Faculty Opinions recommendation of Up-regulation of Bcl-2 by CD147 Through ERK Activation Results in Abnormal Cell Survival in Human Endometriosis.

2015 ◽  
Author(s):  
Kaei Nasu
Keyword(s):  
Cell Survival ◽  
Erk Activation ◽  
Abnormal Cell

The quantity and duration of FcRγ signals determine mast cell degranulation and survival

Blood ◽  
2004 ◽  
Vol 103 (8) ◽  
pp. 3093-3101 ◽  
Author(s):  
Sho Yamasaki ◽  
Eri Ishikawa ◽  
Masayuki Kohno ◽  
Takashi Saito
Keyword(s):  
Mast Cell ◽  
Cell Survival ◽  
Immunoglobulin E ◽  
Mast Cell Degranulation ◽  
Mitogen Activated Protein Kinase ◽  
Cross Linking ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Abstract Immunoglobulin E (IgE) bound to multivalent antigen (Ag) elicits mast cell degranulation but not survival; on the contrary, IgE in the absence of Ag (IgE(-Ag)) induces survival only but not degranulation. Although these distinct responses are mediated through the same receptor, FcϵRI, the molecular mechanism generating the divergence is largely unknown. We recently showed that the signals through FcRγ chain are essential for IgE(-Ag)–induced mast cell survival as well as IgE(+Ag)–induced degranulation. To determine whether the cellular output is regulated by the quantity of FcRγ signal, we expressed CD8/FcRγ chimeras (CD8/γ) in bone marrow–derived mast cells (BMMCs) from FcRγ-/- mice to manipulate the strength of FcRγ signals by anti-CD8 cross-linking. Cross-linking of CD8/γ induced mast cell survival and degranulation. Survival was induced by weaker stimulation than needed for degranulation in terms of anti-CD8 concentration and the valency of chimera. However, sustained extracellular signal-regulated kinase (Erk) activation seems to regulate survival even when the activation signal was strong enough to elicit degranulation. Generation of sustained Erk activation by active mitogen-activated protein kinase kinase (MEK) induced BMMC survival. These results suggest that the duration and the magnitude of FcRγ signals may determine mast cell survival and degranulation, respectively. (Blood. 2004;103:3093-3101)

scholarly journals LAT and NTAL Mediate Immunoglobulin E-Induced Sustained Extracellular Signal-Regulated Kinase Activation Critical for Mast Cell Survival

2007 ◽  
Vol 27 (12) ◽  
pp. 4406-4415 ◽  
Author(s):  
Sho Yamasaki ◽  
Eri Ishikawa ◽  
Machie Sakuma ◽  
Osami Kanagawa ◽  
Alec M. Cheng ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Survival ◽  
Protein Tyrosine Kinase ◽  
Fluorescent Protein ◽  
Immunoglobulin E ◽  
Wild Type ◽  
Protein Fusion ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal

ABSTRACT Immunoglobulin E (IgE) induces mast cell survival in the absence of antigen (Ag) through the high-affinity IgE receptor, Fcε receptor I (FcεRI). Although we have shown that protein tyrosine kinase Syk and sustained extracellular signal-regulated kinase (Erk) activation are required for IgE-induced mast cell survival, how Syk couples with sustained Erk activation is still unclear. Here, we report that the transmembrane adaptors LAT and NTAL are phosphorylated slowly upon IgE stimulation and that sustained but not transient Erk activation induced by IgE was inhibited in LAT−/− NTAL−/− bone marrow-derived mast cells (BMMCs). IgE-induced survival requires Ras activation, and both were impaired in LAT−/− NTAL−/− BMMCs. Sos was preferentially required for FcεRI signals by IgE rather than IgE plus Ag. Survival impaired in LAT−/− NTAL−/− BMMCs was restored to levels comparable to those of the wild type by membrane-targeted Sos, which bypasses the Grb2-mediated membrane recruitment of Sos. The IgE-induced survival of BMMCs lacking Gads, an adaptor critical for the formation of the LAT-SLP-76-phospholipase Cγ (PLCγ) complex, was observed to be normal. IgE stimulation induced the membrane retention of Grb2-green fluorescent protein fusion proteins in wild-type but not LAT−/− NTAL−/− BMMCs. These results suggest that LAT and NTAL contribute to the maintenance of Erk activation and survival through the membrane retention of the Ras-activating complex Grb2-Sos and, further, that the LAT-Gads-SLP-76-PLCγ and LAT/NTAL-Grb2-Sos pathways are differentially required for degranulation and survival, respectively.

