scholarly journals Planarian cell number depends on blitzschnell, a novel gene family that balances cell proliferation and cell death

Development ◽  
2020 ◽  
Vol 147 (7) ◽  
pp. dev184044 ◽  
Author(s):  
Eudald Pascual-Carreras ◽  
Marta Marin-Barba ◽  
Carlos Herrera-Úbeda ◽  
Daniel Font-Martín ◽  
Kay Eckelt ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Gene Family ◽  
Cell Number ◽  
Novel Gene

CATERPILLER: A Novel Gene Family Important in Immunity, Cell Death, and Diseases

2005 ◽  
Vol 23 (1) ◽  
pp. 387-414 ◽  
Author(s):  
Jenny P-Y. Ting ◽  
Beckley K. Davis
Keyword(s):  
Cell Death ◽  
Gene Family ◽  
Novel Gene

Granule cell number, cell death and cell proliferation in the dentate gyrus of wild-living rodents

2004 ◽  
Vol 20 (12) ◽  
pp. 3342-3350 ◽  
Author(s):  
Irmgard Amrein ◽  
Lutz Slomianka ◽  
Hans-Peter Lipp
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Dentate Gyrus ◽  
Granule Cell ◽  
Cell Number

Death in the Life of a Tooth

2004 ◽  
Vol 83 (1) ◽  
pp. 11-16 ◽  
Author(s):  
E. Matalova ◽  
A.S. Tucker ◽  
P.T. Sharpe
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cell Division ◽  
Programmed Cell Death ◽  
Tooth Development ◽  
Cell Number ◽  
Substantial Evidence ◽  
Bud Formation ◽  
Dental Lamina ◽  
Tooth Buds

Programmed cell death (apoptosis) constitutes an important mechanism in embryonic development. Although there is substantial evidence for essential roles of apoptosis in organ shaping and controlling of cell number, the mechanisms of these processes are poorly understood. The regulation of cell proliferation to form tooth buds of the appropriate size and at the correct positions must involve a balance between cell division and cell death. Apoptosis has been suggested to play both passive and active roles in bud formation and morphogenesis and in reduction of the dental lamina, as well as silencing of the enamel knot signaling centers. The location of apoptotic cells during tooth development has been described and suggests their temporospatial roles. Unfortunately, there is little functional evidence on these roles, and the aim of this review is to highlight areas where apoptosis may play key roles in odontogenesis.

Contribution of Kir2 potassium channels to ATP-induced cell death in brain capillary endothelial cells and reconstructed HEK293 cell model

2011 ◽  
Vol 300 (1) ◽  
pp. C75-C86 ◽  
Author(s):  
Daiju Yamazaki ◽  
Hiroaki Kito ◽  
Seiji Yamamoto ◽  
Susumu Ohya ◽  
Hisao Yamamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Death ◽  
Cell Model ◽  
Cell Number ◽  
Brain Capillary ◽  
Relative Population ◽  
Membrane Hyperpolarization ◽  
Brain Capillary Endothelial Cells ◽  
Capillary Endothelial Cells

Cellular turnover of brain capillary endothelial cells (BCECs) by the balance of cell proliferation and death is essential for maintaining the homeostasis of the blood-brain barrier. Stimulation of metabotropic ATP receptors (P2Y) transiently increased intracellular Ca2+ concentration ([Ca2+]i) in t-BBEC 117, a cell line derived from bovine BCECs. The [Ca2+]i rise induced membrane hyperpolarization via the activation of apamin-sensitive small-conductance Ca2+-activated K+ channels (SK2) and enhanced cell proliferation in t-BBEC 117. Here, we found anomalous membrane hyperpolarization lasting for over 10 min in response to ATP in ∼15% of t-BBEC 117, in which inward rectifier K+ channel (Kir2.1) was extensively expressed. Once anomalous hyperpolarization was triggered by ATP, it was removed by Ba2+ but not by apamin. Prolonged exposure to ATPγS increased the relative population of t-BBEC 117, in which the expression of Kir2.1 mRNAs was significantly higher and Ba2+-sensitive anomalous hyperpolarization was observed. The cultivation of t-BBEC 117 in serum-free medium also increased this population and reduced the cell number. The reduction of cell number was enhanced by the addition of ATPγS and the enhancement was antagonized by Ba2+. In the human embryonic kidney 293 cell model, where SK2 and Kir2.1 were heterologously coexpressed, [Ca2+]i rise by P2Y stimulation triggered anomalous hyperpolarization and cell death. In conclusion, P2Y stimulation in BCECs enhances cell proliferation by SK2 activation in the majority of cells but also triggers cell death in a certain population showing a substantial expression of Kir2.1. This dual action of P2Y stimulation may effectively facilitate BCEC turnover.

