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Article ; Online: Trafficking and regulation of the NKCC2 cotransporter in the thick ascending limb.

Mutig, Kerim

Current opinion in nephrology and hypertension

2017 Volume 26, Issue 5, Page(s) 392–397

Abstract: Purpose of review: The kidney Na-K-2Cl cotransporter (NKCC2) is essential for urinary concentration and renal electrolyte handling. Loss of function mutations in the NKCC2 gene cause urinary salt and potassium wasting, whereas excessive NKCC2 function ... ...

Abstract	Purpose of review: The kidney Na-K-2Cl cotransporter (NKCC2) is essential for urinary concentration and renal electrolyte handling. Loss of function mutations in the NKCC2 gene cause urinary salt and potassium wasting, whereas excessive NKCC2 function has been linked to high blood pressure. Loop diuretics, targeting the transporter, are instrumental for relieving edema or hypertension. This review focuses on intrinsic mechanisms regulating NKCC2 activity at the posttranslational level, namely its trafficking and phosphorylation. Recent findings: Protein networks mediating cellular turnover of NKCC2 have recently received major attention. Several key components of its apical trafficking were identified, including respective chaperones, SNARE protein family members and raft-associated proteins. NKCC2 internalization has been characterized qualitatively and quantitatively. Kinase and phosphatase pathways regulating NKCC2 activity have been clarified and links between NKCC2 phosphorylation and trafficking proposed. Constitutive and inducible NKCC2 trafficking and phosphorylation mechanisms have been specified with focus on endocrine control of thick ascending limb (TAL) function by vasopressin. Summary: Proper NKCC2 trafficking and phosphorylation are critical to the TAL function in the physiological context of urinary concentration and extracellular volume regulation. Clarification of the underlying mechanisms and respective protein networks may open new therapeutic perspectives for better management of renal electrolyte disorders and blood pressure control.
Language	English
Publishing date	2017-09
Publishing country	England
Document type	Journal Article
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000351
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Article ; Online: Hyperkalemia and blood pressure regulation.

Mutig, Kerim / Bachmann, Sebastian

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2019 Volume 34, Issue Suppl 3, Page(s) iii26–iii35

Abstract: Hypertension is common in the general population. Management of hypertensive patients at risk of hyperkalemia is challenging due to potential life-threatening complications such as cardiac arrest. Chronic hyperkalemia is often associated with impaired ... ...

Abstract	Hypertension is common in the general population. Management of hypertensive patients at risk of hyperkalemia is challenging due to potential life-threatening complications such as cardiac arrest. Chronic hyperkalemia is often associated with impaired renal ability to excrete excessive potassium ions (K+). This may refer to chronic kidney disease or certain pharmacological interventions, including broadly used renin-angiotensin-aldosterone system and calcineurin inhibitors. Understanding the intrinsic mechanisms permitting kidney adaptations to hyperkalemia is critical for choosing therapeutic strategies. Valuable insights were obtained from the analysis of familial hyperkalemic hypertension (FHHt) syndrome, which became a classic model for coincidence of high blood pressure and hyperkalemia. FHHt can be caused by mutations in several genes, all of them resulting in excessive activity of with-no-lysine kinases (WNKs) in the distal nephron of the kidney. WNKs have been increasingly recognized as key signalling enzymes in the regulation of renal sodium ions (Na+) and K+ handling, enabling adaptive responses to systemic shifts of potassium homoeostasis consequent to variations in dietary potassium intake or disease. The WNK signalling pathway recruits a complex protein network mediating catalytic and non-catalytic effects of distinct WNK isoforms on relevant Na+- or K+-transporting proteins. In this review article, we summarize recent progress in understanding WNK signalling. An update of available models for renal adaptation to hyperkalemic conditions is presented. Consequences for blood pressure regulation are discussed. Pharmacological targeting of WNKs or their substrates offers promising options to manage hypertension while preventing hyperkalemia.
MeSH term(s)	Biomarkers/blood ; Blood Pressure/physiology ; Humans ; Hyperkalemia/blood ; Hyperkalemia/etiology ; Hyperkalemia/physiopathology ; Hypertension/complications ; Hypertension/metabolism ; Hypertension/physiopathology ; Potassium/blood
Chemical Substances	Biomarkers ; Potassium (RWP5GA015D)
Language	English
Publishing date	2019-12-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfz218
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Article ; Online: Angiotensin II receptor blockade alleviates calcineurin inhibitor nephrotoxicity by restoring cyclooxygenase 2 expression in kidney cortex.

