Publications by authors named "DaoHong Lin"

Article Synopsis
  • Kir5.1, when paired with Kir4.2, forms a crucial potassium channel (heterotetramer) in the basolateral membrane of mouse proximal tubules, affecting K+ conductance.
  • Immunofluorescence and immunoblotting show Kir4.2 is found exclusively in proximal tubules, while Kir5.1 is present in both proximal and distal nephrons; however, the absence of Kir5.1 reduces Kir4.2 levels and affects membrane staining.
  • Patch-clamp recordings reveal that Kir5.1-knockout mice lack the 50-pS K channel that is present in wild-type mice, leading to a less negative membrane potential in the proximal tubules, indicating the importance
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Background: Angiotensin-II (Ang-II) perfusion stimulates Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) and thiazide-sensitive Na-Cl-cotransporter (NCC).

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Key Points: Angiotensin II–type-1a-receptor in the distal convoluted tubule (DCT) plays a role in regulating sodium transport in the DCT. Angiotensin II–type-1a-receptor in the DCT plays a role in maintaining potassium homeostasis during sodium restriction.

Background: Chronic angiotensin II perfusion stimulates Kir4.

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Calcineurin, protein phosphatase 2B (PP2B) or protein phosphatase 3 (PP3), is a calcium-dependent serine/threonine protein phosphatase. Calcineurin is widely expressed in the kidney and regulates renal Na and K transport. In the thick ascending limb, calcineurin plays a role in inhibiting NKCC2 function by promoting the dephosphorylation of the cotransporter and an intracellular sorting receptor, called sorting-related-receptor-with-A-type repeats (SORLA), is involved in modulating the effect of calcineurin on NKCC2.

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Key Points: High K stimulates mechanistic target of rapamycin complex 2 (mTORc2) in the distal convoluted tubule (DCT). Inhibition of mTORc2 decreased the basolateral Kir4.1/Kir5.

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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).

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Purpose Of Review: Kir5.1 interacts with Kir4.2 in proximal tubule and with Kir4.

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Article Synopsis
  • - Low potassium levels activate the kidney sodium-chloride cotransporter (NCC) through the With-No-Lysine kinase 4 (WNK4), which is modulated by chloride levels; lower intracellular chloride promotes NCC activation by releasing it from WNK4's regulation.
  • - A mutant version of WNK4 (WNK4-L319F) was created in mice, showing that even without chloride, it leads to increased NCC activity and mild hyperkalemia, especially under low potassium conditions.
  • - The study suggests that low potassium also affects WNK4 activity and degradation via phosphorylation, indicating the involvement of various chloride-regulated mechanisms in regulating NCC under low potassium.
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The inwardly rectifying potassium channel (Kir) 4.1 (encoded by ) interacts with Kir5.1 (encoded by ) to form a major basolateral K channel in the renal distal convoluted tubule (DCT), connecting tubule (CNT), and the cortical collecting duct (CCD).

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We used whole cell recording to examine the renal outer medullary K channel (ROMK or Kir1.1) and epithelial Na channel (ENaC) in the late distal convoluted tubule (DCT2)/initial connecting tubule (CNT) and in the cortical collecting duct (CCD) of kidney tubule-specific neural precursor cell-expressed developmentally downregulated protein 4-2 (Nedd4-2) knockout mice (Ks-Nedd4-2 KO) and floxed neural precursor cell-expressed developmentally downregulated 4-like () mice (control). Tertiapin Q (TPNQ)-sensitive K currents (ROMK) were smaller in both the DCT2/CNT and CCD of Ks-Nedd4-2 KO mice on a normal diet than in control mice.

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High-dietary K (HK) intake inhibits basolateral Kir4.1/Kir5.1 activity in the distal convoluted tubule (DCT), and HK-induced inhibition of Kir4.

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High sodium (HS) intake inhibited epithelial Na channel (ENaC) in the aldosterone-sensitive distal nephron and Na-Cl cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT), thereby increasing renal Na excretion but not affecting K excretion.

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Neural precursor cell expressed developmentally downregulated protein 4-2 (Nedd4-2) regulates the expression of Kir4.1, thiazide-sensitive NaCl cotransporter (NCC), and epithelial Na channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN), and Nedd4-2 deletion causes salt-sensitive hypertension. We now examined whether Nedd4-2 deletion compromises the effect of high-salt (HS) diet on Kir4.

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Background Angiotensin II stimulates epithelial Na channel (ENaC) by aldosterone-independent mechanism. We now test the effect of angiotensin II on ENaC in the distal convoluted tubule (DCT) and cortical collecting duct (CCD) of wild-type (WT) and kidney-specific mineralocorticoid receptor knockout mice (KS-MR-KO). Methods and Results We used electrophysiological, immunoblotting and renal-clearance methods to examine the effect of angiotensin II on ENaC in KS-MR-KO and wild-type mice.

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The inhibition of Type II angiotensin II receptor (AT2R) or BK2R (bradykinin type II receptor) stimulates basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT) and activates thiazide-sensitive NCC (Na-Cl cotransporter).

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Hypomagnesemia is associated with reduced kidney function and life-threatening complications and sustains hypokalemia. The distal convoluted tubule (DCT) determines final urinary Mg excretion and, via activity of the Na-Cl cotransporter (NCC), also plays a key role in K homeostasis by metering Na delivery to distal segments. Little is known about the mechanisms by which plasma Mg concentration regulates NCC activity and how low-plasma Mg concentration and K concentration interact to modulate NCC activity.

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Background: The basolateral potassium channel in the distal convoluted tubule (DCT), comprising the inwardly rectifying potassium channel Kir4.1/Kir5.1 heterotetramer, plays a key role in mediating the effect of dietary potassium intake on the thiazide-sensitive NaCl cotransporter (NCC).

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The stimulation of β-adrenergic receptor increases thiazide-sensitive NaCl cotransporter (NCC), an effect contributing to salt-sensitive hypertension by sympathetic stimulation. We now test whether the stimulation of β-adrenergic receptor-induced activation of NCC is achieved through activating basolateral Kir4.1 in the distal convoluted tubule (DCT).

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Background: Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Whether the basolateral, inwardly rectifying potassium channel Kir4.1/Kir5.

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Stimulation of BK2R (bradykinin [BK] B2 receptor) has been shown to increase renal Na excretion. The aim of the present study is to explore the role of BK2R in regulating Kir4.1 and NCC (NaCl cotransporter) in the distal convoluted tubule (DCT).

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Kir4.1/5.1 heterotetramer participates in generating the negative cell membrane potential in distal convoluted tubule (DCT) and plays a critical role in determining the activity of Na-Cl cotransporter (NCC).

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AT2R (AngII [angiotensin II] type 2 receptor) is expressed in the distal nephrons. The aim of the present study is to examine whether AT2R regulates NCC (Na-Cl cotransporter) and Kir4.1 of the distal convoluted tubule.

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Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we tested whether dietary potassium intake modulates Kir4.

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