scholarly journals Apoptosis and Predisposition To Oral Cancer

1999 ◽  
Vol 10 (2) ◽  
pp. 139-152 ◽  
Author(s):  
PJ Polverini ◽  
J.E. Nor
Keyword(s):  
Cell Death ◽  
Tumor Suppressor ◽  
Gene Family ◽  
Tumor Suppressor Genes ◽  
Mammalian Cells ◽  
Defense Mechanism ◽  
Clonal Selection ◽  
Cell Number ◽  
Suppressor Genes ◽  
Apoptosis Pathway

The term apoptosis, also known as programmed cell death (PCD), was coined by developmental biologists a number of years ago to describe a form of cell death characterized by several unique morphological and biochemical features. Genetic studies of the round worm Caeneorhabditis elegans, a simple multicellular organism, first revealed apoptosis to be an integral part of the developmental program. Subsequently, the importance of apoptosis in higher organisms was demonstrated in several eukaryotic systems. In mammals, apoptosis is widespread during embryogenesis and in adult tissues. It is required for normal tissue homeostasis and for clonal selection in the immune system. In both developing and adult organisms, apoptosis plays a central role in reinforcing appropriate cellular patterns and in regulating cell number by eliminating cells that are harmful or no longer needed. It is becoming increasingly clear that disruption in the apoptosis pathway can contribute to the development of a number of developmental, inflammatory, degenerative, and neoplastic diseases. The effector arm of the apoptotic program includes members of the Bcl-2 gene family that function as either death agonists or death antagonists. These proteins participate in an elaborate genetically controlled biochemical pathway that functions to maintain tissue and organ homeostasis and serve as a critical defense mechanism to guard against malignant transformation. Cancer is the result of a series of genetic lesions that include activation of oncogenes and inactivation or loss of tumor suppressor genes. Several groups of investigators have observed that deregulated expression of oncogenes can subvert apoptotic pathways, resulting in prolonged cell survival. In pathological settings such as cancer, members of the Bcl-2 gene family are able to synergize with oncogenes and tumor suppressor genes to transform cells. In this review, we describe the process of apoptosis in mammalian cells and define the role and biochemical pathways through which the Bcl-2 gene family induce and/or protect cells from apoptosis. Last, we will discuss the evidence which suggests that alterations in this pathway may play a central role in tumorigenesis by allowing genetically damaged cells normally destined for elimination to persist, predisposing them to additional mutations and driving them to malignancy.

scholarly journals Cytotoxicity of NiO and Ni(OH)2 Nanoparticles Is Mediated by Oxidative Stress-Induced Cell Death and Suppression of Cell Proliferation

2020 ◽  
Vol 21 (7) ◽  
pp. 2355 ◽  
Author(s):  
Melissa H. Cambre ◽  
Natalie J. Holl ◽  
Bolin Wang ◽  
Lucas Harper ◽  
Han-Jung Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Cell Death ◽  
A549 Cells ◽  
Chemical Properties ◽  
Total Surface Area ◽  
Cell Number ◽  
Specific Cytotoxicity ◽  
Hepg2 Cell Lines ◽  
Physical And Chemical

The use of nanomaterial-based products continues to grow with advancing technology. Understanding the potential toxicity of nanoparticles (NPs) is important to ensure that products containing them do not impose harmful effects to human or environmental health. In this study, we evaluated the comparative cytotoxicity between nickel oxide (NiO) and nickel hydroxide (Ni(OH)2) in human bronchoalveolar carcinoma (A549) and human hepatocellular carcinoma (HepG2) cell lines. Cellular viability studies revealed cell line-specific cytotoxicity in which nickel NPs were toxic to A549 cells but relatively nontoxic to HepG2 cells. Time-, concentration-, and particle-specific cytotoxicity was observed in A549 cells. NP-induced oxidative stress triggered dissipation of mitochondrial membrane potential and induction of caspase-3 enzyme activity. The subsequent apoptotic events led to reduction in cell number. In addition to cell death, suppression of cell proliferation played an essential role in regulating cell number. Collectively, the observed cell viability is a function of cell death and suppression of proliferation. Physical and chemical properties of NPs such as total surface area and metal dissolution are in agreement with the observed differential cytotoxicity. Understanding the properties of NPs is essential in informing the design of safer materials.

scholarly journals Ion channels and apoptosis in cancer

2014 ◽  
Vol 369 (1638) ◽  
pp. 20130104 ◽  
Author(s):  
Carl D. Bortner ◽  
John A. Cidlowski
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Ion Channels ◽  
Cell Growth ◽  
Cancer Cells ◽  
Critical Role ◽  
Cell Number ◽  
Tumour Formation ◽  
Constant Cell ◽  
Critical Components