Hu, Junda / Xu, Yan / Bachmann, Sebastian / Mutig, Kerim

Acta physiologica (Oxford, England)

2021 Volume 232, Issue 1, Page(s) e13612

Abstract: Aim: The use of calcineurin inhibitors such as cyclosporine A (CsA) for immunosuppression after solid organ transplantation is commonly limited by renal side effects. CsA-induced deterioration of glomerular filtration rate and sodium retention may be ... ...

Abstract	Aim: The use of calcineurin inhibitors such as cyclosporine A (CsA) for immunosuppression after solid organ transplantation is commonly limited by renal side effects. CsA-induced deterioration of glomerular filtration rate and sodium retention may be related to juxtaglomerular dysregulation as a result of suppressed cyclooxygenase 2 (COX-2) and stimulated renin biosynthesis. We tested whether CsA-induced COX-2 suppression is caused by hyperactive renin-angiotensin system (RAS) and whether RAS inhibition may alleviate the related side effects. Methods: Rats received CsA, the RAS inhibitor candesartan, or the COX-2 inhibitor celecoxib acutely (3 days) or chronically (3 weeks). Molecular pathways mediating effects of CsA and RAS on COX-2 were studied in cultured macula densa cells. Results: Pharmacological or siRNA-mediated calcineurin inhibition in cultured cells enhanced COX-2 expression via p38 mitogen-activated protein kinase and NF-kB signalling, whereas angiotensin II abolished these effects. Acute and chronic CsA administration to rats led to RAS activation along with reduced cortical COX-2 expression, creatinine clearance and fractional sodium excretion. Evaluation of major distal salt transporters, NKCC2 and NCC, showed increased levels of their activating phosphorylation upon CsA. Concomitant candesartan treatment blunted these effects acutely and completely normalized the COX-2 expression and renal functional parameters at long term. Celecoxib prevented the candesartan-induced improvements of creatinine clearance and sodium excretion. Conclusion: Suppression of juxtaglomerular COX-2 upon CsA results from RAS activation, which overrides the cell-autonomous, COX-2-stimulatory effects of calcineurin inhibition. Angiotensin II antagonism alleviates CsA nephrotoxicity via the COX-2-dependent normalization of creatinine clearance and sodium excretion.
MeSH term(s)	Angiotensin II/chemistry ; Animals ; Calcineurin Inhibitors ; Cyclooxygenase 2 ; Cyclosporine/chemistry ; Kidney ; Kidney Cortex/physiology ; Rats ; Receptors, Angiotensin
Chemical Substances	Calcineurin Inhibitors ; Receptors, Angiotensin ; Angiotensin II (11128-99-7) ; Cyclosporine (83HN0GTJ6D) ; Cyclooxygenase 2 (EC 1.14.99.1)
Language	English
Publishing date	2021-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13612
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Article: Metabolic effects of vasopressin in pathophysiology of diabetic kidney disease.

Lebedeva, Svetlana / Margaryan, Arus / Smolyarchuk, Elena / Nedorubov, Andrey / Materenchuk, Maria / Tonevitsky, Alexander / Mutig, Kerim

Frontiers in endocrinology

2023 Volume 14, Page(s) 1176199

Abstract: The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose- ... ...

