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Book ; Online ; Thesis: Die Rolle von Serin-Threonin-Kinasen für epitheliale Transportvorgänge = The role of serine-threonine-kinases in epithelial transport

Rexhepaj, Rexhep [Verfasser]

2008

Author's details	vorgelegt von Rexhep Rexhepaj
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: The Relevance of JAK2 in the Regulation of Cellular Transport.

Sopjani, Mentor / Konjufca, Vjollca / Rinnerthaler, Mark / Rexhepaj, Rexhep / Dërmaku-Sopjani, Miribane

Current medicinal chemistry

2015 Volume 23, Issue 6, Page(s) 578–588

Abstract: Janus kinase-2 (JAK2) is a non-receptor tyrosine kinase signaling molecule that mediates the effects of various hormones and cytokines, including interferon, erythropoietin, leptin, and growth hormone. It also fosters tumor growth and modifies the ... ...

Abstract	Janus kinase-2 (JAK2) is a non-receptor tyrosine kinase signaling molecule that mediates the effects of various hormones and cytokines, including interferon, erythropoietin, leptin, and growth hormone. It also fosters tumor growth and modifies the activity of several nutrient transporters. JAK2 contributes to the regulation of the cell volume, protectS cells during energy depletion, proliferation, and aids the survival of tumor cells. Recently, JAK2 was identified as a powerful regulator of transport processes across the plasma membrane. Either directly or indirectly JAK2 may stimulate or inhibit transporter proteins, including ion channels, carriers and Na(+)/K(+) pumps. As a powerful regulator of transport mechanisms across the cell membrane, JAK2 regulates a wide variety of potassium, calcium, sodium and chloride ion channels, multiple Na+-coupled cellular carriers including EAAT1-4, NaPi-IIa, SGLT1, BoaT1, PepT1-2, CreaT1, SMIT1, and BGT1 as well as Na(+)/K(+)-ATPase. These cellular transport regulations contribute to various physiological and pathophysiological processes and thus exerting JAK2-sensitive effects. Future investigations will be important to determine whether JAK2 regulates cell-surface expression of other transporters and further elucidate underlying mechanisms governing JAK2 actions.
MeSH term(s)	Animals ; Biological Transport ; Carrier Proteins/metabolism ; Humans ; Ion Channels/metabolism ; Janus Kinase 2/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism
Chemical Substances	Carrier Proteins ; Ion Channels ; Janus Kinase 2 (EC 2.7.10.2) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
Language	English
Publishing date	2015-12-03
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1319315-6
ISSN	1875-533X ; 0929-8673
ISSN (online)	1875-533X
ISSN	0929-8673
DOI	10.2174/0929867323666151207111707
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Zs.A 4432: Show issues

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Article ; Online: Vitamin D-Rich Diet in Mice Modulates Erythrocyte Survival.

Lang, Elisabeth / Jilani, Kashif / Bissinger, Rosi / Rexhepaj, Rexhep / Zelenak, Christine / Lupescu, Adrian / Lang, Florian / Qadri, Syed M

Kidney & blood pressure research

2015 Volume 40, Issue 4, Page(s) 403–412

Abstract: Background/aims: Epidemiological evidence suggests that vitamin D deficiency is associated with anemia. The potent metabolite 1,25(OH)2 vitamin D3 [1,25(OH)2D3] activates various signaling cascades regulating a myriad of cellular functions including ... ...

