Pancreatobiliary Diversion in the Mouse

2020 ◽  
pp. 1-6
Author(s):  
Xijuan Chen ◽  
Shuai Qiu ◽  
Qiuju Li ◽  
Lijuan Hu ◽  
Chuanshan Yao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Molecular Mechanisms ◽  
Nuclear Antigen ◽  
Sham Operation ◽  
Proximal Jejunum ◽  
Proliferating Cells ◽  
Pancreatic Growth ◽  
Surgical Model ◽  
Gut Hormone ◽  
Proliferating Cell

The gut hormone cholecystokinin (CCK) is primarily secreted from I-cells in the duodenum and proximal jejunum. CCK secretion is stimulated by food digests and inhibited by proteases from pancreatic juice. CCK regulates digestion and appetite, stimulates pancreatic growth, and participates in pancreatic carcinogenesis. The molecular mechanisms of CCK-induced effects are not fully understood. When the mechanisms are studied in animals, the surgical model of pancreatobiliary diversion (PBD) is frequently used. After animals have had PBD, their CCK secretion is no longer inhibited by pancreas-derived proteases, so circulating CCK is increased. PBD is established in rats and hamsters, but not in mice. In this study, we modified PBD procedures and established the model in the mouse. In an experiment, we performed PBD and sham operation (SO) in two groups of mice (20 mice per group). Twenty days after operation, 75% of the PBD mice and all SO mice survived. When plasma CCK was determined by radioimmunoassay, the PBD group had higher levels than the SO group (<i>p</i> &#x3c; 0.001). To assess pancreatic growth, we determined pancreatic weight and pancreatic contents of protein and DNA. We also stained pancreatic sections by immunohistochemistry to show the proliferating cells that either expressed the proliferating cell nuclear antigen or were labeled with 5-bromo-2′-deoxyuridine. As a result, the pancreases of the PBD mice were heavier (<i>p</i> &#x3c; 0.001) and had more protein (<i>p</i> &#x3c; 0.001), DNA (<i>p</i> &#x3c; 0.01), and proliferating cells (<i>p</i> &#x3c; 0.01) than those of the SO counterparts. Thus, pancreatic growth was increased as a result of PBD-induced hypercholecystokininemia. The plasma and pancreatic data demonstrated that the PBD model was a success. This model may be used in CCK-related research. For instance, pancreatic cancer is frequently studied in transgenic mice. PBD may be combined with the cancer model to study the role of CCK in the molecular biology of pancreatic cancer.

scholarly journals Proliferating cell nuclear antigen acts as a cytoplasmic platform controlling human neutrophil survival

2010 ◽  
Vol 207 (12) ◽  
pp. 2631-2645 ◽  
Author(s):  
Véronique Witko-Sarsat ◽  
Julie Mocek ◽  
Dikra Bouayad ◽  
Nicola Tamassia ◽  
Jean-Antoine Ribeil ◽  
...  
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Nuclear Antigen ◽  
Neutrophil Apoptosis ◽  
Proliferating Cells ◽  
Rna Transfection ◽  
Neutrophil Survival ◽  
Proliferating Cell

Neutrophil apoptosis is a highly regulated process essential for inflammation resolution, the molecular mechanisms of which are only partially elucidated. In this study, we describe a survival pathway controlled by proliferating cell nuclear antigen (PCNA), a nuclear factor involved in DNA replication and repairing of proliferating cells. We show that mature neutrophils, despite their inability to proliferate, express high levels of PCNA exclusively in their cytosol and constitutively associated with procaspases, presumably to prevent their activation. Notably, cytosolic PCNA abundance decreased during apoptosis, and increased during in vitro and in vivo exposure to the survival factor granulocyte colony-stimulating factor (G-CSF). Peptides derived from the cyclin-dependent kinase inhibitor p21, which compete with procaspases to bind PCNA, triggered neutrophil apoptosis thus demonstrating that specific modification of PCNA protein interactions affects neutrophil survival. Furthermore, PCNA overexpression rendered neutrophil-differentiated PLB985 myeloid cells significantly more resistant to TNF-related apoptosis-inducing ligand– or gliotoxin-induced apoptosis. Conversely, a decrease in PCNA expression after PCNA small interfering RNA transfection sensitized these cells to apoptosis. Finally, a mutation in the PCNA interdomain-connecting loop, the binding site for many partners, significantly decreased the PCNA-mediated antiapoptotic effect. These results identify PCNA as a regulator of neutrophil lifespan, thereby highlighting a novel target to potentially modulate pathological inflammation.

scholarly journals Proliferating cells in human eccrine and apocrine sweat glands.

