Anorexic effect of K+ channel blockade in mesenteric arterial smooth muscle and intestinal epithelial cells

2001 ◽  
Vol 91 (5) ◽  
pp. 2322-2333 ◽  
Author(s):  
Sharon S. McDaniel ◽  
Oleksandr Platoshyn ◽  
Ying Yu ◽  
Michele Sweeney ◽  
Victor A. Miriel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Weight Gain ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Membrane Depolarization ◽  
Intestinal Epithelial ◽  
Whole Cell ◽  
Kv Channel ◽  
Kv Channels ◽  
Α And Β Subunits

Activity of voltage-gated K+ (Kv) channels controls membrane potential ( E m). Membrane depolarization due to blockade of K+ channels in mesenteric artery smooth muscle cells (MASMC) should increase cytoplasmic free Ca2+ concentration ([Ca2+]cyt) and cause vasoconstriction, which may subsequently reduce the mesenteric blood flow and inhibit the transportation of absorbed nutrients to the liver and adipose tissue. In this study, we characterized and compared the electrophysiological properties and molecular identities of Kv channels and examined the role of Kv channel function in regulating E m in MASMC and intestinal epithelial cells (IEC). MASMC and IEC functionally expressed multiple Kv channel α- and β-subunits (Kv1.1, Kv1.2, Kv1.3, Kv1.4, Kv1.5, Kv2.1, Kv4.3, and Kv9.3, as well as Kvβ1.1, Kvβ2.1, and Kvβ3), but only MASMC expressed voltage-dependent Ca2+ channels. The current density and the activation and inactivation kinetics of whole cell Kv currents were similar in MASMC and IEC. Extracellular application of 4-aminopyridine (4-AP), a Kv-channel blocker, reduced whole cell Kv currents and caused E m depolarization in both MASMC and IEC. The 4-AP-induced E m depolarization increased [Ca2+]cyt in MASMC and caused mesenteric vasoconstriction. Furthermore, ingestion of 4-AP significantly reduced the weight gain in rats. These results suggest that MASMC and IEC express multiple Kv channel α- and β-subunits. The function of these Kv channels plays an important role in controlling E m. The membrane depolarization-mediated increase in [Ca2+]cyt in MASMC and mesenteric vasoconstriction may inhibit transportation of absorbed nutrients via mesenteric circulation and limit weight gain.

Activation of K+ channels and increased migration of differentiated intestinal epithelial cells after wounding

2002 ◽  
Vol 282 (4) ◽  
pp. C885-C898 ◽  
Author(s):  
Jaladanki N. Rao ◽  
Oleksandr Platoshyn ◽  
Li Li ◽  
Xin Guo ◽  
Vera A. Golovina ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Fiber Formation ◽  
Intestinal Epithelial ◽  
Membrane Hyperpolarization ◽  
Kv Channel ◽  
Kv Channels ◽  
Channel Expression

Early mucosal restitution occurs by epithelial cell migration to reseal superficial wounds after injury. Differentiated intestinal epithelial cells induced by forced expression of the Cdx2 gene migrate over the wounded edge much faster than undifferentiated parental cells in an in vitro model. This study determined whether these differentiated intestinal epithelial cells exhibit increased migration by altering voltage-gated K+ (Kv) channel expression and cytosolic free Ca2+ concentration ([Ca2+]cyt). Stable Cdx2-transfected IEC-6 cells (IEC-Cdx2L1) with highly differentiated phenotype expressed higher basal levels of Kv1.1 and Kv1.5 mRNAs and proteins than parental IEC-6 cells. Neither IEC-Cdx2L1 cells nor parental IEC-6 cells expressed voltage-dependent Ca2+ channels. The increased expression of Kv channels in differentiated IEC-Cdx2L1 cells was associated with an increase in whole cell K+ currents, membrane hyperpolarization, and a rise in [Ca2+]cyt. The migration rates in differentiated IEC-Cdx2L1 cells were about four times those of parental IEC-6 cells. Inhibition of Kv channel expression by polyamine depletion decreased [Ca2+]cyt, reduced myosin stress fibers, and inhibited cell migration. Elevation of [Ca2+]cyt by ionomycin promoted myosin II stress fiber formation and increased cell migration. These results suggest that increased migration of differentiated intestinal epithelial cells is mediated, at least partially, by increasing Kv channel activity and Ca2+ influx during restitution.

Secretion of human meprin from intestinal epithelial cells depends on differential expression of the α and β subunits

1999 ◽  
Vol 259 (1-2) ◽  
pp. 496-504 ◽  
Author(s):  
Daniel Lottaz ◽  
Dagmar Hahn ◽  
Stefan Müller ◽  
Christoph Müller ◽  
Erwin E. Sterchi
Keyword(s):  
Epithelial Cells ◽  
Differential Expression ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Α And Β Subunits

scholarly journals IL-4 Receptor-Alpha Signalling of Intestinal Epithelial Cells, Smooth Muscle Cells, and Macrophages Plays a Redundant Role in Oxazolone Colitis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jennifer Claire Hoving ◽  
Roanne Keeton ◽  
Maxine A. Höft ◽  
Mumin Ozturk ◽  
Patricia Otieno-Odhiambo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Intestinal Epithelial Cells ◽  
Muscle Cells ◽  
Specific Cell ◽  
Intestinal Epithelial ◽  
Receptor Alpha ◽  
Redundant Role

