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Article ; Online: Calcium regulation of tight junction permeability.

Bleich, Markus / Shan, Qixian / Himmerkus, Nina

Annals of the New York Academy of Sciences

2012 Volume 1258, Page(s) 93–99

Abstract: Calcium transport in the kidney is a key element in Ca(2+) homeostasis. Ca(2+) concentration, or more precisely the activity of freely dissociated Ca(2+) ions, is a prerequisite for the appropriate function of virtually every cell. Along the renal ... ...

Abstract	Calcium transport in the kidney is a key element in Ca(2+) homeostasis. Ca(2+) concentration, or more precisely the activity of freely dissociated Ca(2+) ions, is a prerequisite for the appropriate function of virtually every cell. Along the renal tubule, about 85% of the filtered Ca(2+) is transported across tight junctions at the paracellular route of reabsorption. Therefore, claudins, which form the conductive and selective part of the tight junctions, have moved into the focus of interest with respect to regulatory events in the control of Ca(2+) transport. This control is of particular interest for the kidney since it has to defend itself against nephrocalcinosis and kidney stones. Tight junction proteins provide pathways, driving forces, and regulatory targets for Ca(2+) transport. Direct regulation of tight junctions by changing Ca(2+) concentrations allows fast and efficient feedback loops to adapt Ca(2+) transport to the requirements of kidney function and plasma Ca(2+) concentration.
MeSH term(s)	Calcium/physiology ; Humans ; Permeability ; Tight Junctions/physiology
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2012-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2012.06539.x
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Article: Epithelial K⁺ channels: driving force generation and K⁺ recycling for epithelial transport with physiological and clinical implications.

Bleich, Markus / Shan, Qi-Xian

Sheng li xue bao : [Acta physiologica Sinica

2007 Volume 59, Issue 4, Page(s) 443–453

Abstract: K(+) channels form a large family of membrane proteins that are expressed in a polarized fashion in any epithelial cell. Based on the transmembrane gradient for K(+) that is maintained by the Na(+)-K(+)-ATPase, these channels serve two principal ... ...

Abstract	K(+) channels form a large family of membrane proteins that are expressed in a polarized fashion in any epithelial cell. Based on the transmembrane gradient for K(+) that is maintained by the Na(+)-K(+)-ATPase, these channels serve two principal functions for transepithelial transport: generation of membrane voltage and recycling of K(+). In this brief review, we will outline the importance of this ancient principle by examples of epithelial transport in the renal proximal tubule and gastric parietal cells. In both tissues, K(+) channel activity is rate-limiting for transport processes across the epithelial cells and essential for cell volume regulation. Recent experimental data using pharmacological tools and genetically modified animals have confirmed the original physiological concepts and specified the knowledge down to the molecular level. The development of highly active and tissue selective small molecule therapeutics has been impeded by two typical features of K(+) channels: their molecular architecture challenges the design of molecules with high affinity binding and they are expressed in a variety of tissues at the same time. Nevertheless, new insights into pathophysiology, e.g. that K(+) channel inhibition can block gastric acid secretion, render the clinical use of K(+) channel drugs in gastric disease and as kidney transport inhibitors highly attractive.
MeSH term(s)	Animals ; Biological Transport ; Epithelial Cells/physiology ; Kidney/physiology ; Potassium ; Potassium Channels/physiology ; Sodium-Potassium-Exchanging ATPase/physiology
Chemical Substances	Potassium Channels ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2007-08-25
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	604308-2
ISSN	0371-0874
ISSN	0371-0874
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Article: [Endothelin-1 and nitric oxide mediated the lipopolysaccharide-induced cardiac negative inotropic role].

Yao, Hui / Tu, Jie / Shan, Qi-xian / Xia, Qiang

Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology

2009 Volume 25, Issue 2, Page(s) 228–232

Abstract: Aim: To investigate the effects of endothelin-1 (ET-1) and nitric oxide (NO) on lipopolysaccharide(LPS)-induced myocardial dysfunction, and explore the related underlying mechanisms.: Methods: Experimental septic model was established by ... ...