Abstract	Background/aims: Epidemiological evidence suggests that vitamin D deficiency is associated with anemia. The potent metabolite 1,25(OH)2 vitamin D3 [1,25(OH)2D3] activates various signaling cascades regulating a myriad of cellular functions including suicidal cell death or apoptosis. Suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Stimulation of eryptosis may limit lifespan of circulating erythrocytes and thus cause anemia. In the present study, we explored the effect of a high vitamin D diet (10,000 I.U. vitamin D for 14 days) in mice on eryptosis. Methods: Plasma concentrations of erythropoietin were estimated using an immunoassay kit, blood count using an electronic hematology particle counter, relative reticulocyte numbers using Retic-COUNT® reagent, PS exposure at the cell surface from annexin V binding, cell volume from forward scatter, and cytosolic Ca(2+) ([Ca(2+)]i) from Fluo3-fluorescence in FACS analysis. Results: Vitamin D treatment decreased mean corpuscular volume, reticulocyte count, and plasma erythropoietin levels. Vitamin D treatment slightly but significantly decreased forward scatter but did not significantly modify spontaneous PS exposure and [Ca(2+)]i of freshly drawn erythrocytes. Vitamin D treatment augmented the stimulation of PS exposure and cell shrinkage following exposure to hyperosmotic shock (addition of 550 mM sucrose) or energy depletion (glucose removal) without significantly modifying [Ca(2+)]i. Conclusions: The present observations point to a subtle effect of exogenous vitamin D supplementation on erythrocyte survival.
MeSH term(s)	Animals ; Blood Cell Count ; Calcium/metabolism ; Cell Size/drug effects ; Diet ; Erythrocyte Aging/drug effects ; Erythrocyte Membrane/drug effects ; Erythropoietin/metabolism ; Female ; Mice ; Mice, Inbred C57BL ; Osmotic Pressure/drug effects ; Phosphatidylserines/blood ; Vitamin D/therapeutic use ; Vitamins/therapeutic use
Chemical Substances	Phosphatidylserines ; Vitamins ; Erythropoietin (11096-26-7) ; Vitamin D (1406-16-2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1326018-2
ISSN	1423-0143 ; 1420-4096
ISSN (online)	1423-0143
ISSN	1420-4096
DOI	10.1159/000368517
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Article ; Online: Upregulation of intestinal NHE3 following saline ingestion.

Pasham, Venkanna / Rotte, Anand / Gu, Shuchen / Yang, Wenting / Bhandaru, Madhuri / Rexhepaj, Rexhep / Pathare, Ganesh / Lang, Florian

Kidney & blood pressure research

2013 Volume 37, Issue 1, Page(s) 48–57

Abstract: Background: Little is known about the effect of salt content of ingested fluid on intestinal transport processes. Osmosensitive genes include the serum- and glucocorticoid-inducible kinase SGK1, which is up-regulated by hyperosmolarity and cell ... ...

Abstract	Background: Little is known about the effect of salt content of ingested fluid on intestinal transport processes. Osmosensitive genes include the serum- and glucocorticoid-inducible kinase SGK1, which is up-regulated by hyperosmolarity and cell shrinkage. SGK1 is in turn a powerful stimulator of the intestinal Na(+)/H(+) exchanger NHE3. The present study was thus performed to elucidate, whether the NaCl content of beverages influences NHE3 activity. Methods: Mice were offered access to either plain water or isotonic saline ad libitum. NHE3 transcript levels and protein abundance in intestinal tissue were determined by confocal immunofluorescent microscopy, RT-PCR and western blotting, cytosolic pH (pHi) in intestinal cells from 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF) fluorescence and Na(+)/H(+) exchanger activity from the Na(+) dependent realkalinization following an ammonium pulse. Results: Saline drinking significantly enhanced fluid intake and increased NHE3 transcript levels, NHE3 protein and Na(+)/H(+) exchanger activity. Conclusions: Salt content of ingested fluid has a profound effect on intestinal Na(+)/H(+) exchanger expression and activity.
MeSH term(s)	Animals ; Eating/drug effects ; Eating/physiology ; Female ; Jejunum/drug effects ; Jejunum/metabolism ; Male ; Mice ; Organ Culture Techniques ; Sodium Chloride/administration & dosage ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/biosynthesis ; Up-Regulation/drug effects ; Up-Regulation/physiology
Chemical Substances	Slc9a3 protein, mouse ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Sodium Chloride (451W47IQ8X)
Language	English
Publishing date	2013
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1326018-2
ISSN	1423-0143 ; 1420-4096
ISSN (online)	1423-0143
ISSN	1420-4096
DOI	10.1159/000343401
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Article ; Online: PI3 kinase and PDK1 in the regulation of the electrogenic intestinal dipeptide transport.

Rexhepaj, Rexhep / Rotte, Anand / Pasham, Venkanna / Gu, Shuchen / Kempe, Daniela S / Lang, Florian

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2010 Volume 25, Issue 6, Page(s) 715–722

Abstract: The phosphoinositol 3 kinase (PI3K) and the phosphoinositide dependent kinase (PDK1) stimulate the serum and glucocorticoid inducible kinase (SGK) and protein kinase B (PKB/Akt) isoforms, kinases stimulating a variety of transporters. Most recently, SGK1 ...

