Tentacular and oral-disc regeneration in the sea anemone, Aiptasia diaphana

Autoradiography with [3H]thymidine and electron microscopy were used to determine (a) the patterns of cellular division exhibited by intact anemones, (b) if measurable increases in cellular proliferation accompany oral-disc regeneration, (c) whether interstitial cells are present in Aiptasia, and (d) if these cells could be responsible for the latter proliferative patterns. An oral-aboral gradient in cellular proliferation was exhibited by the epidermis of uncut anemones, with the highest levels in the tentacles. Wound healing did not require cell proliferation and did not immediately stimulatecellular division which was associated with subsequent morphogenetic events. Indices of presumptive oral-disc [3H]thymidine uptake into nuclei increased tenfold with the outgrowth of the new tentacles. This increase occurred in the epidermis, while only small amounts of gastrodermal proliferation were detected. It is hypothesized that the epidermis contributes new cells to the expanding gastrodermis during tentacle budding. Most of the [3H]thymidine-labeled nuclei were localized in the basal portions of the epidermis of intact anemones and 1- to 2-day-old regenerates; very few gastrodermal nuclei accumulated the label. Nests of interstitial cells and transforming interstitial cells were localized in the exact epidermal regions where nuclear labeling took place, suggesting that the proliferative patterns of intact and regenerating Aiptasia are a function of their interstitial cell distribution.

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Goblet Cell Carcinoids of the Appendix

Archives of Pathology & Laboratory Medicine ◽

10.5858/2001-125-0386-gccota ◽

2001 ◽

Vol 125 (3) ◽

pp. 386-390 ◽

Cited By ~ 8

Author(s):

R. Kanthan ◽

A. Saxena ◽

S. C. Kanthan

Keyword(s):

Electron Microscopy ◽

Cell Cycle ◽

Cell Proliferation ◽

Goblet Cell ◽

Cellular Proliferation ◽

Lung Metastases ◽

Periodic Acid ◽

Biological Behavior ◽

Periodic Acid Schiff ◽

Proliferation Markers

Abstract Background.—Goblet cell carcinoids of the appendix are rare neoplasms with uncertain biological behavior. Objective.—The aims of our study were to evaluate the immunophenotype of this neoplasm with cell cycle/cell proliferation markers and to understand their histogenesis with ultrastructural analysis using conventional carcinoids as a frame of reference. Methods.—Clinical data and archival pathologic material of all goblet cell carcinoids of the appendix recorded by the Saskatchewan Cancer Registry between 1970 and 1998 were reviewed and evaluated by light microscopy, histochemistry, immunohistochemistry, and electron microscopy. Results.—Seven cases of goblet cell carcinoids were identified among 110 cases of conventional carcinoids of the appendix. Histopathology revealed widespread infiltration of the periappendiceal fat in all cases, with extensive perineural invasion. The cells stained strongly positive for mucicarmine, periodic acid–Schiff, periodic acid–Schiff diastase, Alcian blue, cytokeratin, and carcinoembryonic antigen. Most cases were positive for synaptophysin. Increased expression of cell proliferation markers and cell cycle markers was observed. Expression of p53 was strong in one case. Electron microscopy demonstrated the presence of mucinous vacuoles of varying sizes and occasional membrane-bound neuroendocrine granules. Conclusions.—Goblet cell carcinoids of the appendix arise from a pluripotent cell with divergent neuroendocrine and mucinous differentiation. These neoplasms are widely invasive; they demonstrate a high cellular proliferation rate and dysregulation of the cell cycle with up-regulation of cyclin D1 and p21, and down-regulation of p16. Complete removal of the tumor is recommended because of the unpredictable biological behavior of this tumor, which includes delayed local recurrences and lung metastases.

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Reactive oxygen species differently regulate renal tubular epithelial and interstitial cell proliferation after ischemia and reperfusion injury

AJP Renal Physiology ◽

10.1152/ajprenal.00701.2009 ◽

2010 ◽

Vol 298 (5) ◽

pp. F1118-F1129 ◽

Cited By ~ 38

Author(s):

Jinu Kim ◽

Kyong-Jin Jung ◽

Kwon Moo Park

Keyword(s):

