Ciliary reversal ofParamecium primaureliamating type I and mating type II cells

1995 ◽  
Vol 62 (1) ◽  
pp. 1-4
Author(s):  
Sebastiano Salvidio ◽  
Paola Ramoino ◽  
Giuseppina Tolino ◽  
Angelo Valetto ◽  
Tina Crippa Franceschi
2004 ◽  
Vol 34 (7) ◽  
pp. 1930-1940 ◽  
Author(s):  
Adriana Eramo ◽  
Massimo Sargiacomo ◽  
Lucia Ricci-Vitiani ◽  
Matilde Todaro ◽  
Giorgio Stassi ◽  
...  

2003 ◽  
Vol 89 (6) ◽  
pp. 3097-3113 ◽  
Author(s):  
Jason S. Rothman ◽  
Paul B. Manis

Using kinetic data from three different K+ currents in acutely isolated neurons, a single electrical compartment representing the soma of a ventral cochlear nucleus (VCN) neuron was created. The K+ currents include a fast transient current ( IA), a slow-inactivating low-threshold current ( ILT), and a noninactivating high-threshold current ( IHT). The model also includes a fast-inactivating Na+ current, a hyperpolarization-activated cation current ( Ih), and 1–50 auditory nerve synapses. With this model, the role IA, ILT, and IHT play in shaping the discharge patterns of VCN cells is explored. Simulation results indicate that IHT mainly functions to repolarize the membrane during an action potential, and IA functions to modulate the rate of repetitive firing. ILT is found to be responsible for the phasic discharge pattern observed in Type II cells (bushy cells). However, by adjusting the strength of ILT, both phasic and regular discharge patterns are observed, demonstrating that a critical level of ILT is necessary to produce the Type II response. Simulated Type II cells have a significantly faster membrane time constant in comparison to Type I cells (stellate cells) and are therefore better suited to preserve temporal information in their auditory nerve inputs by acting as precise coincidence detectors and having a short refractory period. Finally, we demonstrate that modulation of Ih, which changes the resting membrane potential, is a more effective means of modulating the activation level of ILT than simply modulating ILT itself. This result may explain why ILT and Ih are often coexpressed throughout the nervous system.


1995 ◽  
Vol 269 (1) ◽  
pp. L127-L135 ◽  
Author(s):  
W. W. Barton ◽  
S. Wilcoxen ◽  
P. J. Christensen ◽  
R. Paine

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 271 (5) ◽  
pp. L688-L697 ◽  
Author(s):  
P. L. Sannes ◽  
J. Khosla ◽  
P. W. Cheng

The pulmonary alveolar basement membrane (BM) associated with alveolar type II cells has been shown to be significantly less sulfated than that of type I cells. To examine the biological significance of this observation, we measured the incorporation of 5-bromodeoxyuridine (BrdU) as an indicator of DNA synthesis in isolated rat type II cells cultured for 72-120 h on substrata that were naturally sulfated, not sulfated, or chemically desulfated in serum-free, hormonally defined media, with and without selected growth factors. The percentage of cells incorporating BrdU was significantly elevated by desulfated chondroitin sulfate in the presence of fibroblast growth factor-2 (FGF-2 or basic FGF) and depressed by heparin in the presence of either FGF-1 or acidic FGF or FGF-2. This depressive effect was lost by removing sulfate from the heparin. Some responses were dependent on the period of time in culture and concentration and molecular weight of the substrata. These observations support the notion that sulfation per se of certain components of BM is a key determinant of type II cell responses to select growth factors that may define patterns of proliferation and differentiation.


PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e55545 ◽  
Author(s):  
Mandi H. Wong ◽  
Meshell D. Johnson

Author(s):  
Joseph D. Ferrari ◽  
Kazuko Yamamoto ◽  
Matthew T. Blahna ◽  
Lee J. Quinton ◽  
Matthew R. Jones ◽  
...  

1996 ◽  
Vol 270 (6) ◽  
pp. L1017-L1022 ◽  
Author(s):  
I. Y. Adamson ◽  
L. Young

Most of the alveolar epithelium overlies a fused basement membrane produced by epithelial and endothelial cells. To determine how this type of matrix influences type II cell growth and function, we studied the effects of culturing isolated rat alveolar type II cells on an extracellular matrix (ECM) freshly produced by pulmonary vascular endothelial cells grown 5 days in culture. Type II cells from the same rats were cultured on plastic or Matrigel for comparison. A large increase in mitotic activity was seen in type II cells grown on the endothelial ECM at 2 days only; thereafter cells spread rapidly to confluence and lost their lamellar bodies. Cells grown on Matrigel remained cuboidal with lamellar bodies but grew more slowly, as judged by [3H]thymidine uptake and cell numbers. Incorporation of labeled choline into disaturated phosphatidylcholine (DSPC) was used as a marker of surfactant synthesis. After the rapid, brief burst of proliferation, type II cells on endothelial ECM showed a sudden decline in DSPC-DNA by day 4 compared with cells grown on matrigel. Binding of the lectin Bauhinia purpurea (BPA) indicated that after a phase of division, cells on endothelial ECM developed as type I epithelium by 4 days of culture, when > 70% of cells stained positively for BPA binding, whereas few cuboidal cells on Matrigel were stained. The results indicate that type II cells respond briefly to growth factors in pulmonary endothelial ECM; then this type of matrix promotes cell spreading with loss of type II function as cells subsequently resemble type I epithelium.


Nanomaterials ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 36 ◽  
Author(s):  
My Kieu Ha ◽  
Kyung Hwun Chung ◽  
Tae Hyun Yoon

Cellular association of nanoparticles (NPs) and their resultant cytotoxicity are heterogeneous in nature and can be influenced by the variances in NPs’ properties, cell types, and status. However, conventional in vitro assays typically consider the administered NP dose and the averaged cellular responses based on the assumption of a uniform distribution of monodisperse NPs in homogeneous cells, which might be insufficient to describe the complex nature of cell–NP interactions. Here, using flow cytometry, we report observations of the heterogeneity in the cellular association of silver nanoparticles (AgNPs) in A549 cells, which resulted in distinct dose-response relationships and cytotoxicity. Type I and Type II cells were moderately associated with AgNPs but as the cellular AgNP dose increased, Type I cells remained viable while Type II cells became less viable. Type III cells did not have high affinity with AgNPs but were, however, the least viable. Transmission electron microscopic images revealed that the biodistribution and the released Ag+ ions contributed to the distinct toxic effects of AgNPs in different populations. This single-cell dose-response analysis approach enabled the examination of how differently individual cells responded to different cellular NP doses and provided insights into nanotoxicity pathways at a single-cell level.


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