scholarly journals Pericoronal Follicles of Asymptomatic Impacted Teeth: A Radiographic, Histomorphologic, and Immunohistochemical Study

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Laura Villalba ◽  
Federico Stolbizer ◽  
Fabián Blasco ◽  
Néstor Raúl Mauriño ◽  
María Julia Piloni ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Immunohistochemical Study ◽  
Squamous Metaplasia ◽  
Ki 67 ◽  
Impacted Teeth ◽  
Positive Expression ◽  
Dentigerous Cysts ◽  
Proliferation And Apoptosis ◽  
Enamel Epithelium ◽  
Reduced Enamel Epithelium

Objective. To associate radiographic and histopathological features of pericoronal follicles (PFs) of asymptomatic impacted teeth and evaluate cell proliferation and apoptosis in the epithelium.Study Design. Epithelium and mesenchyme of radiographically normal (NPF≤2.5 mm) and hyperplastic (HPF 2.6 to 5 mm) PF (n=140) were studied histologically. Cell proliferation (PI) and epithelial apoptosis were evaluated by Ki-67 and bcl-2 expression in 14 NPFs and 10 dentigerous cysts (DCs).Results. Radiographically, 127 were NPFs and 13 were HPFs; 87.8% of total PFs exhibited epithelium on the surface. Reduced enamel epithelium was observed in 78 (61.4%) NPFs and 6 (46.2%) HPFs, squamous metaplasia in 17 (13.4%) NPFs and 4 (30.8%) HPFs, and cystic epithelium in 15 (11.8%) NPFs and 3 (23%) HPFs. Mean PI was1.97±1.25and7.97±1.74in the epithelial component of NPF and DC, respectively; bcl-2 positive expression was observed in 9 (64.3%) NPFs and 7 (70%) DCs.Conclusion. The scant epithelial remnant proliferation could imply low risk for development of odontogenic pathologies in the absence of an additional stimulus.

scholarly journals miR-195 Regulates Proliferation and Apoptosis through Inhibiting the mTOR/p70s6k Signaling Pathway by Targeting HMGA2 in Esophageal Carcinoma Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yong Li ◽  
Dapeng Wu ◽  
Pei Wang ◽  
Xiaohui Li ◽  
Gongning Shi
Keyword(s):  
Cell Proliferation ◽  
Esophageal Carcinoma ◽  
Signaling Pathway ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Ki 67 ◽  
Proliferation And Apoptosis ◽  
Ec Cells ◽  
Induced Apoptosis

miR-195 is related to tumorigenesis and frequently inhibits cell proliferation and promotes apoptosis in various cancers, including esophageal carcinoma (EC). The mTOR/p70s6k signaling pathway, which is the major target pathway for HMGA2, regulates the survival and cell proliferation of many tumors and is commonly active in EC. The relationships of miR-195, HMGA2, and the mTOR/p70s6k signaling pathway in EC, however, remain unknown. In the present study, we found that the miR-195 level was significantly downregulated in EC tissues, while the mRNA expressions of HMGA2 were significantly upregulated. Dual-luciferase reporter assay demonstrated that HMGA2 is a target of miR-195. MTT assay and flow cytometry revealed that miR-195 overexpression inhibited cell proliferation and induced apoptosis by targeting HMGA2. We also found that HMGA2 restored the inhibitory effect of miR-195 on phosphorylation of mTOR and p70S6K. Furthermore, rapamycin, a specific inhibitor of the mTOR/p70S6K signaling pathway, decreased the levels of Ki-67 and Bcl-2/Bax ratio, inhibited cell proliferation, and promoted apoptosis in EC cells. In conclusion, upregulation of miR-195 significantly suppressed cell growth and induced apoptosis of EC cells via suppressing the mTOR/p70s6k signaling pathway by targeting HMGA2.

