scholarly journals Functional Separation of the Na-K Exchange Pump from the Volume Controlling Mechanism in Enlarged Duck Red Cells

1974 ◽  
Vol 64 (4) ◽  
pp. 393-412 ◽  
Author(s):  
Floyd M. Kregenow ◽  
Keyword(s):  
Cell Size ◽  
Red Cells ◽  
Minimal Volume ◽  
Cation Content ◽  
High K ◽  
Controlling Mechanism ◽  
Cation Pump ◽  
Mechanism Function ◽  
Original Size ◽  
The One

Previous publications have described a "volume controlling mechanism" in duck erythrocytes that returns both enlarged and shrunken cells to their original isotonic volume. Enlarged cells return to their original size by readjusting their K content. To study the specificity of this aspect of the mechanism for K, we prepared enlarged cells with various Na and K contents. Only cells containing a high K content resume their original size in the standard isotonic medium. The process of regulation resembles that described above. In contrast, cells containing a high Na content fail to reestablish this volume, but shrink instead until they reach a limiting minimal volume (four-fifths of normal). Here, another mechanism, the cation pump rather than the volume controlling mechanism, removes Na and is responsible for the changes in cell size. Enlarged cells with an intermediate Na and K content utilize both mechanisms to reduce their cation content. Only if Na is prevented from leaving the cell and sufficient K is present initially, will these cells reestablish their original size. These studies demonstrate that the cation pump and volume controlling mechanism function independently and, when cells enlarge, only K can effectively traverse the pathway associated with the volume controlling mechanism. This route differs from the one used by the cation pump to eject Na.

scholarly journals The Reponse of Duck Erythrocytes to Norepinephrine and an Elevated Extracellular Potassium

1973 ◽  
Vol 61 (4) ◽  
pp. 509-527 ◽  
Author(s):  
Floyd M. Kregenow
Keyword(s):  
Membrane Permeability ◽  
Cell Size ◽  
Monovalent Cation ◽  
Red Cells ◽  
Extracellular Potassium ◽  
Solute Content ◽  
Cation Content ◽  
Controlling Mechanism ◽  
Cation Pump ◽  
Original Size

This paper presents evidence that duck erythrocytes regulate their size in isotonic media by utilizing a previously reported "volume-controlling mechanism." Two different experimental situations are examined. In the first, cells enlarge in a solution containing norepinephrine and an elevated [K]o; and in the second, enlarged cells shrink to their original size if the norepinephrine and excess potassium are removed. As the erythrocytes enlarge, K, Cl, and H2O accumulate. Shrinkage, in contrast, is accompanied by the controlled loss of K, Cl, and H2O. These changes and the associated changes in membrane permeability resemble those reported previously when duck erythrocytes incubate in anisotonic media. There cells, after first shrinking or swelling, utilize a "volume-controlling mechanism" to reestablish their original size. The mechanism regulates cell size by adjusting the total number of osmotically active intracellular particles. The present studies indicate duck red cells use this mechanism to readjust their total monovalent cation content and thus their solute content in isotonic media as well. In addition, evidence is presented which indicates that the "volume-controlling mechanism" and ouabain-inhibitable cation pump differ functionally.

scholarly journals The Response of Duck Erythrocytes to Hypertonic Media

1971 ◽  
Vol 58 (4) ◽  
pp. 396-412 ◽  
Author(s):  
Floyd M. Kregenow
Keyword(s):  
Cell Volume ◽  
Cell Size ◽  
Hypertonic Solution ◽  
Electrochemical Gradient ◽  
Cell Content ◽  
Bathing Medium ◽  
Instantaneous Phase ◽  
Controlling Mechanism ◽  
Pump Mechanism ◽  
The One

The addition of a hypertonic bathing medium to duck erythrocytes results in an initial instantaneous phase of osmotic shrinkage and, when the [K]o of the hypertonic solution is larger than "normal," in a second, more prolonged phase, the volume regulatory phase. During the latter, which also requires extracellular Na, the cells swell until they approach their initial isotonic volume. The increase in cell volume during the volume regulatory phase is accomplished by a gain in the cell content of K, Cl, and H2O. There is also a smaller increase in the Na content of the cell. Potassium is accumulated against an electrochemical gradient and is therefore actively transported into the cell. This accumulation is associated with an increase, although dissimilar, in both K influx and efflux. Changes in cell size during the volume regulatory phase are not altered by 10-4 M ouabain, although this concentration of ouabain does change the cellular cation content. The response is independent of any effect of norepinephrine. The changes in cell size during the volume regulatory phase are discussed as the product of a volume controlling mechanism identical in principle to the one reported in the previous paper which controls cell volume in hypotonic media. Similarly, this mechanism can regulate cell size, when the Na-K exchange, ouabain-inhibitable pump mechanism is blocked.