Abstract	Aim: To investigate the effects of endothelin-1 (ET-1) and nitric oxide (NO) on lipopolysaccharide(LPS)-induced myocardial dysfunction, and explore the related underlying mechanisms. Methods: Experimental septic model was established by intraperitoneal injection of LPS (10 mg x kg(-1)). The study was carried out on the isolated rat hearts to determine the roles of ET-1 and NO in the effect of LPS on the cardiac contractility and on the isolated rat ventricular myocytes model to observe the [Ca2+]i homeostasis in cardiac myocytes. Results: (1) The levels of serum NO2-/NO3- and plasma ET-1 were markedly increased by LPS treatment for 4 hours. (2) LPS induced the decrease in rate-pressure product (RPP), and increase in left ventricular end-diastolic pressure (LVEDP) in the isolated perfused rat hearts. Pretreatment with either aminoguanidine (AMG) (100 mg x kg(-1), i.p.) or BQ-123 (1 mg x kg(-1), i.p.) partially attenuated LPS-induced myocardial depression. When these two drugs were simultaneously given, myocardial depression elicited by LPS was almost abolished. (3) LPS significantly decreased the amplitude of caffeine induced [Ca2+]i transients compared to the control cells. The activity of SR Ca22+ -ATPase was significantly decreased in the cardiac myocytes from LPS-treated rats. Single pretreatment with either AMG or BQ-123 did not attenuate the impairment of SR Ca2+ -ATPase induced by LPS. Conclusion: ET-1 and NO mediate myocardial dysfunction in hearts isolated and decrease [Ca2+]i transients in cardiac myocytes from LPS-treated rats. But neither ET-1 nor NO participates in the impairment of SR Ca2+ -ATPase induced by LPS.
MeSH term(s)	Animals ; Depression, Chemical ; Endothelin-1/physiology ; Lipopolysaccharides/toxicity ; Male ; Myocardial Contraction/drug effects ; Myocardial Contraction/physiology ; Nitric Oxide/physiology ; Rats ; Rats, Sprague-Dawley ; Shock, Septic/chemically induced ; Shock, Septic/physiopathology
Chemical Substances	Endothelin-1 ; Lipopolysaccharides ; Nitric Oxide (31C4KY9ESH)
Language	Chinese
Publishing date	2009-05
Publishing country	China
Document type	English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1000-6834
ISSN	1000-6834
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Article ; Online: Short-term functional adaptation of aquaporin-1 surface expression in the proximal tubule, a component of glomerulotubular balance.

Pohl, Marcus / Shan, Qixian / Petsch, Thomas / Styp-Rekowska, Beata / Matthey, Patricia / Bleich, Markus / Bachmann, Sebastian / Theilig, Franziska

Journal of the American Society of Nephrology : JASN

2014 Volume 26, Issue 6, Page(s) 1269–1278

Abstract: Transepithelial water flow across the renal proximal tubule is mediated predominantly by aquaporin-1 (AQP1). Along this nephron segment, luminal delivery and transepithelial reabsorption are directly coupled, a phenomenon called glomerulotubular balance. ...

Abstract	Transepithelial water flow across the renal proximal tubule is mediated predominantly by aquaporin-1 (AQP1). Along this nephron segment, luminal delivery and transepithelial reabsorption are directly coupled, a phenomenon called glomerulotubular balance. We hypothesized that the surface expression of AQP1 is regulated by fluid shear stress, contributing to this effect. Consistent with this finding, we found that the abundance of AQP1 in brush border apical and basolateral membranes was augmented >2-fold by increasing luminal perfusion rates in isolated, microperfused proximal tubules for 15 minutes. Mouse kidneys with diminished endocytosis caused by a conditional deletion of megalin or the chloride channel ClC-5 had constitutively enhanced AQP1 abundance in the proximal tubule brush border membrane. In AQP1-transfected, cultured proximal tubule cells, fluid shear stress or the addition of cyclic nucleotides enhanced AQP1 surface expression and concomitantly diminished its ubiquitination. These effects were also associated with an elevated osmotic water permeability. In sum, we have shown that luminal surface expression of AQP1 in the proximal tubule brush border membrane is regulated in response to flow. Cellular trafficking, endocytosis, an intact endosomal compartment, and controlled protein stability are the likely prerequisites for AQP1 activation by enhanced tubular fluid shear stress, serving to maintain glomerulotubular balance.
MeSH term(s)	Adaptation, Physiological ; Animals ; Aquaporin 1/genetics ; Aquaporin 1/metabolism ; Cell Membrane Permeability/physiology ; Cells, Cultured ; Disease Models, Animal ; Gene Expression Regulation ; Glomerular Filtration Rate/physiology ; Kidney Tubules, Proximal/physiopathology ; Mice ; Mice, Transgenic ; Microvilli/metabolism ; Osmosis ; Protein Transport/physiology ; Random Allocation ; Sensitivity and Specificity ; Time Factors ; Water-Electrolyte Balance/genetics ; Water-Electrolyte Balance/physiology
Chemical Substances	Aqp1 protein, mouse ; Aquaporin 1 (146410-94-8)
Language	English
Publishing date	2014-09-30
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2014020148
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Article: [Effect of cinobufacini on vascular contractile of rat thoracic aorta].

