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Article ; Online: Laminins in Cellular Differentiation.

Yap, Lynn / Tay, Hwee Goon / Nguyen, Mien T X / Tjin, Monica S / Tryggvason, Karl

2019 Volume 29, Issue 12, Page(s) 987–1000

Abstract: Basement membrane laminins (LNs) have been shown to modulate cellular phenotypes and differentiation both in vitro and during organogenesis in vivo. At least 16 laminin isoforms are present in mammals, and most are available as recombinant proteins. ... ...

Abstract	Basement membrane laminins (LNs) have been shown to modulate cellular phenotypes and differentiation both in vitro and during organogenesis in vivo. At least 16 laminin isoforms are present in mammals, and most are available as recombinant proteins. Ubiquitous LN511 and LN521 promote the clonal derivation and expansion of pluripotent embryonic stem cells (ESCs), and, together with other highly cell type-specific laminins, they can support the differentiation of stem cells into, for example, cardiac muscle fibers, retinal pigmented epithelial (RPE) cells and photoreceptors, dopamine (DA) neurons, and skin keratinocytes. The laminin-supported differentiation methods are highly reproducible and can be made chemically defined and fully xeno-free - a prerequisite for preparing therapeutic stem cell-derived cells. In this review we describe recent work on the use of laminin-based cell culture matrices in stem cell differentiation.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Embryonic Stem Cells/cytology ; Humans ; Keratinocytes/cytology ; Laminin/metabolism ; Myocytes, Cardiac/cytology ; Neurons/cytology ; Organogenesis/physiology ; Photoreceptor Cells, Vertebrate/cytology ; Pluripotent Stem Cells/cytology ; Retinal Pigment Epithelium/cytology ; Stem Cell Niche/physiology
Chemical Substances	Laminin
Language	English
Publishing date	2019-11-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2019.10.001
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Article ; Online: Maintaining Balance Under Pressure: Integrated Regulation of Renal Transporters During Hypertension.

McDonough, Alicia A / Nguyen, Mien T X

Hypertension (Dallas, Tex. : 1979)

2015 Volume 66, Issue 3, Page(s) 450–455

MeSH term(s)	Animals ; Cation Transport Proteins/metabolism ; Humans ; Hypertension/metabolism ; Hypertension/physiopathology ; Ion Transport/physiology ; Kidney/metabolism ; Kidney/physiopathology
Chemical Substances	Cation Transport Proteins
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.115.04593
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Article ; Online: How does potassium supplementation lower blood pressure?

McDonough, Alicia A / Nguyen, Mien T X

American journal of physiology. Renal physiology

2012 Volume 302, Issue 9, Page(s) F1224–5

MeSH term(s)	Animals ; Hypertension/metabolism ; Kidney/metabolism ; Male ; Nephrectomy/methods ; Potassium, Dietary/metabolism ; Sodium Chloride Symporters/metabolism ; Sodium-Potassium-Chloride Symporters/metabolism
Chemical Substances	Potassium, Dietary ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters
Language	English
Publishing date	2012-05-01
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00429.2011
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Article: Short-term nonpressor angiotensin II infusion stimulates sodium transporters in proximal tubule and distal nephron.

Nguyen, Mien T X / Han, Jiyang / Ralph, Donna L / Veiras, Luciana C / McDonough, Alicia A

Physiological reports

2015 Volume 3, Issue 9

Abstract: In Sprague Dawley rats, 2-week angiotensin II (AngII) infusion increases Na(+) transporter abundance and activation from cortical thick ascending loop of Henle (TALH) to medullary collecting duct (CD) and raises blood pressure associated with a pressure ... ...

Abstract	In Sprague Dawley rats, 2-week angiotensin II (AngII) infusion increases Na(+) transporter abundance and activation from cortical thick ascending loop of Henle (TALH) to medullary collecting duct (CD) and raises blood pressure associated with a pressure natriuresis, accompanied by depressed Na(+) transporter abundance and activation from proximal tubule (PT) through medullary TALH. This study tests the hypothesis that early during AngII infusion, before blood pressure raises, Na(+) transporters' abundance and activation increase all along the nephron. Male Sprague Dawley rats were infused via osmotic minipumps with a subpressor dose of AngII (200 ng/kg/min) or vehicle for 3 days. Overnight urine was collected in metabolic cages and sodium transporters' abundance and phosphorylation were determined by immunoblotting homogenates of renal cortex and medulla. There were no significant differences in body weight gain, overnight urine volume, urinary Na(+) and K(+) excretion, or rate of excretion of a saline challenge between AngII and vehicle infused rats. The 3-day nonpressor AngII infusion significantly increased the abundance of PT Na(+)/H(+) exchanger 3 (NHE3), cortical TALH Na-K-2Cl cotransporter 2 (NKCC2), distal convoluted tubule (DCT) Na-Cl cotransporter (NCC), and cortical CD ENaC subunits. Additionally, phosphorylation of cortical NKCC2, NCC, and STE20/SPS1-related proline-alanine-rich kinase (SPAK) were increased; medullary NKCC2 and SPAK were not altered. In conclusion, 3-day AngII infusion provokes PT NHE3 accumulation as well as NKCC2, NCC, and SPAK accumulation and activation in a prehypertensive phase before evidence for intrarenal angiotensinogen accumulation.
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.12496
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Article ; Online: Differentiation of Human Embryonic Stem Cells to Endothelial Progenitor Cells on Laminins in Defined and Xeno-free Systems.