Abstract	The phosphoinositol 3 kinase (PI3K) and the phosphoinositide dependent kinase (PDK1) stimulate the serum and glucocorticoid inducible kinase (SGK) and protein kinase B (PKB/Akt) isoforms, kinases stimulating a variety of transporters. Most recently, SGK1 was shown to stimulate the peptide transporters PepT1 and PepT2, and to mediate the glucocorticoid stimulation of PepT1. Basal electrogenic intestinal peptide transport was, however, not dependent on the presence of SGK1. The present study explored whether basal electrogenic intestinal peptide transport is dependent on PI3K or PDK1. To this end, peptide transport in intestinal segments was determined utilizing Ussing chamber analysis. Cytosolic pH (pH(i)) was determined by BCECF fluorescence. The luminal addition of 5 mM dipeptide gly-gly induced a current (Ip) across intestinal segments. Ip was significantly decreased in the presence of PI3 kinase inhibitors Wortmannin (1 microM) or LY294002 (50 microM). Exposure of isolated intestinal cells to 5 mM gly-gly was followed by cytosolic acidification (DeltapH(i)), which was significantly blunted by Wortmannin and by LY294002. Both, Ip and DeltapHi were significantly smaller in PDK1 hypomorphic mice (pdk(1flfl)) than in their wild type littermates (pdk1(wt)). In conclusion, PI3K and PDK1 participate in the regulation of basal peptide transport.
MeSH term(s)	3-Phosphoinositide-Dependent Protein Kinases ; Animals ; Dipeptides/metabolism ; Intestinal Mucosa/metabolism ; Intestines/cytology ; Mice ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Transport ; Protein-Serine-Threonine Kinases/metabolism
Chemical Substances	Dipeptides ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; 3-Phosphoinositide-Dependent Protein Kinases (EC 2.7.11.1) ; Pdpk1 protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2010-05-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000315091
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Zs.A 3160: Show issues

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Article: PI3-kinase-dependent electrogenic intestinal transport of glucose and amino acids.

Rexhepaj, Rexhep / Artunc, Ferruh / Metzger, Marco / Skutella, Thomas / Lang, Florian

Pflugers Archiv : European journal of physiology

2007 Volume 453, Issue 6, Page(s) 863–870

Abstract: Intestinal glucose and amino acid transport is stimulated by the serum- and glucocorticoid-inducible kinase isoforms SGK1, SGK2, and SGK3 and protein kinase B which are, in turn, stimulated following activation of the phosphoinositol-3 kinase (PI3 kinase) ...

Abstract	Intestinal glucose and amino acid transport is stimulated by the serum- and glucocorticoid-inducible kinase isoforms SGK1, SGK2, and SGK3 and protein kinase B which are, in turn, stimulated following activation of the phosphoinositol-3 kinase (PI3 kinase). The present study has been performed to explore whether pharmacological inhibition of the PI3 kinase affects electrogenic jejunal transport of glucose and amino acids. In Ussing chamber experiments, glucose (20 mM), phenylalanine (20 mM), glutamine (20 mM), cysteine (20 mM), and proline (20 mM) generated lumen negative currents (I (glc), I (phe), I (gln), I (cys), and I (pro)), respectively, which gradually declined following application of the PI3 kinase inhibitor Wortmannin (1 muM). Within 40 min, Wortmannin treatment significantly decreased I (glc) by 39 +/- 10% (n = 5), I (phe) by 70 +/- 7% (n = 4), I (gln) by 69 +/- 8% (n = 4), I (cys) by 67 +/- 8% (n = 6), and I (prol) by 79 +/- 12% (n = 3). A similar decline of I (glc) was observed following application of the PI3 kinase inhibitor LY294002 (50 microM). Exposure to the inhibitors did not significantly alter transepithelial potential difference and resistance in the absence of substrates for electrogenic transport. The observations suggest that the electrogenic transport of glucose and several amino acids requires the continued activity of PI3 kinase.
MeSH term(s)	Amino Acids/pharmacokinetics ; Androstadienes/pharmacology ; Animals ; Biological Transport/drug effects ; Biological Transport/physiology ; Cysteine/pharmacokinetics ; Diffusion Chambers, Culture ; Diuretics, Osmotic/pharmacokinetics ; Electric Impedance ; Glucose/pharmacokinetics ; Glutamine/pharmacokinetics ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Jejunum/drug effects ; Jejunum/metabolism ; Mannitol/pharmacokinetics ; Mice ; Phenylalanine/pharmacokinetics ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Proline/pharmacokinetics ; Protein Kinase Inhibitors/pharmacology
Chemical Substances	Amino Acids ; Androstadienes ; Diuretics, Osmotic ; Protein Kinase Inhibitors ; Glutamine (0RH81L854J) ; Mannitol (3OWL53L36A) ; Phenylalanine (47E5O17Y3R) ; Proline (9DLQ4CIU6V) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Glucose (IY9XDZ35W2) ; Cysteine (K848JZ4886) ; wortmannin (XVA4O219QW)
Language	English
Publishing date	2007-03
Publishing country	Germany
Document type	Journal Article
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-006-0154-6
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Article ; Online: Hyperaldosteronism, hypervolemia, and increased blood pressure in mice expressing defective APC.