Abstract	The diabetic kidney disease (DKD) is the major cause of the chronic kidney disease (CKD). Enhanced plasma vasopressin (VP) levels have been associated with the pathophysiology of DKD and CKD. Stimulation of VP release in DKD is caused by glucose-dependent reset of the osmostat leading to secondary pathophysiologic effects mediated by distinct VP receptor types. VP is a stress hormone exhibiting the antidiuretic action in the kidney along with broad adaptive effects in other organs. Excessive activation of the vasopressin type 2 (V2) receptor in the kidney leads to glomerular hyperfiltration and nephron loss, whereas stimulation of vasopressin V1a or V1b receptors in the liver, pancreas, and adrenal glands promotes catabolic metabolism for energy mobilization, enhancing glucose production and aggravating DKD. Increasing availability of selective VP receptor antagonists opens new therapeutic windows separating the renal and extra-renal VP effects for the concrete applications. Improved understanding of these paradigms is mandatory for further drug design and translational implementation. The present concise review focuses on metabolic effects of VP affecting DKD pathophysiology.
MeSH term(s)	Humans ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/etiology ; Vasopressins/metabolism ; Receptors, Vasopressin/metabolism ; Renal Insufficiency, Chronic ; Glucose ; Diabetes Mellitus
Chemical Substances	Vasopressins (11000-17-2) ; Receptors, Vasopressin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-09-18
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1176199
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Article ; Online: Immunosuppressive calcineurin inhibitor cyclosporine A induces proapoptotic endoplasmic reticulum stress in renal tubular cells.

Yilmaz, Duygu Elif / Kirschner, Karin / Demirci, Hasan / Himmerkus, Nina / Bachmann, Sebastian / Mutig, Kerim

The Journal of biological chemistry

2022 Volume 298, Issue 3, Page(s) 101589

Abstract: Current immunosuppressive strategies in organ transplantation rely on calcineurin inhibitors cyclosporine A (CsA) or tacrolimus (Tac). Both drugs are nephrotoxic, but CsA has been associated with greater renal damage than Tac. CsA inhibits calcineurin by ...

Abstract	Current immunosuppressive strategies in organ transplantation rely on calcineurin inhibitors cyclosporine A (CsA) or tacrolimus (Tac). Both drugs are nephrotoxic, but CsA has been associated with greater renal damage than Tac. CsA inhibits calcineurin by forming complexes with cyclophilins, whose chaperone function is essential for proteostasis. We hypothesized that stronger toxicity of CsA may be related to suppression of cyclophilins with ensuing endoplasmic reticulum (ER) stress and unfolded protein response (UPR) in kidney epithelia. Effects of CsA and Tac (10 µM for 6 h each) were compared in cultured human embryonic kidney 293 (HEK 293) cells, primary human renal proximal tubule (PT) cells, freshly isolated rat PTs, and knockout HEK 293 cell lines lacking the critical ER stress sensors, protein kinase RNA-like ER kinase or activating transcription factor 6 (ATF6). UPR was evaluated by detection of its key components. Compared with Tac treatment, CsA induced significantly stronger UPR in native cultured cells and isolated PTs. Evaluation of proapoptotic and antiapoptotic markers suggested an enhanced apoptotic rate in CsA-treated cells compared with Tac-treated cells as well. Similar to CsA treatment, knockdown of cyclophilin A or B by siRNA caused proapoptotic UPR, whereas application of the chemical chaperones tauroursodeoxycholic acid or 4-phenylbutyric acid alleviated CsA-induced UPR. Deletion of protein kinase RNA-like ER kinase or ATF6 blunted CsA-induced UPR as well. In summary, inhibition of cyclophilin chaperone function with ensuing ER stress and proapoptotic UPR aggravates CsA toxicity, whereas pharmacological modulation of UPR bears potential to alleviate renal side effects of CsA.
MeSH term(s)	Animals ; Calcineurin/metabolism ; Calcineurin Inhibitors/pharmacology ; Cyclophilins/metabolism ; Cyclosporine/pharmacology ; Endoplasmic Reticulum Stress/drug effects ; HEK293 Cells ; Humans ; Immunosuppressive Agents/pharmacology ; Kidney Tubules/drug effects ; Kidney Tubules/immunology ; Protein Kinases ; RNA ; Rats ; Tacrolimus/pharmacology ; Unfolded Protein Response
Chemical Substances	Calcineurin Inhibitors ; Immunosuppressive Agents ; RNA (63231-63-0) ; Cyclosporine (83HN0GTJ6D) ; Protein Kinases (EC 2.7.-) ; Calcineurin (EC 3.1.3.16) ; Cyclophilins (EC 5.2.1.-) ; Tacrolimus (WM0HAQ4WNM)
Language	English
Publishing date	2022-01-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.101589
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Article ; Online: Regulation of renal Na-(K)-Cl cotransporters by vasopressin.