Li, Xu-yun / Lu, Yuan / Shan, Qi-xian / Xia, Qiang

Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences

2006 Volume 35, Issue 2, Page(s) 178–181

Abstract: Objective: To examine the effect of cinobufacini on rat thoracic aorta and its mechanism.: Methods: Isolated rat thoracic aorta was perfused and isometric tension was recorded by organ bath technique before and after cinobufacini treatment.: Result! ...

Abstract	Objective: To examine the effect of cinobufacini on rat thoracic aorta and its mechanism. Methods: Isolated rat thoracic aorta was perfused and isometric tension was recorded by organ bath technique before and after cinobufacini treatment. Result: Cinobufacini induced contraction of isolated thoracic aorta with or without endothelium in a concentration-dependent manner (at concentration of 2.5,5.0,7.5,10.0 g/L). The vasoconstriction effect of cinobufacini was more potent in endothelium-denuded aorta ring [(16.3+/-3.39)%, (52.5+/-7.70)%, (60.9+/-8.84)%, (69.2+/-11.34)%] than in endothelium-intact aorta ring [(6.2+/-2.07)%, (14.7+/-4.91), (17.6+/-5.86)%, (20.3+/-6.78)% (P<0.01)]. Its contractile effect was attenuated in Ca(2+)-free solution (about 1/10 of that in buffer with 1.25 mmol/L CaCl(2)) or by the treatment with verapamil (10(-7)mol/L), an L-type calcium channel antagonist. Cinobufacini induced contraction on the endothelium-intact rat aorta was augmented by pretreatment with L-NAME (10(-4)mol/L), a nitric oxide synthase inhibitor. Conclusion: Cinobufacini contracts rat thoracic aorta by opening the voltage-dependent Ca(2+) channel and increasing Ca(2+) influx into vascular smooth muscle. Cinobufacini can also stimulate the release of vascular relaxant factor, nitric oxide, from the endothelium and thus antagonize cinobufacini-induced contraction.
MeSH term(s)	Animals ; Aorta, Thoracic/drug effects ; Bufanolides/pharmacology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; In Vitro Techniques ; Male ; Nitric Oxide/biosynthesis ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction/drug effects ; Vasoconstrictor Agents/pharmacology
Chemical Substances	Bufanolides ; Vasoconstrictor Agents ; Nitric Oxide (31C4KY9ESH) ; cinobufagin (T9PSN4R8IR)
Language	Chinese
Publishing date	2006
Publishing country	China
Document type	English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1008-9292
ISSN	1008-9292
DOI	10.3785/j.issn.1008-9292.2006.02.012
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Article ; Online: Insights into driving forces and paracellular permeability from claudin-16 knockdown mouse.

Shan, Qixian / Himmerkus, Nina / Hou, Jianghui / Goodenough, Daniel A / Bleich, Markus

Annals of the New York Academy of Sciences

2009 Volume 1165, Page(s) 148–151

Abstract: Tight junction (TJ) properties are determined by membrane protein complexes of neighboring cells that form both a barrier and a selective pathway for paracellular substrate transport. Our previous work supports the view that paracellular permeability ... ...

