Transformation of catecholaminergic precursors into glucagon (A) cells in the mouse embryonic pancreas

1981 ◽  
pp. 873-883 ◽  
Author(s):  
G. Teitelman ◽  
T. H. Joh ◽  
D. J. Reis
Keyword(s):  
A Cells ◽  
Embryonic Pancreas

Sarsasapogenin stimulates melanogenesis in melan-a cells

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
E Moon ◽  
SY Kim
Keyword(s):  
A Cells

The Role of GLP-1 Receptor Expressed in Pancreatic a Cells in Regulating Glucagon Secretion

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 355-OR ◽  
Author(s):  
YANQING ZHANG ◽  
KESHAB R. PARAJULI ◽  
GENEVIEVE E. SMITH ◽  
RAJESH GUPTA ◽  
WEIWEI XU ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
A Cells

2187-P: Gsα Deficiency in Pancreatic a Cells Leads to Enlarged Islets

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2187-P
Author(s):  
AKIKO TAIRA ◽  
HUI SUN ◽  
CHRISTINA LE ◽  
OKSANA GAVRILOVA ◽  
MIN CHEN ◽  
...  
Keyword(s):  
A Cells

scholarly journals Elevated levels of IL-1β in Fanconi anaemia group A patients due to a constitutively active phosphoinositide 3-kinase-Akt pathway are capable of promoting tumour cell proliferation

2009 ◽  
Vol 422 (1) ◽  
pp. 161-170 ◽  
Author(s):  
Ana Ibáñez ◽  
Paula Río ◽  
José Antonio Casado ◽  
Juan Antonio Bueren ◽  
José Luis Fernández-Luna ◽  
...  
Keyword(s):  
Glycogen Synthase ◽  
Bone Marrow Failure ◽  
Nuclear Factor Κb ◽  
Hereditary Disease ◽  
Akt Pathway ◽  
Fanconi Anaemia ◽  
Primary Glioblastoma ◽  
A Cells ◽  
Group A ◽  
Phosphoinositide 3 Kinase

FA (Fanconi anaemia) is a hereditary disease characterized by congenital malformations, progressive bone marrow failure and an extraordinary elevated predisposition to develop cancer. In the present manuscript we describe an anomalous high level of the proinflammatory cytokine IL-1β (interleukin-1β) present in the serum of FA patients. The elevated levels of IL-1β were completely reverted by transduction of a wild-type copy of the FancA cDNA into FA-A (FA group A) lymphocytes. Although the transcription factor NF-κB (nuclear factor-κB) is a well established regulator of IL-1β expression, our experiments did not show any proof of elevated NF-κB activity in FA-A cells. However, we found that the overexpression of IL-1β in FA-A cells is related to a constitutively activated PI3K (phosphoinositide 3-kinase)-Akt pathway in these cells. We provide evidence that the effect of Akt on IL-1β activation is mediated by the inhibition of GSK3β (glycogen synthase kinase 3β). Finally, our data indicate that the levels of IL-1β produced by FA-A lymphoblasts are enough to promote an activation of the cell cycle in primary glioblastoma progenitor cells. Together, these results demonstrate that the constitutive activation of the PI3K-Akt pathway in FA cells upregulates the expression of IL-1β through an NF-κB-independent mechanism and that this overproduction activates the proliferation of tumour cells.

scholarly journals Overexpression of Transcripts Coding for Renin-b but Not for Renin-a Reduce Oxidative Stress and Increase Cardiomyoblast Survival under Starvation Conditions

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1204
Author(s):  
Heike Wanka ◽  
Philipp Lutze ◽  
Alexander Albers ◽  
Janine Golchert ◽  
Doreen Staar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
B Cells ◽  
Apoptotic Cell ◽  
Renin Angiotensin System ◽  
Glucose Deprivation ◽  
Protective Effects ◽  
Glucose Depletion ◽  
A Cells ◽  
Apoptosis And Necrosis