MAPK activation determines renal epithelial cell survival during oxidative injury

1999 ◽  
Vol 277 (2) ◽  
pp. F195-F203 ◽  
Author(s):  
John F. di Mari ◽  
Roger Davis ◽  
Robert L. Safirstein
Keyword(s):  
Cell Survival ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Cell Counting ◽  
Thick Ascending Limb ◽  
Erk Pathway ◽  
Iodide Uptake ◽  
Renal Epithelial Cell ◽  
Erk Activation ◽  
Igf I

Ischemia/reperfusion (I/R) injury induces both functional and morphological changes in the kidney. Necrosis, predominantly of the proximal tubule (PT), is the hallmark of this model of renal injury, whereas cells of the distal nephron survive, apparently intact. We examined whether differences in cellular outcome of the various regions of the nephron may be due to segmental variation in the activation of the mitogen-activated protein kinases (MAPKs) in response to I/R injury. Whereas c-Jun N-terminal kinase (JNK) is activated in both the cortex and inner stripe of the outer medulla, the extracellular regulated kinase (ERK) pathway is activated only in the inner stripe in which thick ascending limb (TAL) cells predominate. These studies are consistent with the notion that ERK activation is essential for survival. To test this hypothesis directly, we studied an in vitro system in which manipulation of these pathways and their effects on cellular survival could be examined. Oxidant injury was induced in mouse PT and TAL cells in culture by the catabolism of hypoxanthine by xanthine oxidase. PT cells were found to be more sensitive than TAL cells to oxidative stress as assessed by cell counting, light microscopy, propidium iodide uptake, and fluorescence-activated cell sorting (FACS) analysis. Immunoprecipitation/kinase analysis revealed that JNK activation occurred in both cell types, whereas ERK activation occurred only in TAL cells. We then examined the effect of PD-098059, a MAP kinase kinase (MEK)-1 inhibitor of the ERK pathway, on PT and TAL survival. In TAL cells, ERK inhibition reduced cell survival nearly fourfold ( P < 0.001) after oxidant exposure. In PT cells, activation of the ERK pathway by insulin-like growth factor I (IGF-I) increased survival by threefold ( P < 0.001), and this IGF-I-enhanced cell survival was inhibited by PD-098059. These results indicate that cell survival in the kidney after ischemia may be dependent on ERK activation, suggesting that this pathway may be a target for therapeutic treatment in I/R injury.

scholarly journals Overexpression of miR-155 causes expansion, arrest in terminal differentiation and functional activation of mouse natural killer cells

Blood ◽  
2013 ◽  
Vol 121 (16) ◽  
pp. 3126-3134 ◽  
Author(s):  
Rossana Trotta ◽  
Li Chen ◽  
Stefan Costinean ◽  
Srirama Josyula ◽  
Bethany L. Mundy-Bosse ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Cell Survival ◽  
Nk Cells ◽  
Nk Cell ◽  
Terminal Differentiation ◽  
Interferon Γ ◽  
Cell Number ◽  
Erk Activation ◽  
Key Points

Key Points miR-155 tg mice have increased NK-cell number, enhanced NK-cell survival, excess immature CD11blowCD27high NK cells, and an activated phenotype. miR-155 tg NK cells exhibit enhanced expansion, interferon-γ production, AKT and ERK activation, and killing of lymphoma in vivo.

The Response of Testes Cells to Low Level, Single dose Helium Particle Irradiation

1982 ◽  
Vol 40 ◽  
pp. 252-253
Author(s):  
D.E. Philpott ◽  
W. Sapp ◽  
C. Williams ◽  
J. Stevenson ◽  
S. Black ◽  
...  
Keyword(s):  
Stem Cell ◽  
Single Dose ◽  
B Cell ◽  
Cell Survival ◽  
Spermatogonial Stem Cell ◽  
Low Doses ◽  
Particle Irradiation ◽  
Stem Cell Survival ◽  
Irradiation Injury ◽  
Radio Sensitivity

Spermatogonial stem-cell survival after irradiation injury has been studied in rodents by histological counts of surviving cells. Many studies, including previous work from our laboratory, show that the spermatogonial population demonstrates a heterogeneous response to irradiation. The spermatogonia increase in radio-sensitivity as differentiation proceeds through the sequence As - Apr - A1 - A2 - A3 - A4 - In - B. The stem (As) cell is the most resistant and the B cell is the most sensitive. The purpose of this work is to investigate the response of spermatogonial cell to low doses (less than 10 0 rads) of helium particle irradiation.

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