Bhandaru, Madhuri / Kempe, Daniela S / Rotte, Anand / Rexhepaj, Rexhep / Kuhl, Dietmar / Lang, Florian

American journal of physiology. Regulatory, integrative and comparative physiology

2009 Volume 297, Issue 3, Page(s) R571–5

Abstract: Adenomatous polyposis coli (APC) fosters degradation of beta-catenin, a multifunctional protein upregulating the serum- and glucocorticoid-inducible kinase (SGK1). SGK1 regulates a wide variety of renal transport processes. The present study explored the ...

Abstract	Adenomatous polyposis coli (APC) fosters degradation of beta-catenin, a multifunctional protein upregulating the serum- and glucocorticoid-inducible kinase (SGK1). SGK1 regulates a wide variety of renal transport processes. The present study explored the possibility that APC influences renal function. To this end, metabolic cage experiments were performed in mice carrying a loss-of-function mutation in the APC gene (apc(Min/+)), their wild-type littermates (apc(+/+)), and apc(Min/+) mice lacking functional SGK1 (apc(Min/+)/sgk1(-/-)). As a result, mean body weight, food intake, fluid intake, salt appetite, urinary flow, as well as plasma Na(+) and K(+) concentrations were similar in apc(Min/+) mice, apc(+/+) mice, and apc(Min/+)/sgk1(-/-) mice. Glomerular filtration rate and absolute renal Na(+) excretion were decreased, and fractional urinary K(+) excretion was enhanced in apc(Min/+) mice. The antinatriuresis, but not the hypofiltration and kaliuresis was partially reversed by additional lack of SGK1. Plasma corticosterone and aldosterone concentrations were significantly enhanced in apc(Min/+) mice. While the plasma corticosterone concentration was similar in apc(+/+) mice and apc(Min/+)/sgk1(-/-) mice, plasma aldosterone was even higher in apc(Min/+)/sgk1(-/-) mice than in apc(Min/+) mice. The hyperaldosteronism of apc(Min/+) mice was paralleled by significantly elevated plasma volume and blood pressure. The experiments reveal an influence of defective APC on adrenal hormone release and renal function, effects partially but not completely explained by APC dependence of SGK1 expression.
MeSH term(s)	Adenomatous Polyposis Coli Protein/deficiency ; Adenomatous Polyposis Coli Protein/genetics ; Adenomatous Polyposis Coli Protein/metabolism ; Aldosterone/blood ; Animals ; Blood Pressure/genetics ; Blood Volume/genetics ; Body Weight ; Corticosterone/blood ; Drinking ; Eating ; Glomerular Filtration Rate ; Homeostasis ; Hyperaldosteronism/genetics ; Hyperaldosteronism/metabolism ; Hyperaldosteronism/physiopathology ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/physiopathology ; Immediate-Early Proteins/deficiency ; Immediate-Early Proteins/genetics ; Kidney/metabolism ; Kidney/physiopathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Natriuresis ; Potassium/blood ; Potassium/urine ; Protein-Serine-Threonine Kinases/deficiency ; Protein-Serine-Threonine Kinases/genetics ; Signal Transduction ; Sodium/blood ; Sodium/urine ; Sodium Chloride, Dietary/administration & dosage ; Urodynamics ; Wnt Proteins/metabolism
Chemical Substances	Adenomatous Polyposis Coli Protein ; Immediate-Early Proteins ; Sodium Chloride, Dietary ; Wnt Proteins ; Aldosterone (4964P6T9RB) ; Sodium (9NEZ333N27) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Potassium (RWP5GA015D) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2009-06-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00070.2009
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Article ; Online: Glucocorticoids enhance intestinal glucose uptake via the dimerized glucocorticoid receptor in enterocytes.