Bachmann, Sebastian / Mutig, Kerim

Pflugers Archiv : European journal of physiology

2017 Volume 469, Issue 7-8, Page(s) 889–897

Abstract: Vasopressin (AVP) induces antidiuresis, thus playing an essential role in body water and electrolyte homeostasis. Its antidiuretic effects are mediated chiefly by V2 vasopressin receptors (V2R) expressed along the distal nephron and collecting duct ... ...

Abstract	Vasopressin (AVP) induces antidiuresis, thus playing an essential role in body water and electrolyte homeostasis. Its antidiuretic effects are mediated chiefly by V2 vasopressin receptors (V2R) expressed along the distal nephron and collecting duct epithelia. NaCl reabsorption in the distal nephron, which includes the thick ascending limb (TAL) and distal convoluted tubule (DCT), largely depends on the activity of two structurally related Na-(K)-Cl cotransporters, NKCC2 in TAL and NCC in DCT. AVP-induced activation of these transporters contributes to urine concentration and renal electrolyte reabsorption. Previous work has specified molecular pathways mediating the effects of V2R activation in TAL and DCT, and protein networks involved in intracellular trafficking and phosphoregulation of the two transporters have been identified. This review summarizes recent progress in understanding AVP signalling mechanisms that are responsible for the activation of NKCC2 and NCC. Implications in the pathophysiology of diseases such as nephrogenic diabetes insipidus, diabetes mellitus and salt-sensitive hypertension are discussed in this context.
Language	English
Publishing date	2017-08
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-017-2002-2
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Article ; Online: Calcineurin inhibitors stimulate Kir4.1/Kir5.1 of the distal convoluted tubule to increase NaCl cotransporter.

Zhang, Dan-Dan / Duan, Xin-Peng / Mutig, Kerim / Rausch, Franziska / Xiao, Yu / Zheng, Jun-Ya / Lin, Dao-Hong / Wang, Wen-Hui

JCI insight

2023 Volume 8, Issue 7

Abstract: We examine whether calcineurin or protein phosphatase 2B (PP2B) regulates the basolateral inwardly rectifying potassium channel Kir4.1/Kir5.1 in the distal convoluted tubule (DCT). Application of tacrolimus (FK506) or cyclosporine A (CsA) increased whole- ...

Abstract	We examine whether calcineurin or protein phosphatase 2B (PP2B) regulates the basolateral inwardly rectifying potassium channel Kir4.1/Kir5.1 in the distal convoluted tubule (DCT). Application of tacrolimus (FK506) or cyclosporine A (CsA) increased whole-cell Kir4.1/Kir5.1-mediated K+ currents and hyperpolarized the DCT membrane. Moreover, FK506-induced stimulation of Kir4.1/Kir5.1 was absent in kidney tubule-specific 12 kDa FK506-binding protein-knockout mice (Ks-FKBP-12-KO). In contrast, CsA stimulated Kir4.1/Kir5.1 of the DCT in Ks-FKBP-12-KO mice, suggesting that FK506-induced stimulation of Kir4.1/Kir5.1 was due to inhibiting PP2B. Single-channel patch-clamp experiments demonstrated that FK506 or CsA stimulated the basolateral Kir4.1/Kir5.1 activity of the DCT, defined by NPo (a product of channel number and open probability). However, this effect was absent in the DCT treated with Src family protein tyrosine kinase (SFK) inhibitor or hydroxyl peroxide. Fluorescence imaging demonstrated that CsA treatment increased membrane staining intensity of Kir4.1 in the DCT of Kcnj10fl/fl mice. Moreover, CsA treatment had no obvious effect on phosphorylated NaCl cotransporter (pNCC) expression in Ks-Kir4.1-KO mice. Immunoblotting showed acute FK506 treatment increased pNCC expression in Kcnj10fl/fl mice, but this effect was attenuated in Ks-Kir4.1-KO mice. In vivo measurement of thiazide-induced renal Na+ excretion demonstrated that FK506 enhanced thiazide-induced natriuresis. This effect was absent in Ks-FKBP-12-KO mice and blunted in Ks-Kir4.1-KO mice. We conclude that inhibition of PP2B stimulates Kir4.1/Kir5.1 of the DCT and NCC and that PP2B inhibition-induced stimulation of NCC is partially achieved by stimulation of the basolateral Kir4.1/Kir5.1.
MeSH term(s)	Animals ; Mice ; Solute Carrier Family 12, Member 3/metabolism ; Calcineurin Inhibitors/pharmacology ; Sodium Chloride/metabolism ; Tacrolimus/pharmacology ; Tacrolimus Binding Protein 1A/metabolism ; Mice, Knockout ; Thiazides
Chemical Substances	Solute Carrier Family 12, Member 3 ; Calcineurin Inhibitors ; Sodium Chloride (451W47IQ8X) ; Tacrolimus (WM0HAQ4WNM) ; Tacrolimus Binding Protein 1A (EC 5.2.1.-) ; Thiazides
Language	English
Publishing date	2023-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.165987
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Book ; Online ; Thesis: Rolle des antidiuretischen Hormons in der Regulation der renalen Na-(K)-Cl Transporter