Cell Proliferation ◽

Epithelial Cells ◽

Interstitial Cell ◽

Interstitial Cells ◽

Ischemia And Reperfusion ◽

Oxygen Species ◽

Tubular Epithelial Cells ◽

Cell Type ◽

A Cell ◽

Cell Type Specific

Reactive oxygen species (ROS) function as an inducer of cell death and survival or proliferative factor, in a cell-type-specific and concentration-dependent manner. All of these roles are critical to ischemia-induced renal functional impairment and progressive fibrotic changes in the kidney. In an effort to define the role of ROS in the proliferation of tubular epithelial cells and of interstitial cells in kidneys recovering after ischemia and reperfusion (I/R) injury, experimental mice were subjected to 30 min of bilateral kidney ischemia and administered with manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP), a superoxide dismutase mimetic, from 2 to 15 days after I/R for 14 days daily (earlier and longer) and from 8 to 15 days after I/R for 8 days daily (later and shorter). Cell proliferation was assessed via 5′-bromo-2′-deoxyuridine (BrdU) incorporation assays for 20 h before the harvest of kidneys. After I/R, the numbers of BrdU-incorporating cells increased both in the tubules and interstitium. MnTMPyP administration was shown to accelerate the proliferation of tubular epithelial cells, presenting tubule-specific marker proteins along tubular segments, whereas it attenuated the proliferation of interstitial cells, evidencing α-smooth muscle actin, fibroblast-specific protein-1, F4/80, and NADPH oxidase-2 proteins; these results indicated that ROS attenuates tubular cell regeneration, but accelerates interstitial cell proliferation. Earlier and longer MnTMPyP treatment more effectively inhibited tissue superoxide formation, the increment of interstitial cells, and the decrement of epithelial cells compared with later and shorter treatment. After I/R, apoptotic cells appeared principally in the tubular epithelial cells, but not in the interstitial cells, thereby indicating that ROS is harmful in tubule cells, but is not in interstitial cells. In conclusion, ROS generated after I/R injury in cell proliferation and death performs a cell-type-specific and concentration-dependent role, even within the same tissues, and timely intervention of ROS is crucial for effective therapies.

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Proliferation control of kidney interstitial cells

10.1101/2020.04.11.037259 ◽

2020 ◽

Author(s):

Sarah S. McCarthy ◽

Lindsey Gower ◽

Michele Karolak ◽

Alicia England ◽

Thomas Carroll ◽

...

Keyword(s):

Cell Proliferation ◽

Interstitial Cell ◽

Cell Lineage ◽

Interstitial Cells ◽

Target Number ◽

Kidney Medulla ◽

Proliferation Control ◽

Adult Kidney ◽

Feedback Inhibitor ◽

Cell Proliferation Control

ABSTRACTExpansion of interstitial cells in the adult kidney is a hallmark of chronic disease, whereas their proliferation during fetal development is necessary for organ formation. An intriguing difference between adult and neonatal kidneys is that the neonatal kidney has the capacity to control interstitial cell proliferation when the target number has been reached. In this study, we define the consequences of inactivating the TGFβ/Smad response in the interstitial cell lineage. We find that pathway inactivation through loss of Smad4 leads to over-proliferation of interstitial cells regionally in the kidney medulla. Genetic and molecular interaction studies showed that Smad3/4 participates in the Wnt/β-catenin signaling pathway, which is responsible for promoting proliferation of interstitial cells. Specifically, Smad4 is required for the expression of the Wnt feedback inhibitor Apcdd1, and based on these findings we propose a model for interstitial cell proliferation control in which the Wnt/β-catenin proliferative signal is attenuated by TGFβ/Smad signaling to ensure that proliferation ceases when the target number of interstitial cells has been reached in the neonatal medulla.Summary statementThis study describes a novel function for TGFβ signaling in the developing renal interstitium. Mice with Foxd1-Cre-mediated deletion of Smad4 have interstitial expansion and activated Wnt signaling.

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Fibroblasts During Hypertrophic Scar Formation and Resolution

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100072587 ◽

1973 ◽

Vol 31 ◽

pp. 428-429

Author(s):

C. W. Kischer

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Cell Proliferation ◽

Fine Structure ◽

Metabolic Activity ◽

Hypertrophic Scar ◽

Normal Skin ◽

Ground Substance ◽

Hypertrophic Scars ◽

Scanning Electron

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).

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Correlation Between Cellular Functions and Morphological Changes of Human Trophoblast in Vitro

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100116620 ◽

1975 ◽

Vol 33 ◽

pp. 600-601

Author(s):

John C. Garancis ◽

Robert O. Hussa ◽

Michael T. Story ◽

Donald Yorde ◽

Roland A. Pattillo

Keyword(s):