Reichardt, Sybille D / Föller, Michael / Rexhepaj, Rexhep / Pathare, Ganesh / Minnich, Kerstin / Tuckermann, Jan P / Lang, Florian / Reichardt, Holger M

Endocrinology

2012 Volume 153, Issue 4, Page(s) 1783–1794

Abstract: Glucocorticoid (GC) treatment of inflammatory disorders, such as inflammatory bowel disease, causes deranged metabolism, in part by enhanced intestinal resorption of glucose. However, the underlying molecular mechanism is poorly understood. Hence, we ... ...

Abstract	Glucocorticoid (GC) treatment of inflammatory disorders, such as inflammatory bowel disease, causes deranged metabolism, in part by enhanced intestinal resorption of glucose. However, the underlying molecular mechanism is poorly understood. Hence, we investigated transcriptional control of genes reported to be involved in glucose uptake in the small intestine after GC treatment and determined effects of GC on electrogenic glucose transport from transepithelial currents. GR(villinCre) mice lacking the GC receptor (GR) in enterocytes served to identify the target cell of GC treatment and the requirement of the GR itself; GR(dim) mice impaired in dimerization and DNA binding of the GR were used to determine the underlying molecular mechanism. Our findings revealed that oral administration of dexamethasone to wild-type mice for 3 d increased mRNA expression of serum- and GC-inducible kinase 1, sodium-coupled glucose transporter 1, and Na(+)/H(+) exchanger 3, as well as electrogenic glucose transport in the small intestine. In contrast, GR(villinCre) mice did not respond to GC treatment, neither with regard to gene activation nor to glucose transport. GR(dim) mice were also refractory to GC, because dexamethasone treatment failed to increase both, gene expression and electrogenic glucose transport. In addition, the rise in blood glucose levels normally observed after GC administration was attenuated in both mutant mouse strains. We conclude that enhanced glucose transport in vivo primarily depends on gene regulation by the dimerized GR in enterocytes, and that this mechanism contributes to GC-induced hyperglycemia.
MeSH term(s)	Animals ; Dexamethasone/pharmacology ; Dimerization ; Down-Regulation/drug effects ; Enterocytes/cytology ; Enterocytes/drug effects ; Enterocytes/metabolism ; Female ; Glucocorticoids/pharmacology ; Glucose/metabolism ; Immediate-Early Proteins/metabolism ; Interleukin-6/metabolism ; Intestinal Absorption/drug effects ; Jejunum/cytology ; Matrix Metalloproteinase 13/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Models, Animal ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Glucocorticoid/deficiency ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism ; Sodium-Glucose Transporter 1/metabolism ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Up-Regulation/drug effects
Chemical Substances	Glucocorticoids ; Immediate-Early Proteins ; Interleukin-6 ; Receptors, Glucocorticoid ; Slc5a1 protein, mouse ; Sodium-Glucose Transporter 1 ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Dexamethasone (7S5I7G3JQL) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Matrix Metalloproteinase 13 (EC 3.4.24.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2012-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2011-1747
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Article ; Online: OSR1-sensitive small intestinal Na+ transport.

Pasham, Venkanna / Pathare, Ganesh / Fajol, Abul / Rexhepaj, Rexhep / Michael, Diana / Pakladok, Tatsiana / Alesutan, Ioana / Rotte, Anand / Föller, Michael / Lang, Florian

American journal of physiology. Gastrointestinal and liver physiology

2012 Volume 303, Issue 11, Page(s) G1212–9

Abstract: The oxidative stress responsive kinase 1 (OSR1) contributes to WNK (with no K)-dependent regulation of renal tubular salt transport, renal salt excretion, and blood pressure. Little is known, however, about a role of OSR1 in the regulation of intestinal ... ...

