver immune cell subsets and cytokine production were analyzed. Results: PD-1 was significantly upregulated in CD4+ and CD8+ T cells in patients with BA compared with control subjects. PD-1 expression in T cells was negatively associated with IFN-γ concentration in liver. Blockade of PD-1 increased IFN-g expression in CD4+ T and CD8+ T cells, suppressed bilirubin production and exacerbated liver immunopathology.Conclusions: PD-1 plays a protective role in infants with BA by suppressing IFN-g production in T cells. Increasing PD-1 signaling may serve as a therapeutic strategy for BA.


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