Electron Microscopy ◽

Cellular Proliferation ◽

Morphological Changes ◽

Culture Fluid ◽

Cellular Functions ◽

Human Trophoblast ◽

Transmission Electron ◽

Marked Activity ◽

Malignant Trophoblast

Human malignant trophoblast cells in continuous culture were incubated for 3 days in medium containing 1 mM N6-O2'-dibutyryl cyclic adenosine 3':5'-monophosphate (dibutyryl cyclic AMP) and 1 mM theophylline. The culture fluid was replenished daily. Stimulated cultures secreted many times more chorionic gonadotropin and estrogens than did control cultures in the absence of increased cellular proliferation. Scanning electron microscopy revealed remarkable surface changes of stimulated cells. Control cells (not stimulated) were smooth or provided with varying numbers of microvilli (Fig. 1). The latter, usually, were short and thin. The surface features of stimulated cells were considerably different. There was marked increase of microvilli which appeared elongated and thick. Many cells were covered with confluent polypoid projections (Fig. 2). Transmission electron microscopy demonstrated marked activity of cytoplasmic organelles. Mitochondria were increased in number and size; some giant forms with numerous cristae were observed.

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HIF1A is Overexpressed in Medulloblastoma and its Inhibition Reduces Proliferation and Increases EPAS1 and ATG16L1 Methylation

Current Cancer Drug Targets ◽

10.2174/1568009617666170315162525 ◽

2018 ◽

Vol 18 (3) ◽

pp. 287-294 ◽

Cited By ~ 8

Author(s):

Gustavo Alencastro Veiga Cruzeiro ◽

Maristella Bergamo dos Reis ◽

Vanessa Silva Silveira ◽

Regia Caroline Peixoto Lira ◽

Carlos Gilberto Carlotti Jr ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Line ◽

Cellular Proliferation ◽

Mrna Level ◽

Relevant Information ◽

Protein Stabilization ◽

Mrna Levels ◽

Medulloblastoma Cell Line ◽

Pediatric Medulloblastoma ◽

Fresh Frozen

Background: Genetic and epigenetic modifications are closely related to tumor initiation and progression and can provide guidance for understanding tumor functioning, potentially leading to the discovery of new therapies. Studies have associated hypoxia-related genes to tumor progression and chemo/radioresistance in brain tumors. Information on the expression profile of hypoxiarelated genes in pediatric medulloblastoma, although scarce, may reveal relevant information that could support treatment decisions. Objective: Our study focused on evaluation the of CA9, CA12, HIF1A, EPAS1, SCL2A1 and VEGF genes in 41 pediatric fresh-frozen medulloblastoma sample. Additionally, we analyzed the effect of hypoxia and normoxia in the pediatric medulloblastoma cell-line UW402. Furthermore, we assessed the effects of HIF1A knockdown in cell-proliferation and methylation levels of genes related to hypoxia, apoptosis and autophagy. Method: qPCR was performed to evaluate mRNA levels, and Western blot to confirm HIF1A silencing in both patient samples and cell line. Pyrosequencing was performed to asses the methylation levels after HIF1A knockdown in the UW402 cell line. Results: A higher HIF1A mRNA level was observed in MB patients when compared to the cerebellum (non-tumor match). In UW402 MB cell-line, chemically induced hypoxic resulted in an increase of mRNA levels of HIF1A, VEGF, SCL2A1 and CA9 genes. Additionally, HIF1A knockdown induced a decrease in the expression of hypoxia related genes and a decrease of 30% in cell proliferation was also observed. Also, a significant increase in the methylation of ATG16L1 promoter and decrease in the methylation of EPAS1 promoter were observed after HIF1A knockdown. Conclusion: HIF1A knockdown in medulloblastoma cells lead to decreased cellular proliferation, suggesting that HIF1A can be a potential therapeutic target to be explored in the medulloblastoma. However, the mechanisms behind HIF1A protein stabilization and function are very complex and more data need to be generated to potentially use HIF1A as a therapeutical target.

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The KLF6 Super Enhancer Modulates Cell Proliferation via MiR-1301 in Human Hepatoma Cells

MicroRNA ◽

10.2174/2211536608666190314122725 ◽

2019 ◽

Vol 9 (1) ◽

pp. 64-69 ◽

Cited By ~ 1

Author(s):

KumChol Ri ◽

Chol Kim ◽

CholJin Pak ◽

PhyongChol Ri ◽

HyonChol Om

Keyword(s):