A stimulated renin-angiotensin system is known to promote oxidative stress, apoptosis, necrosis and fibrosis. Renin transcripts (renin-b; renin-c) encoding a cytosolic renin isoform have been discovered that may in contrast to the commonly known secretory renin (renin-a) exert protective effects Here, we analyzed the effect of renin-a and renin-b overexpression in H9c2 cardiomyoblasts on apoptosis and necrosis as well as on potential mechanisms involved in cell death processes. To mimic ischemic conditions, cells were exposed to glucose starvation, anoxia or combined oxygen–glucose deprivation (OGD) for 24 h. Under OGD, control cells exhibited markedly increased necrotic and apoptotic cell death accompanied by enhanced ROS accumulation, loss of mitochondrial membrane potential and decreased ATP levels. The effects of OGD on necrosis were exaggerated in renin-a cells, but markedly diminished in renin-b cells. However, with respect to apoptosis, the effects of OGD were almost completely abolished in renin-b cells but interestingly also moderately diminished in renin-a cells. Under glucose depletion we found opposing responses between renin-a and renin-b cells; while the rate of necrosis and apoptosis was aggravated in renin-a cells, it was attenuated in renin-b cells. Based on our results, strategies targeting the regulation of cytosolic renin-b as well as the identification of pathways involved in the protective effects of renin-b may be helpful to improve the treatment of ischemia-relevant diseases.

Properties of visceral primary afferent neurons in the nodose ganglion of the rabbit

1985 ◽  
Vol 54 (2) ◽  
pp. 245-260 ◽  
Author(s):  
C. E. Stansfeld ◽  
D. I. Wallis
Keyword(s):  
Action Potentials ◽  
Input Resistance ◽  
Nodose Ganglion ◽  
Time Dependent ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
C Cells ◽  
Axonal Conduction ◽  
A Cells

The active and passive membrane properties of rabbit nodose ganglion cells and their responsiveness to depolarizing agents have been examined in vitro. Neurons with an axonal conduction velocity of less than 3 m/s were classified as C-cells and the remainder as A-cells. Mean axonal conduction velocities of A- and C-cells were 16.4 m/s and 0.99 m/s, respectively. A-cells had action potentials of brief duration (1.16 ms), high rate of rise (385 V/s), an overshoot of 23 mV, and relatively high spike following frequency (SFF). C-cells typically had action potentials with a "humped" configuration (duration 2.51 ms), lower rate of rise (255 V/s), an overshoot of 28.6 mV, an after potential of longer duration than A-cells, and relatively low SFF. Eight of 15 A-cells whose axons conducted at less than 10 m/s had action potentials of longer duration with a humped configuration; these were termed Ah-cells. They formed about 10% of cells whose axons conducted above 2.5 m/s. The soma action potential of A-cells was blocked by tetrodotoxin (TTX), but that of 6/11 C-cells was unaffected by TTX. Typically, A-cells showed strong delayed (outward) rectification on passage of depolarizing current through the soma membrane and time-dependent (inward) rectification on inward current passage. Input resistance was thus highly sensitive to membrane potential close to rest. In C-cells, delayed rectification was not marked, and slight time-dependent rectification occurred in only 3 of 25 cells; I/V curves were normally linear over the range: resting potential to 40 mV more negative. Data on Ah-cells were incomplete, but in our sample of eight cells time-dependent rectification was absent or mild. C-cells had a higher input resistance and a higher neuronal capacitance than A-cells. In a proportion of A-cells, RN was low at resting potential (5 M omega) but increased as the membrane was hyperpolarized by a few millivolts. A-cells were depolarized by GABA but were normally unaffected by 5-HT or DMPP. C-cells were depolarized by GABA in a similar manner to A-cells but also responded strongly to 5-HT; 53/66 gave a depolarizing response, and 3/66, a hyperpolarizing response. Of C-cells, 75% gave a depolarizing response to DMPP.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Understanding heterogeneity of fetal hemoglobin induction through comparative analysis of F and A erythroblasts