S100A4 promotes the progression of lipopolysaccharide-induced acute epididymitis in mice†

2020 ◽  
Vol 102 (6) ◽  
pp. 1213-1224 ◽  
Author(s):  
Yingjie Wu ◽  
Haoran Li ◽  
Yinghe Qin
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Mrna Levels ◽  
Ki 67 ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Sperm Membrane ◽  
Marked Cell ◽  
Acute Epididymitis

Abstract S100A4 has been suggested to be a critical regulator of tumor metastasis and is implicated in the progression of inflammation. The aim of this study is to investigate the expression and possible role of S100A4 in epididymitis. Using a mouse model of epididymitis induced by the injection of lipopolysaccharide (LPS) in the deferent duct, we found that LPS administration induced an upregulation of S100a4 transcription (P < 0.05) and a recruitment of S100A4 positive cells in the epididymal interstitium of wild type (WT) mice. Co-immunofluorescence showed that S100A4 was mainly expressed by granulocytes, CD4 lymphocytes, and macrophages. Deficiency of S100A4 reduced epididymal pathological reaction and the mRNA levels of the pro-inflammatory cytokines IL-1β and TNF-α (P < 0.01), suggesting that S100A4 promotes the progression of epididymitis. Furthermore, S100A4 deficiency alleviated the decline of sperm motility and rectified the abnormal expression of sperm membrane protein AMAD3, which suggested that in the progression of epididymitis, S100A4 aggravates the damage to sperm vitality. In addition, both Ki-67 marked cell proliferation and transferase-mediated dUTP-biotin nick end labeling detected cell apoptosis were reduced in S100a4−/− mice compared with WT mice after LPS treatment, indicating that S100A4 promotes both cell proliferation and cell apoptosis in epididymitis. Overall, these results demonstrate that S100A4 promotes the progression of LPS-induced epididymitis and facilitates a decline in sperm vitality, and its function may be related to the process of cell proliferation and apoptosis during inflammation.

The Effect of miR-155 on the Regulation of Hyperplasia of Middle Membrane of Blood Vessel in Rat Hypertension Model

2019 ◽  
Vol 9 (7) ◽  
pp. 982-987
Author(s):  
Xiaoying Wang ◽  
Yanke Hao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bioinformatics Analysis ◽  
Luciferase Assay ◽  
Ki 67 ◽  
Vsmc Proliferation ◽  
Tunica Media ◽  
Proliferation And Apoptosis ◽  
The Relationship

Vascular smooth muscle cell (VSMC) abnormal proliferation is related to hypertension. P27 can arrest cell cycle and its downregulation is associated with hypertension. miR-155 plays a regulatory role in VSMC proliferation, while its relationship with hypertension is still unclear. Bioinformatics analysis reveals a relationship between p27 mRNA and miR-155. The present study explores miR-155's role in p27 expression, VSMC proliferation and apoptosis, as well as in the pathogenesis of hypertension. Dual luciferase assay verified the relationship between miR-155 and p27. miR155, p27, α-SMA, and Ki-67 expressions in the thoracic aorta media of rat hypertension model were detected. VSMCs were cultured in vitro and grouped into, anti-miR-NC, anti-miR-155, pIRES2-blank, pIRES2-p27, and anti-miR-155 + pIRES2-p27 groups followed by analysis of cell cycle by flow cytometry and cell proliferation by EdU staining. Hypertension rats were randomly divided into antagomir-155 and antagomir-control. Caudal artery systolic and diastolic pressures were measured. miR-155 suppressed p27 expression. miR-155 and Ki-67 expressions were significantly enhanced, while p27 and α-SMA levels were reduced in the tunica media from hypertension rats compared with control. Downregulation of miR-155 and/or upregulation of p27 obviously declined cell proliferation and arrested cell cycle in G1 phase. Antagomir-155 injection significantly decreased systolic and diastolic pressures, elevated p27 and α-SMA expressions in media, and reduced the thickness of tunica media. miR-155 enhances VSMC proliferation via regulating p27. miR-155 enhancement was related to hypertension. miR-155 plays a therapeutic effect in hypertension.

scholarly journals Management of Dentigerous Cyst: A Review Article

2021 ◽  
Vol 2 (1) ◽  
pp. 01-04
Author(s):  
Nanda Gofur
Keyword(s):  
Epithelial Cells ◽  
Dentigerous Cyst ◽  
Inflammatory Cells ◽  
Cyst Fluid ◽  
Enamel Organ ◽  
Fluid Accumulation ◽  
Venous Flow ◽  
Dentigerous Cysts ◽  
Enamel Epithelium ◽  
Reduced Enamel Epithelium