Abstract	Tight junction (TJ) properties are determined by membrane protein complexes of neighboring cells that form both a barrier and a selective pathway for paracellular substrate transport. Our previous work supports the view that paracellular permeability changes in the thick ascending limb (TAL) may underlie the mechanism for familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), a rare autosomal recessive disease linked to mutations in claudin-16 (CLDN16) and claudin-19 (CLDN19). CLDN16 knockdown (KD) mice are lacking CLDN16 expression by transgenic RNA interference. We observed that the transport defect for Mg(2+) and Ca(2+) in this animal model is caused by a loss of paracellular cation selectivity. The permeability ratio for Na(+) over Cl(-) in KD mice was lower by a factor of two without a change in paracellular conductance, compared to wild type (WT). This resulted in a collapse of the transepithelial voltage, which is the driving force for Mg(2+) and Ca(2+) absorption in TAL. Since CLDN16 KD mice revealed lower blood pressure and an increased aldosterone plasma concentration, we hypothesize that the reduction in paracellular selectivity could allow backflow of Na(+) and Cl(-) into the lumen of the TAL, thus enhancing the distal NaCl load and challenging the organism with a latent NaCl loss.
MeSH term(s)	Animals ; Calcium/metabolism ; Cell Membrane Permeability/genetics ; Claudins ; Magnesium/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; RNA Interference ; Sodium/metabolism ; Tight Junctions/metabolism
Chemical Substances	Claudins ; Membrane Proteins ; claudin 16 ; Sodium (9NEZ333N27) ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2009-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2009.04041.x
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Article: Adrenomedullin: a cardiac depressant factor in septic shock.

Hyvelin, Jean-Marc / Shan, Qixian / Bourreau, Jean-Pierre

Journal of cardiac surgery

2002 Volume 17, Issue 4, Page(s) 328–335

Abstract: Despite intensive research, septic shock is still the most common cause of death in surgical intensive care, and its incidence keeps increasing. No curative treatment is yet available. The critical aspect of septic shock is the refractory hypotension ... ...

Abstract	Despite intensive research, septic shock is still the most common cause of death in surgical intensive care, and its incidence keeps increasing. No curative treatment is yet available. The critical aspect of septic shock is the refractory hypotension that develops during its late phase which leads to a progressive deterioration of cell and organ functions, and in most instances, death. During septic shock, following the overproduction of cytokines, many factors such as nitric oxide and adrenomedullin (ADM) are produced in abnormally large quantities, but our understanding of their contribution to the pathophysiology of sepsis is limited. Here we show that adrenomedullin (22-52), an adrenomedullin receptor antagonist, improves the contractility of myocytes isolated from lipopolysaccharide (LPS)-treated rats, whereas in normal myocytes, adrenomedullin, acting through an adrenomedullin (22-52) sensitive receptor, decreases their contractility. In addition, adrenomedullin antiserum and inducible nitric oxide (NO) synthase inhibitor improve the survival of LPS-treated rats. The data indicate that adrenomedullin is a cardiac depressant factor, which along with NO precipitates ventricular failure during septic shock.
MeSH term(s)	Adenylyl Cyclases/drug effects ; Adrenomedullin ; Animals ; Biomarkers/blood ; Blood Pressure/drug effects ; Cardiotonic Agents/blood ; Cardiotonic Agents/pharmacology ; Disease Models, Animal ; Electric Stimulation ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Guanidines/pharmacology ; Heart Ventricles/cytology ; Heart Ventricles/drug effects ; Humans ; Lipopolysaccharides/pharmacology ; Male ; Myocardial Contraction/drug effects ; Myocytes, Cardiac/drug effects ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitrates/blood ; Peptides/blood ; Peptides/pharmacology ; Rats ; Rats, Sprague-Dawley ; Shock, Septic/blood ; Time Factors ; Vascular Resistance/drug effects ; Ventricular Function/drug effects
Chemical Substances	Biomarkers ; Cardiotonic Agents ; Enzyme Inhibitors ; Guanidines ; Lipopolysaccharides ; Nitrates ; Peptides ; Adrenomedullin (148498-78-6) ; Adenylyl Cyclases (EC 4.6.1.1) ; pimagedine (SCQ4EZQ113) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2002-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639059-6
ISSN	1540-8191 ; 0886-0440
ISSN (online)	1540-8191
ISSN	0886-0440
DOI	10.1111/j.1540-8191.2001.tb01152.x
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Zs.A 2221: Show issues

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Article: Salt and acid-base metabolism in claudin-16 knockdown mice: impact for the pathophysiology of FHHNC patients.

