Histology and histopathology Vol.20, nº 2 (2005)
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- PublicationOpen AccessBioactive lysophospholipids and mesangial cell intracellular signaling pathways: role in the pathobiology of kidney disease(Murcia : F. Hernández, 2005) Kamanna, V.S.; Bassa, B.V.; Ganji, S.H.; Roh, D.D.Lysophosphatidic acid (LPA), lysophosphatidylcholine (LPC), and sphingosine -1- phosphate (S1P) are major biologically active lysophospholipids (LPLs) that are produced by activated platelets, monocyte/macrophages, and many types of mammalian cells. LPLs have been shown to induce a wide array of physiological and pathophysiological properties including cellular differentiation, proliferation, migration, extracellular matrix deposition, change in morphology, and chemotactic responses. The recent cloning and identification of G protein-coupled receptors as specific receptors for LPLs created a great deal of interest in LPLs signaling and diverse biological responses. The pathobiological role of LPLs has been implicated in a number of pathological states and human diseases including atherosclerosis, glomerulosclerosis, post-ischemic renal failure, polycystic kidney disease, and ovarian cancer. Although the research in this area is growing at an enormous rate, this review is specifically focused on the recent understanding of the pathophysiological properties of LPA and LPC with special reference to kidney diseases, and their specific G-protein-coupled receptors and intracellular signaling pathways.
- PublicationOpen AccessMicrotubules regulate aortic endothelial cell actin microfilament reorganization in intact and repairing monolayers(Murcia : F. Hernández, 2005) Lee, J.S.Y.; Gotlieb, A.I.To understand the role of microtubules and microfilaments in regulating endothelial monolayer integrity and repair, and since microtubules and microfilaments show some co-alignment in endothelial cells, we tested the hypothesis that microtubules organize microfilament distribution. Disruption of microtubules with colchicine in resting confluent aortic endothelial monolayers resulted in disruption of microfilament distribution with a loss of dense peripheral bands, an increase in actin microfilament bundles, and an associated increase of focal adhesion proteins at the periphery of the cells. However, when microfilaments were disrupted with cytochalasin B, microtubule distribution did not change. During the early stages of wound repair of aortic endothelial monolayers, microtubules and microfilaments undergo a sequential series of changes in distribution prior to cell migration. They are initially distributed randomly relative to the wound edge, then align parallel to the wound edge and then elongate perpendicular to the wound edge. When microtubules in wounded cultures were disrupted, dense peripheral bands and lamellipodia formation were lost with increases in central stress fibers. However, following microfilament disruption, microtubule redistribution was not disrupted and the microtubules elongated perpendicular to the wound edge similar to non-treated cultures. Microtubules may organize independently of microfilaments while microfilaments require microtubules to maintain normal organization in confluent and repairing aortic endothelial monolayers.
- PublicationOpen AccessImmunohistochemical localization of phosphatidylcholine in rat mandibular condylar surface and lower joint cavity by cryotechniques(Murcia : F. Hernández, 2005) Zea-Aragón, Z.; Terada, N.; Ohtsuki, K.; Ohnishi, M.; Ohno, S.The immunolocalization of phospholipids has not yet been clearly demonstrated in temporomandibular joints (TMJs). We have examined the distribution of one of phospholipids, phosphatidylcholine (PC), in the rat mandibular condylar surface and lower joint cavity. Some fresh resected TMJs with their disks attached were immediately plunged into isopentane-propane cryogen (-193 °C). Cryostat sections were cut, mounted on NH3 +-coated slides, and fixed with paraformaldehyde (PF). Cryosections were first immunostained with anti-mouse PC antibody (JE-1). Subsequently, they were labeled with immunogold particles following silver enhancing for light microscopic analyses. Some cryosections were subjected to double immunofluoresecence labeling with antifibronectin antibody or hyaluronic acid-binding protein in combination with the anti-PC antibody. As an immunocontrol, other cryosections were pretreated with phospholipase A2 before such immunofluorescence labeling. We have confirmed the presence of PC in the lower joint cavity of rat TMJs as well as on the mandibular condylar surface layer, which was colocalized with hyaluronic acid and fibronectin respectively. However, by treatment with phospholipase A2, such immunolabeling for PC was clearly decreased, showing that the PC is a component in the rat in vivo TMJ. These findings suggest that PC, hyaluronic acid and fibronectin may interact each other in the TMJ articular surface areas to play a functional role for lubrication in TMJ.
- PublicationOpen AccessEffects of single, double or triple combinations of octreotide, galanin and serotonin on a human pancreatic cancer cell line(Murcia : F. Hernández, 2005) Tjomsland, V.; El-Salhy, M.The human pancreatic cancer cell line (SW 1990) was exposed to 0.2 µg/ml of octreotide, galanin or serotonin as single, double or triple combinations. The tumor cells were checked at 3, 6 and 12 hours. In order to determine the number of viable cancer cells, the MTTassay was used. Proliferation, apoptosis and the expression of epidermal growth factor were detected with immunohistochemistry using the avidin-biotin complex method. In addition, apoptosis was also detected with (TUNEL) method. The primary antibodies used were proliferating cell nuclear antigen (PCNA), anti-poly (ADP-ribose) polymerase (PARP) and antihuman epidermal growth factor. Single treatment with octreotide or serotonin reduced, the number of viable cells and the proliferation index at all observation times. Galanin increased the number of viable cells and the proliferation index. Whereas double treatments containing octreotide reduced the number of viable cells, those containing galanin increased the number. The effect of single, double or triple treatment on the apoptotic index obtained with both TUNEL method and PARP expression varied depending on the combination and the observation time. Octreotide did not affect the tumor cell expression of EGF. Galanin and serotonin, on the other hand, increased the expression of EGF Whereas triple combination increased the expression of EGF after 6 h, all the other double combinations decreased this expression. It has been concluded that treatment with a combination of octreotide and serotonin may be useful in clinical settings.
- PublicationOpen AccessHuman and animal spongiform encephalopathies are the result of chronic autoimmune attack in the CNS: A novel medical theory supported by overwhelming experimental evidence(Murcia : F. Hernández, 2005) Ting Zhu, BaoSpongiform encephalopathies, also called "prion diseases", are fatal degenerative diseases of the central nervous system which can occur in animals (such as the "mad cow disease" in cattle) and also in humans. This paper presents a novel medical theory concerning the pathogenic mechanisms for various human and animal spongiform encephalopathies. It is hypothesized that various forms of prion diseases are essentially autoimmune diseases, resulting from chronic autoimmune attack of the central nervous system. A key step in the pathogenic process leading towards the development of spongiform encephalopathies involves the production of specific autoimmune antibodies against the disease-causing prion protein (PrPsc) and possibly other immunogenic macromolecules present in the brain. As precisely explained in this paper, the autoimmune antibodies produced against PrPsc are responsible for the conversion of the normal cellular prion protein (PrPc) to PrPsc, for the accumulation of PrPsc in the brain and other peripheral tissues, and also for the initiation of an antibody-mediated chronic autoimmune attack of the central nervous system neurons, which would contribute to the development of characteristic pathological changes and clinical symptoms associated with spongiform encephalopathies. The validity and correctness of the proposed theory is supported by an overwhelming body of experimental observations that are scattered in the biomedical literature. In addition, the theory also offers practical new strategies for early diagnosis, treatment, and prevention of various human and animal prion diseases.