Humans maintain a constant cell number throughout their lifespan. This equilibrium of cell number is accomplished when cell proliferation and cell death are kept balanced, achieving a steady-state cell number. Abnormalities in cell growth or cell death can lead to an overabundance of cells known as neoplasm or tumours. While the perception of cancer is often that of an uncontrollable rate of cell growth or increased proliferation, a decrease in cell death can also lead to tumour formation. Most cells when detached from their normal tissue die. However, cancer cells evade cell death, tipping the balance to an overabundance of cell number. Therefore, overcoming this resistance to cell death is a decisive factor in the treatment of cancer. Ion channels play a critical role in cancer in regards to cell proliferation, malignant angiogenesis, migration and metastasis. Additionally, ion channels are also known to be critical components of apoptosis. In this review, we discuss the modes of cell death focusing on the ability of cancer cells to evade apoptosis. Specifically, we focus on the role ion channels play in controlling and regulating life/death decisions and how they can be used to overcome resistance to apoptosis in the treatment of cancer.

EMBJ08, a novel gene promoting cell proliferation

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Jing Li ◽  
Dongxia Hao ◽  
Weiwei Deng ◽  
Na Li ◽  
Shai Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Novel Gene

The P-MAPA immunomodulator partially prevents apoptosis induced by Zika virus infection in THP-1 cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Morganna C. Lima ◽  
Elisa A. N. Azevedo ◽  
Clarice N. L. de Morais ◽  
Larissa I. O. de Sousa ◽  
Bruno M. Carvalho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Virus Infection ◽  
Virus Replication ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Caspase 3 ◽  
Neurological Complications ◽  
Zika Virus Infection

Background: Zika virus is an emerging arbovirus of global importance. ZIKV infection is associated with a range of neurological complications such as the Congenital Zika Syndrome and Guillain Barré Syndrome. Despite the magnitude of recent outbreaks, there is no specific therapy to prevent or to alleviate disease pathology. Objective: To investigate the role of P-MAPA immunomodulator in Zika-infected THP-1 cells. Methods: THP-1 cells were subjected at Zika virus infection (Multiplicity of Infection = 0.5) followed by treatment with P-MAPA for until 96 hours post-infection. After that, the cell death was analyzed by annexin+/ PI+ and caspase 3/ 7+ staining by flow cytometry. In addition, the virus replication and cell proliferation were accessed by RT-qPCR and Ki67 staining, respectively. Results: We demonstrate that P-MAPA in vitro treatment significantly reduces Zika virus-induced cell death and caspase-3/7 activation on THP-1 infected cells, albeit it has no role in virus replication and cell proliferation. Conclusions: Our study reveals that P-MAPA seems to be a satisfactory alternative to inhibits the effects of Zika virus infection in mammalian cells.

Single-chain Antibody Against Reg4 Suppresses Gastric Cancer Cell Growth and Enhances 5-FU-induced Cell Death in vitro

2019 ◽  
Vol 19 (5) ◽  
pp. 610-619 ◽  
Author(s):  
Xue-Qing Zhang ◽  
Lu-Ting Yu ◽  
Pei Du ◽  
Tian-Qi Yin ◽  
Zhi-Yuan Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Single Chain ◽  
Single Chain Antibody ◽  
Ags Cells ◽  
Thiazolyl Blue Tetrazolium Bromide

Background:Regenerating islet-derived gene family member 4 (Reg4), a well-investigated growth factor in the regenerative pancreas, has recently been reported to be highly associated with a majority of gastrointestinal cancers. Pathological hyper-expression or artificial over-expression of Reg4 causes acceleration of tumor growth, migration, and resistance to chemotherapeutic 5-Fluorouracil (5-FU). Until now, no method has been successfully established for eliminating the effects of Reg4 protein.Methods:This study reports the production of an engineered immunoglobin, a single-chain variable fragment (scFv-Reg4), to specifically bind Reg4 and block the bioactivity. The complementary-determining regions (CDRs) against Reg4 were assigned using MOE and ZDOCK servers. The binding affinity (KD) was determined by bio-layer interferometry (BLI). MKN45 and AGS cell proliferation was determined by Thiazolyl blue tetrazolium bromide (MTT) method and the cell apoptosis was detected by flow cytometry assay.Results:The KD of scFv-Reg4 to Reg4 was determined to be 1.91×10-8. In MKN45 and AGS cell lines, scFv- Reg4 depressed Reg4-stimulated cell proliferation and the inhibitory rates were 27.7±1.5% and 17.3±2.6%, respectively. Furthermore, scFv significantly enhanced 5-FU-induced cell death, from 23.0±1.0% to 28.4±1.2% in MKN45 and 28.2±0.7% to 36.6±0.6% in AGS cells. Treatment with scFv alone could lyse cancer cells to a certain extent, but no significance has been observed.Conclusion:The single-chain antibody (scFv-Reg4) significantly inhibited gastric cancer cell proliferation and synergistically enhanced the lethal effect of 5-FU. Thus, traditional chemo-/radio- therapeutics supplemented with scFv-Reg4 may provide advances in the strategy for gastrointestinal cancer treatment.

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