scholarly journals Influence of indomethacin on the regenerative process of the tail fin of teleost: morphometric and ultrastructural analysis

2010 ◽  
Vol 70 (3 suppl) ◽  
pp. 889-897 ◽  
Author(s):  
PK. Böckelmann ◽  
IJ. Bechara
Keyword(s):  
Regenerative Process ◽  
Severely Injured ◽  
Epidermal Layer ◽  
Epimorphic Regeneration ◽  
Differentiated Cells ◽  
Distal Migration ◽  
Blastemal Cell ◽  
Matrix Components ◽  
Tissue Restoration ◽  
Different Doses

When partially amputated or severely injured, teleost fins suffer a regenerative process called epimorphic regeneration characterised by the following stages: the formation of a multistratified epidermal layer, the disorganisation and distal migration of multipotent mesenchymal cells, the proliferation of these cells in order to form the blastema, continuous proliferation of distal blastema to facilitate the growth, and differentiation of the proximal blastema in order to restore its lost structure. The regeneration of the fin is extremely sensitive to the action of some drugs that can interfere in its structure restoration. For this reason, and also based on papers relating that indomethacin can interfere somehow in the tissue restoration of many different organisms, the aim of this work is to evaluate the possible effects of this drug in three different doses in the regeneration of the teleost fish tail fin, taking into consideration the synthesis, the disposition and organisation of lepidotrichial matrix components, the restoration of actinotrichia, as well as the fin area itself. Therefore, histochemical, ultrastructural and morphometric analysis were done and it was observed that indomethacin in doses of 20 and 30 mg.L-1 caused a delay in the regenerative process of the dermal skeleton (lepidotrichia and actinotrichia) of the tail fins. These doses could have interfered, momentarily, in the process of blastemal cell differentiation in the cells responsible for the synthesis and disposition of actinotrichia and lepidotrichia or, even interfered in the signalling necessary for the recent differentiated cells to begin synthesising the components of the dermal skeleton.

The role of ionic currents in establishing developmental pattern

1981 ◽  
Vol 295 (1078) ◽  
pp. 553-566 ◽  
Keyword(s):  
Cell Membranes ◽  
Direct Evidence ◽  
Ionic Currents ◽  
Regenerative Process ◽  
Thyroid Cell ◽  
Ion Pumps ◽  
Epimorphic Regeneration ◽  
Charged Macromolecules ◽  
Further Development

This paper reviews a theory of pattern establishment and pattern restoration by endogenous ionic currents. These currents are supposed to be generated by a certain separation of ion leaks and ion pumps in cell membranes. In so far as these currents act back to further this separation, they would be part of a regenerative process that initially establishes positional values. Later in development, particularly in epimorphic regeneration, when positional values are restored or extended, these currents are supposed to leak through sites of discontinuity in such values and thus trigger growth. This paper also reviews the factual evidence for this view: evidence that developmental currents are, indeed, very widespread; evidence in a few cases, particularly in Cecropia follicles and in wounded cavy skin, that they can generate substantial voltage differences or gradients; evidence that comparable artificial fields can move charged macromolecules along cell membranes and polarize cell growth; and direct evidence in a few cases, particularly fucoid eggs, Cecropia follicles and regenerating amphibian limbs, that ion currents do, in fact, act back to direct or further development. The paper also presents a particular theory, based upon ionic currents, of the reversal of thyroid cell polarity by serum.

scholarly journals Human ARF Specifically Inhibits Epimorphic Regeneration in the Zebrafish Heart

Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 666
Author(s):  
Solomon Lee ◽  
Robert Hesse ◽  
Stanley Tamaki ◽  
Catharine Garland ◽  
Jason H. Pomerantz
Keyword(s):  
Kinase Inhibitor ◽  
Regenerative Process ◽  
Reading Frame ◽  
Mesenchymal Transition ◽  
Epimorphic Regeneration ◽  
Context Sensitive ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Murine Skeletal Muscle ◽  
Zebrafish Heart

The Alternative Reading Frame (ARF) protein is a tumor suppressor encoded by the Cyclin Dependent Kinase Inhibitor 2A gene in mammals but not lower regenerative vertebrates, and has been previously implicated as a context-sensitive suppressor of regeneration in murine skeletal muscle and humanized ARF-expressing zebrafish fins. This study extends our investigation of the role of ARF in the regeneration of other solid tissues, including the zebrafish heart and the mammalian digit. Heart regeneration after cryoinjury was used to mimic massive myocardial infarction. ARF gene expression was upregulated during the cardiac regenerative process and slowed the rate of morphological recovery. ARF specifically impacts cardiomyocytes, neovascularization, and the endothelial-mesenchymal transition, while not affecting epicardial proliferation. This suggests that in the context of regeneration, ARF is specifically expressed in cells undergoing dedifferentiation. To investigate ARF as a suppressor of epimorphic regeneration in mammalian systems, we also tested whether the absence of ARF was permissive for murine digit regeneration, but found that ARF absence alone was insufficient to significantly alter digit restoration. These findings provide additional evidence that ARF suppresses epimorphic regeneration, but suggests that modulation of ARF alone is insufficient to permit regeneration.