Introduction: Dentigerous cyst is a pathological epithelial cavity that surrounds an unerupted tooth crown. Dentigerous cysts are usually associated with impacted teeth, mandibular third molars, first and second premolars and canines. Dentigerous cysts can occur at any age, but most cases of these cysts occur at the age of approximately 20 years. Men are affected more often than women. Purpose.To find out how the mechanism of dentigerous cysts. The cyst cavity is lined with epithelial cells derived from the epithelial enamel that is reduced from the tooth-forming organs. According to its pathogenesis, the pressure exerted by an erupted tooth on the follicle can block venous flow leading to accumulation of exudate between the reduced enamel epithelium and the crown of the tooth. These cysts are mostly due to fluid accumulation either between the reduced enamel epithelium and the enamel or between the layers of the enamel organ. This fluid accumulation occurs as a result of the pressure exerted by the erupting tooth on the affected follicle, which blocks venous flow, thus inducing rapid transudation of serum in the capillary walls. Discussion: The expansion of the dentigerous cyst causes the release of bone resorbing factor and an increase in the osmolarity of the cyst fluid as a result of the discharge of inflammatory cells, the discharge of residual epithelial enamel and tooth enamel, and desquamation of epithelial cells into the lumen of the cyst. In theory, the fluid will cause cystic proliferation. because the hyperosmolar content produced by cellular breakdown and cell products causes an osmotic gradient to pump fluid into the lumen of the cyst or it can also be said that an increase in the osmolarity of cyst fluid is the result of a shortcut to inflammatory cells and desquamation of epithelial cells into the lumen of the cyst resulting in a dentigerous cyst. Conclusion: The dentigerous cysts that surround the unerupted dental crowns are caused by the accumulation of fluid either between the reduced enamel epithelium or between the layers of the enamel organs. Dentigerous cysts can cause infection, pain, swelling, root dislocation, and resorption of adjacent tooth roots.

scholarly journals Bilateral ectopic third molar in the maxillary sinuses associated with dentigerous cyst: a case report

2021 ◽  
Author(s):  
Antoine Berberi ◽  
Georges Aoun ◽  
Bouchra Hjeij ◽  
Maissa AboulHosn ◽  
Hiba Alassaad ◽  
...  
Keyword(s):  
Dentigerous Cyst ◽  
Third Molar ◽  
Third Molars ◽  
Unerupted Tooth ◽  
Sinus Cavity ◽  
Dentigerous Cysts ◽  
Enamel Epithelium ◽  
Ectopic Third Molar ◽  
Reduced Enamel Epithelium ◽  
Maxillary Sinuses

A dentigerous cyst is an epithelial-lined odontogenic cyst formed by an accumulation of fluid between the reduced enamel epithelium and the crown of an unerupted tooth. About 70% of dentigerous cysts occur in the mandible and 30% in the maxilla and the most involved teeth are maxillary canines and maxillary third molar. Dentigerous cysts often displace the related tooth into an ectopic position. In the maxilla when the cyst expands into the sinus, usually causes total or partial occupation of the sinus cavity and can extend to the nose. We report a rare case of a 24-year-old female with bilateral maxillary third molars inside the maxillary sinuses attached to a dentigerous cyst and treated with a minimally invasive endoscopic surgery through the middle meatal meatotomy.

miR-338-3p inhibits HIF-1α to Attenuate Nucleus Pulposus Cell Proliferation and Promote Apoptosis Through the Hippo-YAP Pathway

2021 ◽  
Author(s):  
Daolu Zhan ◽  
Jian Liu ◽  
Mingxia Lin ◽  
Jian Chen ◽  
Yehan Fang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nucleus Pulposus ◽  
Intervertebral Disc Degeneration ◽  
Nucleus Pulposus Cell ◽  
Luciferase Assay ◽  
Ki 67 ◽  
Pathway Activation ◽  
Proliferation And Apoptosis ◽  
Related Proteins