Mutig, Kerim [Verfasser]

2015

Author's details	Kerim Mutig
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	German
Publisher	Medizinische Fakultät Charité - Universitätsmedizin Berlin
Publishing place	Berlin
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Calcium-Sensing Receptor and Regulation of WNK Kinases in the Kidney.

Ostroverkhova, Daria S / Hu, Junda / Tarasov, Vadim V / Melnikova, Tatiana I / Porozov, Yuri B / Mutig, Kerim

Cells

2020 Volume 9, Issue 7

Abstract: The kidney is essential for systemic calcium homeostasis. Urinary calcium excretion can be viewed as an integrative renal response to endocrine and local stimuli. The extracellular calcium-sensing receptor (CaSR) elicits a number of adaptive reactions to ...

Abstract	The kidney is essential for systemic calcium homeostasis. Urinary calcium excretion can be viewed as an integrative renal response to endocrine and local stimuli. The extracellular calcium-sensing receptor (CaSR) elicits a number of adaptive reactions to increased plasma Ca
MeSH term(s)	Animals ; Humans ; Kidney/cytology ; Kidney/enzymology ; Kidney/metabolism ; Nephrons/cytology ; Nephrons/enzymology ; Nephrons/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Calcium-Sensing/genetics ; Receptors, Calcium-Sensing/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Calcium-Sensing ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-07-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9071644
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Article ; Online: Furosemide rescues hypercalciuria in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis model.

Kriuchkova, Natalia / Breiderhoff, Tilman / Müller, Dominik / Yilmaz, Duygu Elif / Demirci, Hasan / Drewell, Hoora / Günzel, Dorothee / Himmerkus, Nina / Bleich, Markus / Persson, Pontus B / Mutig, Kerim

Acta physiologica (Oxford, England)

2023 Volume 237, Issue 3, Page(s) e13927

Abstract: Aim: Perturbed calcium homeostasis limits life expectancy in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC). This rare disease occurs by loss-of-function mutations in CLDN16 or CLDN19 genes, causing impaired paracellular ... ...

Abstract	Aim: Perturbed calcium homeostasis limits life expectancy in familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC). This rare disease occurs by loss-of-function mutations in CLDN16 or CLDN19 genes, causing impaired paracellular reabsorption of divalent cations along the cortical thick ascending limb (cTAL). Only partial compensation takes place in the ensuing late distal convoluted tubule, connecting tubule, and collecting duct, where the luminal transient receptor potential channel V5 (TRPV5), as well as basolateral plasma membrane calcium ATPase (PMCA) and sodium-potassium exchanger (NCX1) mediate transcellular Ca Methods: Cldn16-deficient mice (Cldn16 Results: Cldn16 Conclusions: Furosemide significantly reduces hypercalciuria, likely via upregulation of luminal and basolateral Ca
MeSH term(s)	Animals ; Mice ; Calcium/metabolism ; Carrier Proteins ; Claudins/metabolism ; Furosemide/pharmacology ; Furosemide/therapeutic use ; Hypercalciuria/drug therapy ; Hypercalciuria/metabolism ; Magnesium/metabolism ; Nephrocalcinosis/drug therapy ; Nephrocalcinosis/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Carrier Proteins ; Claudins ; Furosemide (7LXU5N7ZO5) ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2023-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13927
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