1995 ◽  
Vol 43 (12) ◽  
pp. 1217-1221 ◽  
Author(s):  
Y Morimoto ◽  
K Saga
Keyword(s):  
Proliferating Cell Nuclear Antigen ◽  
Myoepithelial Cells ◽  
Nuclear Antigen ◽  
Sweat Glands ◽  
Secretory Cells ◽  
Proliferating Cells ◽  
Peripheral Cells ◽  
Proliferating Cell ◽  
Eccrine Sweat Glands

Morphological observations of sweat glands showed degenerated debris of secretory cells in the secretory lumen in both apocrine and eccrine sweat glands. This suggested that dead secretory cells of human eccrine and apocrine sweat glands were released into the lumen and replaced by other cells. However, we did not know which type of cells replaced lost secretory cells. Therefore, we studied the proliferating cells in human eccrine and apocrine sweat glands by labeling S-phase cells in vitro with 5-bromo-2'-deoxyuridine (BrdUrd) and by immunostaining proliferation-associated proliferating cell nuclear antigen (PCNA) with anti-PCNA monoclonal antibody. BrdUrd and anti-PCNA antibody labeled a few secretory cells in eccrine and apocrine sweat glands, but neither method labeled myoepithelial cells. Luminal and peripheral cells of the eccrine and apocrine coiled duct were labeled with both BrdUrd and PCNA. However, we could not find any highly proliferative germinative cells in coiled ducts. Our results suggest that lost secretory cells could be replaced by proliferation of secretory cells themselves rather than by proliferation of myoepithelial cells or duct cells.

scholarly journals Control of PCNA deubiquitylation in yeast

2010 ◽  
Vol 38 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Alfonso Gallego-Sánchez ◽  
Francisco Conde ◽  
Pedro San Segundo ◽  
Avelino Bueno
Keyword(s):  
Dna Damage ◽  
Crucial Role ◽  
Proliferating Cell Nuclear Antigen ◽  
Molecular Mechanisms ◽  
Damage Tolerance ◽  
Nuclear Antigen ◽  
Dna Damage Tolerance ◽  
Sliding Clamp ◽  
Evolutionarily Conserved ◽  
Proliferating Cell

Eukaryotes ubiquitylate the replication factor PCNA (proliferating-cell nuclear antigen) so that it tolerates DNA damage. Although, in the last few years, the understanding of the evolutionarily conserved mechanism of ubiquitylation of PCNA, and its crucial role in DNA damage tolerance, has progressed impressively, little is known about the deubiquitylation of this sliding clamp in most organisms. In the present review, we will discuss potential molecular mechanisms regulating PCNA deubiquitylation in yeast.

scholarly journals In Situ Analysis of Cellular Proliferation in Canine, Feline and Equine Tumors by Immunohistochemistry: A Comparison of Bromodeoxyuridine, Proliferating Cell Nuclear Antigen, and Interchromatin-Associated Antigen Immunostaining Techniques

1994 ◽  
Vol 6 (4) ◽  
pp. 453-457 ◽  
Author(s):  
Alain Pierre Théon ◽  
Loretta Metzger ◽  
Stephen Griffey
Keyword(s):  
Cell Proliferation ◽  
Proliferating Cell Nuclear Antigen ◽  
Cellular Proliferation ◽  
Nuclear Antigen ◽  
Brdu Incorporation ◽  
Immunohistochemical Detection ◽  
Proliferating Cells ◽  
Proliferating Cell

Cell proliferation in canine, feline, and equine tumors was evaluated using immunohistochemical detection of in vitro 5–bromodeoxyuridine (BrdU) incorporation, proliferating cell nuclear antigen (PCNA), and interchromatin-associated antigen (p105). Ten tumors in each species were analyzed. The tumor proliferative fraction (PF) was defined as the percentage of labeled nuclei for 5,000 tumor nuclei counted. Immunoreactivity was observed with all techniques in all species. A good correlation was observed between the proliferative fractions measured with the BrdU (PFBrdU) and PCNA (PFPCNA) techniques ( rs = 0.523, P = 0.0026). There was no correlation between the PFs measured with the BrdU (PFBrdU) and p105 (PFP105) techniques. Using the median values obtained from the different approaches as cutoff points to define slowly and rapidly proliferating tumors, there was an 80% agreement ( P = 0.009) between PFBrdU and PFPCNA and no agreement between PFBrdU and PFP105 The results of this study indicate that both BrdU and PCNA labeling methods can be used reliably for identifying proliferating cells in animal tumors. In addition, PCNA could be used to replace the BrdU method to assess tumor proliferative fraction because it does not require pretreatment of tissues.

scholarly journals Apoptosis and Proliferation of Myoepithelial Cells in Atrophic Rat Submandibular Glands

2001 ◽  
Vol 49 (12) ◽  
pp. 1557-1563 ◽  
Author(s):  
Shigeru Takahashi ◽  
Shiro Nakamura ◽  
Katsuhiro Shinzato ◽  
Takanori Domon ◽  
Tsuneyuki Yamamoto ◽  
...  
Keyword(s):  
Submandibular Gland ◽  
Myoepithelial Cells ◽  
Nuclear Antigen ◽  
Double Staining ◽  
Proliferating Cells ◽  
Submandibular Glands ◽  
Transmission Electron ◽  
Duct Ligation ◽  
The Right ◽  
Proliferating Cell