Effect of basement membrane and colloid osmotic pressure on renal tubule cell volume

1977 ◽  
Vol 233 (4) ◽  
pp. F325-F332
Author(s):  
M. A. Linshaw ◽  
F. B. Stapleton ◽  
F. E. Cuppage ◽  
J. J. Grantham
Keyword(s):  
Basement Membrane ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Cell Size ◽  
Renal Tubule ◽  
Colloid Osmotic Pressure ◽  
Outer Diameter ◽  
Tubule Cell ◽  
Cation Pump ◽  
Renal Tubule Cell

Renal tubule cell volume is thought to be kept constant by a cation pump. When active transport is blocked, intracellular impermeant solutes cause cells to swell. Cell size is then determined by transmembrane hydrostatic and colloid osmotic forces. We studied the importance of passive transmembrane forces in determining cell size in isolated rabbit proximal straight tubules (PST). We blocked active solute transport with ouabain and evaluated subsequent changes in cell size by measuring outer diameter of nonperfused tubules. Tubules in a ouabain and 6 g/100 ml protein bath swelled only 40% above control. However, removal of the tubule basement membrane with collagenase dissipated a transmembrane hydrostatic pressure and caused more swelling. Final cell volume was determined largely by bath protein concentration. Tubules in ouabain and collagenase swelled enormously in hyponcotic protein, moderately in isoncotic protein, and could be shrunk below control in hyperoncotic protein. Intracellular colloid osmotic pressure was estimated to exceed 38 cmH20. We conclude that hydrostatic and colloid osmotic forces are major determinants of cell size in isolated PST treated with ouabain.

scholarly journals The molecular link between auxin and ROS-Mediated polar root hair growth

2017 ◽  
Author(s):  
Silvina Mangano ◽  
Silvina Paola Denita-Juarez ◽  
Hee-Seung Choi ◽  
Eliana Marzol ◽  
Youra Hwang ◽  
...  
Keyword(s):  
Cell Size ◽  
Root Hair ◽  
Hair Growth ◽  
Molecular Mechanisms ◽  
Root Hairs ◽  
Oxygen Species ◽  
Polar Growth ◽  
Genes Encoding ◽  
Root Hair Growth ◽  
Original Size

AbstractRoot hair polar growth is endogenously controlled by auxin and sustained by oscillating levels of reactive oxygen species (ROS). These cells extend several hundred-fold their original size toward signals important for plant survival. Although their final cell size is of fundamental importance, the molecular mechanisms that control it remain largely unknown. Here, we show that ROS production is controlled by the transcription factors RSL4, which in turn is transcriptionally regulated by auxin through several Auxin Responsive Factors (ARFs). In this manner, auxin controls ROS-mediated polar growth by activating RSL4, which then upregulates the expression of genes encoding NADPH oxidases (also known as RBOHs, RESPIRATORY BURST OXIDASE HOMOLOG proteins) and Class-III Peroxidases (PER), which catalyse ROS production. Chemical or genetic interference with the ROS balance or peroxidase activity affect root hair final cell size. Overall, our findings establish a molecular link between auxin regulated ARFs-RSL4 and ROS-mediated polar root hair growth.Significance StatementTip-growing root hairs are excellent model systems to decipher the molecular mechanism underlying reactive oxygen species (ROS)-mediated cell elongation. Root hairs are able to expand in response to external signals, increasing several hundred-fold their original size, which is important for survival of the plant. Although their final cell size is of fundamental importance, the molecular mechanisms that control it remain largely unknown. In this study, we propose a molecular mechanism that links the auxin-Auxin Response Factors (ARFs) module to activation of RSL4, which directly targets genes encoding ROS-producing enzymes, such as NADPH oxidases (or RBOHs) and secreted type-III peroxidases (PERs). Activation of these genes impacts apoplastic ROS homeostasis, thereby stimulating root hair cell elongation.