Blood ◽  
2020 ◽  
Vol 135 (22) ◽  
pp. 1957-1968 ◽  
Author(s):  
Eugene Khandros ◽  
Peng Huang ◽  
Scott A. Peslak ◽  
Malini Sharma ◽  
Osheiza Abdulmalik ◽  
...  
Keyword(s):  
Fetal Hemoglobin ◽  
Erythroid Cell ◽  
Transcriptional Level ◽  
Globin Genes ◽  
Proteomic Profiling ◽  
A Cells ◽  
F Cells ◽  
Adult Hemoglobin ◽  
Differentiation Stage ◽  
Developmental Switch

Abstract Reversing the developmental switch from fetal hemoglobin (HbF, α2γ2) to adult hemoglobin (HbA, α2β2) is an important therapeutic approach in sickle cell disease (SCD) and β-thalassemia. In healthy individuals, SCD patients, and patients treated with pharmacologic HbF inducers, HbF is present only in a subset of red blood cells known as F cells. Despite more than 50 years of observations, the cause for this heterocellular HbF expression pattern, even among genetically identical cells, remains unknown. Adult F cells might represent a reversion of a given cell to a fetal-like epigenetic and transcriptional state. Alternatively, isolated transcriptional or posttranscriptional events at the γ-globin genes might underlie heterocellularity. Here, we set out to understand the heterogeneity of HbF activation by developing techniques to purify and profile differentiation stage-matched late erythroblast F cells and non–F cells (A cells) from the human HUDEP2 erythroid cell line and primary human erythroid cultures. Transcriptional and proteomic profiling of these cells demonstrated very few differences between F and A cells at the RNA level either under baseline conditions or after treatment with HbF inducers hydroxyurea or pomalidomide. Surprisingly, we did not find differences in expression of any known HbF regulators, including BCL11A or LRF, that would account for HbF activation. Our analysis shows that F erythroblasts are not significantly different from non-HbF–expressing cells and that the primary differences likely occur at the transcriptional level at the β-globin locus.

scholarly journals p53-dependent and p53-independent activation of apoptosis in mammary epithelial cells reveals a survival function of EGF and insulin.

1995 ◽  
Vol 128 (6) ◽  
pp. 1185-1196 ◽  
Author(s):  
G R Merlo ◽  
F Basolo ◽  
L Fiore ◽  
L Duboc ◽  
N E Hynes
Keyword(s):  
Mammary Epithelial Cells ◽  
P53 Protein ◽  
Survival Function ◽  
Mammary Epithelial ◽  
Nuclear Accumulation ◽  
Temperature Sensitive ◽  
Dna Damaging Agents ◽  
A Cells ◽  
Hc11 Cells ◽  
P53 Tumor Suppressor Protein

The p53 tumor suppressor protein has been implicated as a mediator of programmed cell death (PCD). A series of nontransformed mammary epithelial cell (MEC) lines were used to correlate p53 function with activation of PCD. Treatment of MECs expressing mutant, inactive, or no p53 with DNA-damaging agents did not induce apoptosis. Upon introduction of temperature-sensitive p53 into HC11 cells, which lack wild-type (wt) p53, PCD was observed after mitomycin treatment at 32 degrees, when the ts p53 protein is in wt conformation. Thus, wt p53 mediates activation of PCD in response to mitomycin in HC11 cells. Treatment of the MCF10-A cells, which express wt p53, with various DNA-damaging agents led to nuclear accumulation of p53. Only mitomycin treatment led to an increase in the number of apoptotic nuclei. ErbB-2-transformed MCF10-A cells responded to mitomycin, cisplatin, and 5-Fl-uracil, suggesting that signaling from activated ErbB-2 enhances the cells ability to respond to DNA damage. A combination of high cell density and serum-free medium induces apoptosis in all MECs tested, irrespective of their p53 status. Under these conditions, EGF or insulin act as survival factors in preventing PCD. These data might elucidate some aspects of breast involution and tumorigenesis.

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