This study was designed to determine whether apoptosis and proliferation of myoepithelial cells occur in atrophic rat submandibular glands. The excretory duct of the right submandibular gland was doubly ligated with metal clips. The atrophic right submandibular glands removed after 1–28 days of duct ligation were investigated using immunohistochemical double staining for actin as a marker for myoepithelial cells and proliferating cell nuclear antigen (PCNA) as a marker for proliferating cells, double staining for actin immunohistochemistry, nick end-labeling (TUNEL) as a marker for apoptotic cells, and transmission electron microscopy (TEM). A few PCNA- and no TUNEL-positive myoepithelial cells were found in the control submandibular glands taken from animals with no operation. In the experimental glands, PCNA-positive myoepithelial cells were common 2 and 3 days after duct ligation and then decreased in number. TUNEL-positive myoepithelial cells appeared at 2 days and were observed most frequently at 5 days. Apoptotic myoepithelial cells were also identified by TEM. These observations suggest that both apoptosis and proliferation of myoepithelial cells occur, especially in the early phase of atrophy, in the rat submandibular gland.

scholarly journals Differences in the cellular composition of small versus large uterine fibroids

Reproduction ◽  
2016 ◽  
Vol 152 (5) ◽  
pp. 467-480 ◽  
Author(s):  
Sarah J Holdsworth-Carson ◽  
Dong Zhao ◽  
Leonie Cann ◽  
Sophie Bittinger ◽  
Cameron J Nowell ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Uterine Fibroids ◽  
Nuclear Antigen ◽  
Cellular Composition ◽  
Proliferating Cells ◽  
Cellular Phenotypes ◽  
Proliferating Cell ◽  
Fibroid Growth

Uterine fibroids are clonally derived from a single cell; however, despite being monoclonal, the cellular phenotypes that make up uterine fibroids are heterogeneous consisting of predominantly smooth muscle cells (SMC) and fibroblasts. This raises the question as to when clonal cell differentiation occurs during fibroid development, and does this information provide clues about possible mechanisms regulating the growth process that leads to fibroids of symptom-causing size? This study investigated the differences in the cellular composition of fibroids by immunohistochemistry (IHC). A tissue microarray (n = 21 hysterectomy cases) was used for the investigation of large uterine fibroids and normal myometrium. An investigation of small fibroids (≤ 5mm) used a separate group of samples (n = 7 hysterectomy cases, total ofn = 17 fibroids). A panel of cell phenotypic markers was selected based on our previousin situinvestigations and included aldehyde dehydrogenase 1 (ALDH1A1) and vimentin for different fibroblast sub-populations, smooth muscle actin (SMA) as a marker for SMCs, CD31 for endothelial cells and CD45 for leucocytes. Proliferating cell nuclear antigen (PCNA) was also studied to identify proliferating cells. The cellular composition of small fibroids differs significantly from large fibroids. Small fibroids are more cellular (increased cells/mm2) than large fibroids, have more blood vessels and also have a higher ratio of SMC to fibroblasts than large fibroids. Large fibroids have more cell proliferation (measured by PCNA) and fewer leucocytes (measured by CD45) than adjacent myometrium, whereas small fibroids are less proliferative and have similar number of leucocytes to myometrium. Different cellular composition between fibroids of different sizes may provide important clues as to the mechanisms that drive fibroid growth.

scholarly journals Effect of Cryptorchidism on the Histomorphometry, Proliferation, Apoptosis, and Autophagy in Boar Testes

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1379
Author(s):  
Xiaorui Fan ◽  
Yihui Liu ◽  
Meishan Yue ◽  
Weidong Yue ◽  
Gaoya Ren ◽  
...  
Keyword(s):  
Germ Cells ◽  
Sertoli Cells ◽  
Proliferating Cell Nuclear Antigen ◽  
Molecular Mechanisms ◽  
Inguinal Canal ◽  
The Body ◽  
Nuclear Antigen ◽  
Seminiferous Tubules ◽  
Mrna Levels ◽  
Proliferating Cell

Spontaneous unilateral cryptorchid boars have one testis in the abdomen or inguinal canal, causing its temperature to be at or near the body temperature, which impairs spermatogenesis, although the histomorphometry and molecular mechanisms underlying this process remain unclear. The aim of the present study was to determine the histomorphometry, proliferation, apoptosis, and autophagy alterations in spermatogonia and Sertoli cells in unilateral cryptorchid, scrotal (contrascrotal), and preweaning piglet (preweaning) testes. Histomorphometrical analysis of cryptorchid testes showed that the seminiferous tubules contained only Sertoli cells and a few spermatogonia, but did not contain post-meiotic germ cells. The number of spermatogonia markedly decreased, and the number of Sertoli cells did not change remarkably in cryptorchid testes. TUNEL assay results showed that apoptosis signals were predominantly observed in spermatogonia. In cryptorchid and contrascrotal testes, proliferating cell nuclear antigen (PCNA) and LC3 were located in spermatogonia. The number of PCNA-positive, TUNEL-positive, and LC3-positive germ cells was low, and the protein and mRNA levels of PCNA and LC3 were significantly decreased in cryptorchid testes. Taken together, the number of Sertoli cells did not change remarkably, whereas the number of germ cells decreased in the cryptorchid testes, compared with that in the contrascrotal testes. Insufficient proliferation, excessive apoptosis, and autophagy were involved in the regulation of the decrease in spermatogonia in cryptorchid boar testes.

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