Himmerkus, Nina / Shan, Qixian / Goerke, Boeren / Hou, Jianghui / Goodenough, Daniel A / Bleich, Markus

American journal of physiology. Renal physiology

2008 Volume 295, Issue 6, Page(s) F1641–7

Abstract: Claudin-16 is defective in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Claudin-16 knockdown (CLDN16 KD) mice show reduced cation selectivity in the thick ascending limb. The defect leads to a collapse of the lumen-positive ... ...

Abstract	Claudin-16 is defective in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC). Claudin-16 knockdown (CLDN16 KD) mice show reduced cation selectivity in the thick ascending limb. The defect leads to a collapse of the lumen-positive diffusion voltage, which drives Ca(2+) and Mg(2+) absorption. Because of the reduced tight junction permeability ratio for Na(+) over Cl(-), we proposed a backleak of NaCl into the lumen. Systemic analysis had revealed lower blood pressure and a moderately increased plasma aldosterone concentration. In this study, we measured the amiloride-sensitive equivalent short-circuit current in isolated, perfused collecting ducts and found it increased by fivefold in CLDN16 KD mice compared with wild-type (WT) mice. Amiloride treatment unmasked renal Na(+) loss in the thick ascending limb of the nephron. Under amiloride treatment, CLDN16 KD mice developed hyponatremia and the renal fractional excretion of Na(+) was twofold higher in CLDN16 KD compared with WT mice. The loss of claudin-16 also resulted in increased urinary flow, reduced HCO(3)(-) excretion, and lower urine pH. We conclude that perturbation in salt and acid-base metabolism in CLDN16 KD mice has its origin in the defective cation permselectivity of the thick ascending limb of the nephron. This study has contributed to the still incomplete understanding of the symptoms of FHHNC patients.
MeSH term(s)	Adsorption ; Animals ; Calcium/blood ; Calcium/metabolism ; Calcium/urine ; Cell Membrane Permeability ; Claudins ; Creatinine/blood ; Creatinine/urine ; Female ; Humans ; Hypercalciuria/genetics ; Kidney Tubules/physiology ; Kidney Tubules/physiopathology ; Magnesium/blood ; Magnesium/metabolism ; Magnesium/urine ; Magnesium Deficiency/genetics ; Male ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Nephrocalcinosis/genetics ; Nephrons/physiology ; Nephrons/physiopathology ; Perfusion ; Sodium/blood ; Sodium/urine ; Tight Junctions/physiology
Chemical Substances	Claudins ; Membrane Proteins ; claudin 16 ; Sodium (9NEZ333N27) ; Creatinine (AYI8EX34EU) ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2008-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.90388.2008
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Article: [The alterations of nitric oxide synthase activity of ventricular cardiac muscle of rats in two septic shock models].

Ye, Ting-mei / Xu, Ce / Gao, Qin / Zhou, Xin-mei / Shan, Qi-xian / Xia, Qiang

Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology

2007 Volume 23, Issue 2, Page(s) 194–198

Abstract: Aim: To observe the differences of hemodynamics and nitric oxide synthase(NOS) activity of ventricular cardiac muscle in two septic shock models and explore the possible mechanism.: Methods: Two rat models of septic shock[lipopolysaccharide(LPS)- ... ...