Cell Proliferation ◽

Cellular Proliferation ◽

Hepatoma Cells ◽

Regulation Mechanism ◽

Dependent Manner ◽

Human Hepatoma ◽

Human Hepatoma Cells ◽

Over Expression ◽

Super Enhancer ◽

Engineering Changes

Background: Recent studies have attempted to elucidate the function of super enhancers by means of microRNAs. Although the functional outcomes of miR-1301 have become clearer, the pathways that regulate the expressions of miR-1301 remain unclear. Objective: The objective of this paper was to consider the pathway regulating expression of miR- 1301 and miR-1301 signaling pathways with the inhibition of cell proliferation. Methods: In this study, we prepared the cell clones that the KLF6 super enhancer was deleted by means of the CRISPR/Cas9 system-mediated genetic engineering. Changes in miR-1301 expression after the deletion of the KLF6 super enhancer were evaluated by RT-PCR analysis, and the signal pathway of miR-1301 with inhibition of the cell proliferation was examined using RNA interference technology. Results: The results showed that miR-1301 expression was significantly increased after the deletion of the KLF6 super enhancer. Over-expression of miR-1301 induced by deletion of the KLF6 super enhancer also regulated the expression of p21 and p53 in human hepatoma cells. functional modeling of findings using siRNA specific to miR-1301 showed that expression level changes had direct biological effects on cellular proliferation in Human hepatoma cells. Furthermore, cellular proliferation assay was shown to be directly associated with miR-1301 levels. Conclusion: As a result, it was demonstrated that the over-expression of miR-1301 induced by the disruption of the KLF6 super enhancer leads to a significant inhibition of proliferation in HepG2 cells. Moreover, it was demonstrated that the KLF6 super enhancer regulates the cell-proliferative effects which are mediated, at least in part, by the induction of p21and p53 in a p53-dependent manner. Our results provide the functional significance of miR-1301 in understanding the transcriptional regulation mechanism of the KLF6 super enhancer.

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TP53 Abnormalities and MMR Preservation in 5 Cases of Proliferating Trichilemmal Tumours

Dermatopathology ◽

10.3390/dermatopathology8020021 ◽

2021 ◽

Vol 8 (2) ◽

pp. 147-158

Author(s):

Raquel Martín-Sanz ◽

José María Sayagués ◽

Pilar García-Cano ◽

Mikel Azcue-Mayorga ◽

María del Carmen Parra-Pérez ◽

...

Keyword(s):

Cell Proliferation ◽

Ultraviolet Radiation ◽

Mismatch Repair ◽

Squamous Cell ◽

Cellular Proliferation ◽

P53 Expression ◽

Dna Mismatch ◽

Molecular Alterations ◽

Root Sheath ◽

Close Relationship

Proliferating trichilemmal tumours (PTT) are defined by a benign squamous cell proliferation inside a trichilemmal cystic (TC) cavity. A possible explanation of this proliferative phenomenon within the cyst may be molecular alterations in genes associated to cell proliferation, which can be induced by ultraviolet radiation. Among other genes, alterations on TP53 and DNA mismatch repair proteins (MMR) may be involved in the cellular proliferation observed in PTT. Based on this assumption, but also taking into account the close relationship between the sebaceous ducts and the external root sheath where TC develop, a MMR, a p53 expression assessment and a TP53 study were performed in a series of 5 PTT cases, including a giant one. We failed to demonstrate a MMR disorder on studied PTT, but we agree with previous results suggesting increased p53 expression in these tumours, particularly in proliferative areas. TP53 alteration was confirmed with FISH technique, demonstrating TP53 deletion in most cells.

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Validation of MicroRNA-188-5p Inhibition Power on Tumor Cell Proliferation in Papillary Thyroid Carcinoma

Cell Transplantation ◽

10.1177/0963689720918300 ◽

2020 ◽

Vol 29 ◽

pp. 096368972091830 ◽

Cited By ~ 1

Author(s):

Ping Zhou ◽

Andrew Irving ◽

Huifang Wu ◽

Juan Luo ◽

Johana Aguirre ◽

...

Keyword(s):

Cell Proliferation ◽

Papillary Thyroid Carcinoma ◽

Thyroid Carcinoma ◽

Tumor Cell ◽

Cellular Proliferation ◽

Tumor Cell Proliferation ◽

Papillary Thyroid ◽

Tumor Tissues ◽

Potential Biomarker ◽

And Function

Given the crucial role of microRNAs in the cellular proliferation of various types of cancers, we aimed to analyze the expression and function of a cellular proliferation-associated miR-188-5p in papillary thyroid carcinoma (PTC). Here we demonstrate that miR-188-5p is downregulated in PTC tumor tissues compared with the associated noncancerous tissues. We also validate that the miR-188-5p overexpression suppressed the PTC cancer cell proliferation. In addition, fibroblast growth factor 5 (FGF5) is observed to be downregulated in the PTC tumor tissues compared with the associated noncancerous tissues. Subsequently, FGF5 is identified as the direct functional target of miR-188-5p. Moreover, the silencing of FGF5 was found to inhibit PTC cell proliferation, which is the same pattern as miR-188-5p overexpression. These results suggest that miR-188-5p-associated silencing of FGF5 inhibits tumor cell proliferation in PTC. It also highlights the importance of further evaluating miR-188-5p as a potential biomarker and therapy target in PTC.

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