Abstract	The oxidative stress responsive kinase 1 (OSR1) contributes to WNK (with no K)-dependent regulation of renal tubular salt transport, renal salt excretion, and blood pressure. Little is known, however, about a role of OSR1 in the regulation of intestinal salt transport. The present study thus explored whether OSR1 is expressed in intestinal tissue and whether small intestinal Na(+)/H(+) exchanger (NHE), small intestinal Na(+)-glucose cotransport (SGLT1), and/or colonic epithelium Na(+) channel (ENaC) differ between knockin mice carrying one allele of WNK-resistant OSR1 (osr1(+/KI)) and wild-type mice (osr1(+/+)). OSR1 protein abundance was determined by Western blotting, cytosolic pH from BCECF fluorescence, NHE activity from Na(+)-dependent realkalinization following an ammonium pulse, SGLT1 activity from glucose-induced current, and colonic ENaC activity from amiloride-sensitive transepithelial current in Ussing chamber experiments. As a result, OSR1 protein was expressed in small intestine of both osr1(+/KI) mice and osr1(+/+) mice. Daily fecal Na(+), K(+), and H(2)O excretion and jejunal SGLT1 activity were lower, whereas small intestinal NHE activity and colonic ENaC activity were higher in osr1(+/KI) mice than in osr1(+/+) mice. NHE3 inhibitor S-3226 significantly reduced NHE activity in both genotypes but did not abrogate the difference between the genotypes. Plasma osmolarity, serum antidiuretic hormone, plasma aldosterone, and plasma corticosterone concentrations were similar in both genotypes. Small intestinal NHE3 and colonic α-ENaC protein abundance were not significantly different between genotypes, but colonic phospho-β-ENaC (ser633) was significantly higher in osr1(+/KI) mice. In conclusion, OSR1 is expressed in intestine and partial WNK insensitivity of OSR1 increases intestinal NHE activity and colonic ENaC activity.
MeSH term(s)	Animals ; Epithelial Sodium Channels/metabolism ; Gene Knock-In Techniques ; Guanidines/pharmacology ; Methacrylates/pharmacology ; Mice ; Protein-Serine-Threonine Kinases/metabolism ; Sodium-Glucose Transporter 1/metabolism ; Sodium-Hydrogen Exchangers/metabolism
Chemical Substances	3-(2-(3-guanidino-2-methyl-3-oxo-propenyl)-5-methylphenyl)-N-isopropylidene-2-methyl-acrylamide dihydrochloride ; Epithelial Sodium Channels ; Guanidines ; Methacrylates ; Slc5a1 protein, mouse ; Sodium-Glucose Transporter 1 ; Sodium-Hydrogen Exchangers ; OXSR1 protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2012-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00367.2011
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Article ; Online: Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2.

Bissinger, Rosi / Lang, Elisabeth / Ghashghaeinia, Mehrdad / Singh, Yogesh / Zelenak, Christine / Fehrenbacher, Birgit / Honisch, Sabina / Chen, Hong / Fakhri, Hajar / Umbach, Anja T / Liu, Guilai / Rexhepaj, Rexhep / Liu, Guoxing / Schaller, Martin / Mack, Andreas F / Lupescu, Adrian / Birnbaumer, Lutz / Lang, Florian / Qadri, Syed M

Scientific reports

2016 Volume 6, Page(s) 30925

Abstract: Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, ... ...

Abstract	Putative functions of the heterotrimeric G-protein subunit Gαi2-dependent signaling include ion channel regulation, cell differentiation, proliferation and apoptosis. Erythrocytes may, similar to apoptosis of nucleated cells, undergo eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure. Eryptosis may be triggered by increased cytosolic Ca(2+) activity and ceramide. In the present study, we show that Gαi2 is expressed in both murine and human erythrocytes and further examined the survival of erythrocytes drawn from Gαi2-deficient mice (Gαi2(-/-)) and corresponding wild-type mice (Gαi2(+/+)). Our data show that plasma erythropoietin levels, erythrocyte maturation markers, erythrocyte counts, hematocrit and hemoglobin concentration were similar in Gαi2(-/-) and Gαi2(+/+) mice but the mean corpuscular volume was significantly larger in Gαi2(-/-) mice. Spontaneous PS exposure of circulating Gαi2(-/-) erythrocytes was significantly lower than that of circulating Gαi2(+/+) erythrocytes. PS exposure was significantly lower in Gαi2(-/-) than in Gαi2(+/+) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 ceramide. Erythrocyte Gαi2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+) activity and cell shrinkage. Moreover, Gαi2(-/-) erythrocytes were more resistant to osmosensitive hemolysis as compared to Gαi2(+/+) erythrocytes. In conclusion, Gαi2 deficiency in erythrocytes confers partial protection against suicidal cell death.
MeSH term(s)	Animals ; Cell Survival ; Eryptosis ; Erythrocyte Indices ; Erythrocytes/chemistry ; Erythrocytes/cytology ; Erythrocytes/physiology ; GTP-Binding Protein alpha Subunit, Gi2/deficiency ; GTP-Binding Protein alpha Subunit, Gi2/metabolism ; Humans ; Mice ; Mice, Knockout ; Phosphatidylserines/analysis
Chemical Substances	Phosphatidylserines ; GTP-Binding Protein alpha Subunit, Gi2 (EC 3.6.5.1)
Language	English
Publishing date	2016-08-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep30925
Database	MEDical Literature Analysis and Retrieval System OnLINE

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