Abstract	Aim: To observe the differences of hemodynamics and nitric oxide synthase(NOS) activity of ventricular cardiac muscle in two septic shock models and explore the possible mechanism. Methods: Two rat models of septic shock[lipopolysaccharide(LPS)-induced and cecal ligation and puncture (CLP)-induced septic shock] were used. The hemodynamic parameters and nitric oxide synthase activity of ventricular cardiac muscle were measured. Results: The hemodynamic parameters in CLP-induced model were increased in the early stage and decreased in the late stage while in LPS-induced model the parameters showed the same change of the CLP late stage. Both LPS model and CLP model (late stage) showed significant increase in NOS activity, but there was no difference between the two models. After treatment of the NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME), the parameters of CLP-late stage and LPS model increased significantly. The NOS activity reached the highest level in the CLP-middle stage. The production of nitrite/nitrate decreased significantly in LPS model and CLP model(late stage) after treatment of L-NAME, but the nitrite/nitrate produced by constitutive NOS in LPS model was higher than CLP model(late stage). Conclusion: The increase of the NOS activity may be the main reason to lead to the depression of the hemodynamic parameters. Inducible NOS may play the leading role in the LPS model while cNOS and iNOS have the same effect in the CLP model.
MeSH term(s)	Animals ; Hemodynamics ; Lipopolysaccharides ; Male ; Myocytes, Cardiac/metabolism ; Nitric Oxide Synthase/metabolism ; Rats ; Rats, Sprague-Dawley ; Shock, Septic/classification ; Shock, Septic/metabolism
Chemical Substances	Lipopolysaccharides ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	Chinese
Publishing date	2007-05
Publishing country	China
Document type	Comparative Study ; English Abstract ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1000-6834
ISSN	1000-6834
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Article ; Online: Human beta-defensin-2 increases cholinergic response in colon epithelium.

Himmerkus, Nina / Vassen, Veit / Sievers, Birte / Goerke, Boeren / Shan, Qixian / Harder, Jürgen / Schröder, Jens-Michael / Bleich, Markus

Pflugers Archiv : European journal of physiology

2010 Volume 460, Issue 1, Page(s) 177–186

Abstract: The human beta-defensin-2 (hBD-2) is expressed in epithelial cells of skin and respiratory and gastrointestinal tracts. Defensins are arginine-rich small cationic peptides with six intramolecular disulfide bonds and are antimicrobially active against a ... ...

Abstract	The human beta-defensin-2 (hBD-2) is expressed in epithelial cells of skin and respiratory and gastrointestinal tracts. Defensins are arginine-rich small cationic peptides with six intramolecular disulfide bonds and are antimicrobially active against a broad spectrum of pathogens. In addition, they have cytokine-like immunomodulatory properties. We hypothesized that hBD-2 also might influence epithelial cells themselves, thereby altering fluid composition in the gastrointestinal tract. We therefore tested its impact on electrogenic ion transport properties of distal colon in Ussing chamber experiments. Application of hBD-2 did not affect transepithelial voltage or resistance in cAMP-stimulated distal colon. However, it increased cholinergic Ca(2+)-dependent Cl(-) secretion. After 20 min of incubation with hBD-2, the effect of carbachol (CCh) on the equivalent short circuit current (I'(sc)) was enhanced twofold compared to vehicle-treated colon. Modulation of Ca(2+) signaling by hBD-2 was validated by Fura-2 measurements in human colon carcinoma HT29 cells. Twenty-minute incubation with hBD-2 increased the CCh-induced Ca(2+) transient by 20-30% compared to either vehicle-treated cells or cells treated with the defensins hBD-1, hBD-3, or HD-5. This effect was concentration-dependent, with an EC(50) of 0.043 microg/ml, and still present in the absence of extracellular Ca(2+). Also, the ionomycin-induced Ca(2+) transient was increased by hBD-2 treatment. We conclude that hBD-2 facilitates cholinergic Ca(2+)-regulated epithelial Cl(-) secretion. These findings contribute to the concept of a specific interaction of antimicrobial peptides with epithelial function.
MeSH term(s)	Acetylcholine/metabolism ; Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calcium Signaling ; Carbachol/pharmacology ; Chlorides/metabolism ; Cholinergic Agonists/pharmacology ; Colon/drug effects ; Colon/metabolism ; Dose-Response Relationship, Drug ; Electric Impedance ; HT29 Cells ; Humans ; In Vitro Techniques ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Ionomycin/pharmacology ; Ionophores/pharmacology ; Membrane Potentials ; Molecular Sequence Data ; Rats ; Time Factors ; beta-Defensins/metabolism
Chemical Substances	Chlorides ; Cholinergic Agonists ; DEFB103A protein, human ; DEFB105A protein, human ; DEFB4A protein, human ; Ionophores ; beta-Defensins ; Ionomycin (56092-81-0) ; Carbachol (8Y164V895Y) ; Acetylcholine (N9YNS0M02X) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2010-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-009-0780-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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