scholarly journals Midkine-a functions as a universal regulator of proliferation during epimorphic regeneration in adult zebrafish

2020 ◽  
Author(s):  
Nicholas B Ang ◽  
Alfonso Saera-Vila ◽  
Caroline Walsh ◽  
Peter F. Hitchcock ◽  
Alon Kahana ◽  
...  
Keyword(s):  
Extraocular Muscle ◽  
Molecular Mechanisms ◽  
Tissue Injury ◽  
Loss Of Function ◽  
Caudal Fin ◽  
Epimorphic Regeneration ◽  
Differentiated Cells ◽  
Ability To Regenerate ◽  
Stem And Progenitor Cells ◽  
Fundamental Biological Process

ABSTRACTZebrafish have the ability to regenerate damaged cells and tissues by activating quiescent stem and progenitor cells or reprogramming differentiated cells into regeneration-competent precursors. Proliferation among the cells that will functionally restore injured tissues is a fundamental biological process underlying regeneration. Midkine-a is a cytokine growth factor, whose expression is strongly induced by injury in a variety of tissues across a range of vertebrate classes. Using a zebrafish Midkine-a loss of function mutant, we evaluated regeneration of caudal fin, extraocular muscle and retinal neurons to investigate the function of Midkine-a during epimorphic regeneration. In wildtype zebrafish, injury among these tissues induces robust proliferation and rapid regeneration. In Midkine-a mutants, the initial proliferation in each of these tissues is significantly diminished or absent. Regeneration of the caudal fin and extraocular muscle is delayed; regeneration of the retina is nearly completely absent. These data demonstrate that Midkine-a is universally required in the signaling pathways that convert tissue injury into the initial burst of cell proliferation. Further, these data highlight differences in the molecular mechanisms that regulate epimorphic regeneration in zebrafish.

Aging delays epimorphic regeneration in mice

2021 ◽  
Author(s):  
Regina Brunauer ◽  
Ian G Xia ◽  
Shabistan N Asrar ◽  
Lindsay A Dawson ◽  
Connor P Dolan ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tissue Regeneration ◽  
Wound Closure ◽  
Cell Plasticity ◽  
Epimorphic Regeneration ◽  
Blastema Formation ◽  
Differentiated Cells ◽  
Spatiotemporal Regulation ◽  
First Time ◽  
Regulation Of Regeneration

Abstract Epimorphic regeneration is a multi-tissue regeneration process where amputation does not lead to scarring, but blastema formation and patterned morphogenesis for which cell plasticity and concerted cell-cell interactions are pivotal. Tissue regeneration declines with aging, yet if and how aging impairs epimorphic regeneration is unknown. Here we show for the first time that aging derails the spatiotemporal regulation of epimorphic regeneration in mammals, first, by exacerbating tissue histolysis and delaying wound closure, and second, by impairing blastema differentiation and skeletal regrowth. Surprisingly, aging did not limit stem cell availability in the blastema, but reduced osteoblast-dependent bone formation. Our data suggest that aging delays regeneration not by stem cell exhaustion, but functional defects of differentiated cells that may be driven by an aged wound environment and alterations in the spatiotemporal regulation of regeneration events. Our findings emphasize the importance of accurate timing of signaling events for regeneration, and highlight the need for carefully timed interventions in regenerative medicine.

Motility of leukemic lymphocytes

1990 ◽  
Vol 48 (3) ◽  
pp. 368-369
Author(s):  
Manoj Raje ◽  
Karvita B. Ahluwalia
Keyword(s):  
Quantitative Data ◽  
Laser Doppler Velocimetry ◽  
Acute Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Cellular Space ◽  
Differentiated Cells ◽  
Poorly Differentiated ◽  
Solid Tissues ◽  
Well Differentiated ◽  
Reduced Mobility

In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.