A hallmark of ulcerative colitis is the chronic colonic inflammation, which is the result of a dysregulated intestinal mucosal immune response. Epithelial barrier disruption which allows the entry of microorganisms eventually leads to more aggressive inflammation and potentially the removal of the colon. We have previously shown that the T helper- (Th-) type 2 cytokines, Interleukin- (IL-) 4 and IL-13, mediate CD4+ T cell- or B cell-driven inflammation in the oxazolone-induced mouse model of ulcerative colitis. In contrast, mice deficient in the shared receptor of IL-4 and IL-13, IL-4 receptor-alpha (IL-4Rα), on all cells develop an exacerbated disease phenotype. This suggests that a regulatory role of IL-4Rα is required to protect against severe colitis. However, the cell populations responsible for regulating the severity of disease onset through IL-4Rα in colitis are yet to be identified. By deleting IL-4Rα on specific cell subsets shown to play a role in mediating colitis, we determined their role in a loss of function approach. Our data demonstrated that the loss of IL-4Rα signalling on intestinal epithelial cells, smooth muscle cells, and macrophages/neutrophils had no effect on alleviating the pathology associated with colitis. These results suggest that IL-4/IL-13 signalling through IL-4Rα on nonhematopoietic intestinal epithelial or smooth muscle cells and hematopoietic macrophage/neutrophils has a redundant role in driving acute oxazolone colitis.

Primary culture of salamander intestinal epithelial cells from nests: whole cell Na+ currents induced by valine

1994 ◽  
Vol 267 (1) ◽  
pp. G59-G66
Author(s):  
J. F. White
Keyword(s):  
Epithelial Cells ◽  
Intestinal Mucosa ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cells ◽  
Small Intestinal Mucosa ◽  
Intestinal Epithelial ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Inward Current ◽  
Small Intestinal

Methods are described for isolating the cell nests, subepithelial clusters of germinative cells, from salamander intestinal mucosa and for growing the nests in culture into polarized monolayers of intestinal epithelial cells. Cells were viable in culture for up to 3 wk. The capacity of the monolayer cells to engage in membrane transport was evaluated using the patch-clamp technique in the whole cell mode. L-Valine (25 mM) induced an inward current in small intestinal cells of 25.8 +/- 5.7 pA and depolarized the cell membrane 14.5 +/- 1.6 mV. L-Alanine and L-phenylalanine were similarly effective, whereas D-valine was ineffective. The Km of the transporter for valine was 90 mM. Replacement of bath Na with tris(hydroxymethyl)aminomethane eliminated the inward current induced by valine. The basal (solute-independent) inward current was also reduced by Na+ replacement. Glucose did not induce a Na+ current. In contrast to the effect of valine on small intestinal cells, large intestinal cells were unresponsive to valine. It is concluded that the cultured small intestinal cells possess Na-amino acid but not Na-sugar cotransport. This profile of behavior is characteristic of undifferentiated small intestinal cells. Primary cultures of salamander small intestinal cells should be useful for studying enterocyte function and the developmental biology of the small intestinal mucosa.

scholarly journals Expression of actin isoforms in developing rat intestinal epithelium.

1989 ◽  
Vol 37 (8) ◽  
pp. 1225-1233 ◽  
Author(s):  
A L Hartman ◽  
N M Sawtell ◽  
J L Lessard
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Developmental Regulation ◽  
Adult Life ◽  
Developmental Expression ◽  
Intestinal Epithelial ◽  
Actin Isoforms ◽  
Adult Rat ◽  
Specific Distribution

A minimum of six very similar but distinct actin isoforms are encoded by the mammalian genome. Developmental regulation of these genes results in a tissue-specific distribution of the isoforms in the adult. Using a panel of actin specific monoclonal antibodies (MAb), we recently reported the expression of two unique actin isoforms in adult rat intestinal brush border. In this report, we examine the developmental expression of these and other actin isoforms in rat intestinal epithelial cells. Isoforms containing the HUC 1-1 and/or C4 epitopes are present by day 15 of gestation and are continuously expressed throughout adult life. Unexpectedly, the gamma-enteric smooth muscle isoactin, defined by the B4 epitope, is transiently expressed in these non-muscle cells late in gestation. The alpha-vascular smooth muscle isoform, however, is not expressed in intestinal epithelial cells during development and, as previously reported, both smooth muscle isoforms are absent in epithelial cells of adult intestine. In addition, we demonstrate that although multiple isoforms are expressed simultaneously in these cells, they are not uniformly distributed at the subcellular level, suggesting that the cell recognizes the actin isoforms as functionally distinct entities.

Three-dimensional organization and functional relationships of endocytotic compartments in pig intestinal epithelial cells

1992 ◽  
Vol 50 (1) ◽  
pp. 576-577
Author(s):  
Julian P. Heath ◽  
Buford L. Nichols ◽  
László G. Kömüves
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Three Dimensional ◽  
Intestinal Epithelial ◽  
Cell Surfaces ◽  
Basal Surface ◽  
Functional Relationships

The newborn pig intestine is adapted for the rapid and efficient absorption of nutrients from colostrum. In enterocytes, colostral proteins are taken up into an apical endocytotic complex of channels that transports them to target organelles or to the basal surface for release into the circulation. The apical endocytotic complex of tubules and vesicles clearly is a major intersection in the routes taken by vesicles trafficking to and from the Golgi, lysosomes, and the apical and basolateral cell surfaces.Jejunal tissues were taken from piglets suckled for up to 6 hours and prepared for electron microscopy and immunocytochemistry as previously described.

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