Swelling, NEM, and A23187 activate Cl(-)-dependent K+ transport in high-K+ sheep red cells

1987 ◽  
Vol 252 (2) ◽  
pp. C197-C204 ◽  
Author(s):  
H. Fujise ◽  
P. K. Lauf
Keyword(s):  
Metal Ion ◽  
Red Cells ◽  
Common Mechanism ◽  
Ionophore A23187 ◽  
Sheep Red Cells ◽  
High K ◽  
Sh Group ◽  
Low K ◽  
K Transport ◽  
Significant Activation

In low K+ (LK) sheep red cells a significant fraction of the total ouabain-resistant (OR) K+ flux is inhibited when Cl- is replaced by other anions of the Hofmeister series except Br- (Cl(-)-dependent K+ flux). In contrast, high K+ (HK) sheep red cells in isosmotic media did not possess any significant OR Cl(-)-dependent K+ flux when Cl- was replaced by NO3- or I-. However, exposure to hyposmotic solutions, treatment with the sulfhydryl (SH) group reagent N-ethylmaleimide (NEM) or with the bivalent metal ion (Me2+) ionophore A23187 in absence of external Me2+ caused a significant activation of Cl(-)-dependent K+ transport as measured with Rb+ as K+ congener. There was no Cl(-)-dependent Rb+ flux in A23187-treated cells when Mn2+, Mg2+, and Ca2+ were present at 1 mM concentrations, suggesting that cellular accumulation of these Me2+ is inhibitory. Similar to LK red cells, HK red cells failed to respond to A23187 when pretreated with NEM supporting the hypothesis proposed recently (Lauf, P. K. J. Membr. Biol. 88: 1-13, 1985) of a common mechanism of Cl(-)-dependent K+ transport activation. The magnitudes of the Cl(-)-dependent Rb+ fluxes in HK cells were much smaller than those elicited by identical treatments in LK red cells, and the effect of all interventions was not due to the presence of reticulocytes known to possess Cl(-)-dependent K+ transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Ion and water shifts produced by ammonium chloride in high K and low K red cells

1966 ◽  
Vol 68 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Simo Salminen ◽  
Vesa Manninen
Keyword(s):  
Ammonium Chloride ◽  
Red Cells ◽  
High K ◽  
Low K

scholarly journals The Erythropoietin Receptor Stimulates Rapid Cycling and Formation of Larger Red Cells During Mouse and Human Erythropoiesis

2020 ◽  
Author(s):  
Daniel Hidalgo ◽  
Jacob Bejder ◽  
Ramona Pop ◽  
Kyle Gellatly ◽  
S. Maxwell Scalf ◽  
...  
Keyword(s):  
Cell Size ◽  
Erythropoietin Receptor ◽  
Red Cells ◽  
Red Cell ◽  
Cell Cycles ◽  
Erythroid Terminal Differentiation ◽  
Unique Effect ◽  
Human Volunteers ◽  
Eif2α Kinase ◽  
Survival Signaling

AbstractErythroid terminal differentiation entails cell divisions that are coupled to progressive decreases in cell size. EpoR signaling is essential for the survival of erythroid precursors, but it is unclear whether it has other functions in these cells. Here we endowed mouse precursors that lack the EpoR with survival signaling, finding that this was sufficient to support their differentiation into enucleated red cells, but that the process was abnormal. Precursors underwent fewer and slower cell cycles and yet differentiated into smaller red cells. Surprisingly, EpoR further accelerated cycling of early erythroblasts, the fastest cycling cells in the bone marrow, while simultaneously increasing their cell size. EpoR-mediated formation of larger red cells was independent of the established pathway regulating red cell size by iron through Heme-regulated eIF2α kinase (HRI). We confirmed the effect of Epo on red cell size in human volunteers, whose mean corpuscular volume (MCV) increased following Epo administration. This increase persisted after Epo declined and was not the result of increased reticulocytes. Our work reveals a unique effect of EpoR signaling on the interaction between the cell cycle and cell growth. Further, it suggests new diagnostic interpretations for increased red cell volume, as reflecting high Epo and erythropoietic stress.

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