Abstract The proliferation and apoptosis of nucleus pulposus (NP) cells (NPCs) play a crucial role in intervertebral disc degeneration (IDD). we aimed to discover the role of miRNA-induced IDD. We analyzed the miRNA expression of three NP tissues from IDD patients and three normal NP samples using the GEO2R tool, and The results revealed that miR-338-3p was upregulated in NPCs from IDD patients. miR-338-3p suppressed NPCs proliferation, and the related proteins PCNA and Ki-67 were downregulated, as demonstrated via western blotting. miR-338-3p promoted apoptosis. Furthermore, we predicted that HIF-1α was targeted by miR-338-3p, using the miRDB database, and this target was validated via dual luciferase assay. HIF-1α reversed miR-338-3p-induced NPCs proliferation and apoptosis. The Hippo-YAP pathway activation proteins YAP, CTGF, and PCNA were upregulated, unlike the inhibitory YAP phosphorylation. In conclusions, our results suggestive that miR-338-3p inhibited HIF-1α/ Hippo-YAP pathway to attenuate NPCs proliferation and apoptosis.

scholarly journals Maxillary Dentigerous Cyst Associated With Supernumerary Tooth

2019 ◽  
Vol 27 (1) ◽  
Author(s):  
Prashant Nanwani
Keyword(s):  
Case Report ◽  
Dentigerous Cyst ◽  
Third Molar ◽  
Developmental Abnormality ◽  
Supernumerary Tooth ◽  
Anterior Maxilla ◽  
Present Case Report ◽  
Dentigerous Cysts ◽  
Enamel Epithelium ◽  
Reduced Enamel Epithelium

Introduction Dentigerous cysts are caused by a developmental abnormality derived from the reduced enamel epithelium of the tooth-forming organ. Dentigerous cyst rarely involve impacted supernumerary tooth in anterior maxilla while commonly involve third molar tooth.   Case Report A case of dentigerous cyst in association with supernumerary tooth in a 15-year-old male patient is reported causing right nasal cavity obstruction. The present case report describes the management of a dentigerous cyst by surgical enucleation.

Regular Voluntary Running Inhibits Androgen-Independent Prostate Cancer Growth in Mice

2021 ◽  
pp. 1-7
Author(s):  
Mário Esteves ◽  
Carina Silva ◽  
Sofia S. Pereira ◽  
Tiago Morais ◽  
Ângela Moreira ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Study Groups ◽  
Cancer Cell Growth ◽  
Ki 67 ◽  
Voluntary Running ◽  
Proliferation And Apoptosis ◽  
Phosphate Buffered Saline ◽  
Androgen Independent

Introduction: Benefits of regular physical exercise were demonstrated as preventive and coadjuvant nonpharmacological anticancer therapy. However, the role of exercise in modulating prostate cancer behavior has yet to be established. Methods: Prostate tumors were induced in C57BL/6 male mice (n = 28) by subcutaneous inoculation of a suspension of murine androgen-independent RM1 cells (1.5 × 105 cells/500 μL phosphate-buffered saline) in the dorsal region. Mice were randomly allocated into 2 study groups: sedentary tumor-induced (n = 14) and exercised tumor-induced (n = 14). Exercise consisted of voluntary running in wheeled cages. Mice (n = 7 per group) were sacrificed either 14 or 28 days after cell inoculation to evaluate tumor weight and percentage of area occupied by immunohistochemistry stained cells for Ki-67 and TdT-mediated dUTP-biotin nick end labeling, used as surrogate markers of cell proliferation and apoptosis, respectively. Results: Compared with sedentary tumor-induced mice, the tumors developed by exercised tumor-induced mice were significantly smaller at 14 days (0.17 [0.12] g vs 0.48 [0.24] g, P < .05) and at 28 days (0.92 [0.73] g vs 2.09 [1.31] g, P < .05), with smaller Ki-67 and greater TdT-mediated dUTP-biotin nick end-labeling stained areas (P < .05). Conclusion: These results suggest that regular voluntary running inhibits prostate cancer cell growth by reducing cell proliferation and enhancing apoptosis.

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