Structure, compositon and function of the dermal-epidermal junction: Relevance in cutaneous disease and diagnosis

1989 ◽  
Vol 47 ◽  
pp. 868-869
Author(s):  
K. A. Holbrook
Keyword(s):  
Basement Membrane ◽  
Epidermolysis Bullosa ◽  
Normal Skin ◽  
Lamina Densa ◽  
Inherited Disorders ◽  
Ultrastructural Studies ◽  
Type Iv ◽  
Type Vii Collagen ◽  
Attachment Structures ◽  
Matrix Components

The dermal-epidermal junction (DEJ), or basement membrane rone, is the boundary between the epithelial and mesenchymal compartments of the skin; epidermal and fibroblastic cells in these two regions collaborate to synthesire its components. Ultrastructural studies (TEM and SEM) have defined a series of planes or layers (basal epidermal, lamina lucida, lamina densa, sublamina densa) and the morphology and density of attachment structures (hemidesmosomes, anchoring filaments, anchoring fibrils and anchoring plaques) in this region of normal skin. Change in structure of the DEJ provides information about the history of the tissue; reduplication of the lamina densa, for example, indicates a site of cell detachment or migration, or remodelling that accompanies repair of focal damage. In normal skin the structure of the DEJ is stable; in pathologic conditions it can be compromised by the congenital absence of certain structures or antigens (e.g., in the inherited disorders, epidermolysis bullosa [EB]) or by enzymatic degradation (e.g., in tumor invasion). Dissolution of the DEJ can also occur normally during the formation of epidermal appendages (e.g., hair follicles) and as melanocytes and Langerhans cells migrate into the epidermis during development.Biochemical and immunohisto/cytochemical studies have identified more than 20 molecules at the DEJ. These include well known matrix molecules (e.g., types IV and V collagen, laminin and fibronectin) and skin-specific antigens. The latter have been identified by autoantibodies or specific polyclonal or monoclonal antibodies raised against the skin, cultured cells and other epithelia. Some of the molecules of the DEJ are are present in basement membrane zones of many epithelia and thus are considered ubiquitous components (type IV, V, laminin, fibronectin, nidogen, entactin, HSPG, LDA-1, CSP [3B3]). All of them (that have been investigated in developing skin) appear ontogenetically as early as human embryonic tissue can be obtained and their expression is typically normal in patients with EB. The known properties of many of these molecules (particularly the matrix components) suggest functions they might impart to the DEJ: support of an epithelium (type IV collagen), regulation of permeability (heparan sulfate proteoglycan) or facilitation of cell attachment (fibronectin) and movement (laminin). Another group of matrix components and antigens of the DEJ includes molecules that are skin-specific or characteristic of stratified squamous epithelia (type VII collagen=LH 7:2 antigen, bullous pemphigoid antigen, AA3, GB3, KF-1,19-DEJ-1, epidermolysis bullosa acquisita antigen [EBA], AF-1 and AF-2, cicatricial pemphigoid antigen [CPA]) . These molecules are expressed in the DEJ later in development than the first group of molecules, in conjunction with the morphologic appearance of the structure they represent. Their appearance is also coordinated with specific developmental events (e.g., epidermal stratification) and the expression of molecules of differentiation in the epidermis and dermis. One or more of them is typically absent or reduced in expression in the skin of patients with heritable disorders affecting this region. There is no apparent correlation between the location of molecules in the DEJ and the stability of their expression.

No effect of vitamin D supplementation on metabolic parameters but on lipids in patients with type 2 diabetes and chronic kidney disease

2020 ◽  
pp. 1-10
Author(s):  
Jiwoon Kim ◽  
Ji Sun Nam ◽  
Heejung Kim ◽  
Hye Sun Lee ◽  
Jung Eun Lee
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Supplementation ◽  
Lipid Profiles ◽  
Metabolic Parameters ◽  
Injection Group ◽  
Different Doses

Abstract. Background/Aims: Trials on the effects of cholecalciferol supplementation in type 2 diabetes with chronic kidney disease patients were underexplored. Therefore, the aim of this study was to investigate the effects of two different doses of vitamin D supplementation on serum 25-hydroxyvitamin D [25(OH)D] concentrations and metabolic parameters in vitamin D-deficient Korean diabetes patients with chronic kidney disease. Methods: 92 patients completed this study: the placebo group (A, n = 33), the oral cholecalciferol 1,000 IU/day group (B, n = 34), or the single 200,000 IU injection group (C, n = 25, equivalent to 2,000 IU/day). 52% of the patients had less than 60 mL/min/1.73m2 of glomerular filtration rates. Laboratory test and pulse wave velocity were performed before and after supplementation. Results: After 12 weeks, serum 25(OH)D concentrations of the patients who received vitamin D supplementation were significantly increased (A, -2.4 ± 1.2 ng/mL vs. B, 10.7 ± 1.2 ng/mL vs. C, 14.6 ± 1.7 ng/mL; p < 0.001). In addition, the lipid profiles in the vitamin D injection group (C) showed a significant decrease in triglyceride and a rise in HDL cholesterol. However, the other parameters showed no differences. Conclusions: Our data indicated that two different doses and routes of vitamin D administration significantly and safely increased serum 25(OH)D concentrations in vitamin D-deficient diabetes patients with comorbid chronic kidney disease. In the group that received the higher vitamin D dose, the lipid profiles showed significant improvement, but there were no beneficial effects on other metabolic parameters.

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