Nguyen, Mien T X / Okina, Elena / Chai, Xiaoran / Tan, Kok Hian / Hovatta, Outi / Ghosh, Sujoy / Tryggvason, Karl

Stem cell reports

2016 Volume 7, Issue 4, Page(s) 802–816

Abstract: A major hurdle for in vitro culturing of primary endothelial cells (ECs) is that they readily dedifferentiate, hampering their use for therapeutic applications. Human embryonic stem cells (hESCs) may provide an unlimited cell source; however, most ... ...

Abstract	A major hurdle for in vitro culturing of primary endothelial cells (ECs) is that they readily dedifferentiate, hampering their use for therapeutic applications. Human embryonic stem cells (hESCs) may provide an unlimited cell source; however, most current protocols deriving endothelial progenitor cells (EPCs) from hESCs use direct differentiation approaches albeit on undefined matrices, yet final yields are insufficient. We developed a method to culture monolayer hESCs on stem cell niche laminin (LN) LN511 or LN521 matrix. Here, we report a chemically defined, xeno-free protocol for differentiation of hESCs to EPCs using LN521 as the main culture substrate. We were able to generate ∼95% functional EPCs defined as VEGFR2
Language	English
Publishing date	2016-10-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2016.08.017
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Article ; Online: Differential regulation of Na+ transporters along nephron during ANG II-dependent hypertension: distal stimulation counteracted by proximal inhibition.

Nguyen, Mien T X / Lee, Donna H / Delpire, Eric / McDonough, Alicia A

American journal of physiology. Renal physiology

2013 Volume 305, Issue 4, Page(s) F510–9

Abstract: During angiotensin II (ANG II)-dependent hypertension, ANG II stimulates, while hypertension inhibits, Na(+) transporter activity to balance Na(+) output to input. This study tests the hypothesis that ANG II infusion activates Na(+) transporters in the ... ...

Abstract	During angiotensin II (ANG II)-dependent hypertension, ANG II stimulates, while hypertension inhibits, Na(+) transporter activity to balance Na(+) output to input. This study tests the hypothesis that ANG II infusion activates Na(+) transporters in the distal nephron while inhibiting transporters along the proximal nephron. Male Sprague-Dawley rats were infused with ANG II (400 ng·kg(-1)·min(-1)) or vehicle for 2 wk. Kidneys were dissected (cortex vs. medulla) or fixed for immunohistochemistry (IHC). ANG II increased mean arterial pressure by 40 mmHg, urine Na(+) by 1.67-fold, and urine volume by 3-fold, evidence for hypertension and pressure natriuresis. Na(+) transporters' abundance and activation [assessed by phosphorylation (-P) or proteolytic cleavage] were measured by immunoblot. During ANG II infusion Na(+)/H(+) exchanger 3 (NHE3) abundance decreased in both cortex and medulla; Na-K-2Cl cotransporter 2 (NKCC2) decreased in medullary thick ascending loop of Henle (TALH) and increased, along with NKCC2-P, in cortical TALH; Na-Cl cotransporter (NCC) and NCC-P increased in the distal convoluted tubule; and epithelial Na(+) channel subunits and their cleaved forms were increased in both cortex and medulla. Like NKCC2, STE20/SPS1-related proline alanine-rich kinase (SPAK) and SPAK-P were decreased in medulla and increased in cortex. By IHC, during ANG II NHE3 remained localized to proximal tubule microvilli at lower abundance, and the differential regulation of NKCC2 and NKCC2-P in cortex versus medulla was evident. In summary, ANG II infusion increases Na(+) transporter abundance and activation from cortical TALH to medullary collecting duct while the hypertension drives a natriuresis response evident as decreased Na(+) transporter abundance and activation from proximal tubule through medullary TALH.
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Blood Pressure/drug effects ; Epithelial Sodium Channels/drug effects ; Epithelial Sodium Channels/metabolism ; Hypertension/metabolism ; Immunoblotting ; Immunohistochemistry ; Kidney/metabolism ; Male ; Membrane Transport Proteins/drug effects ; Membrane Transport Proteins/metabolism ; Nephrons/drug effects ; Nephrons/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium/metabolism
Chemical Substances	Epithelial Sodium Channels ; Membrane Transport Proteins ; Angiotensin II (11128-99-7) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2013-05-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00183.2013
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Article ; Online: Intrarenal localization of the plasma membrane ATP channel pannexin1.

Hanner, Fiona / Lam, Lisa / Nguyen, Mien T X / Yu, Alan / Peti-Peterdi, János

American journal of physiology. Renal physiology

2012 Volume 303, Issue 10, Page(s) F1454–9

Abstract: In the renal tubules, ATP released from epithelial cells stimulates purinergic receptors, regulating salt and water reabsorption. However, the mechanisms by which ATP is released into the tubular lumen are multifaceted. Pannexin1 (Panx1) is a newly ... ...

Abstract	In the renal tubules, ATP released from epithelial cells stimulates purinergic receptors, regulating salt and water reabsorption. However, the mechanisms by which ATP is released into the tubular lumen are multifaceted. Pannexin1 (Panx1) is a newly identified. ubiquitously expressed protein that forms connexin-like channels in the plasma membrane, which have been demonstrated to function as a mechanosensitive ATP conduit. Here, we report on the localization of Panx1 in the mouse kidney. Using immunofluorescence, strong Panx1 expression was observed in renal tubules, including proximal tubules, thin descending limbs, and collecting ducts, along their apical cell membranes. In the renal vasculature, Panx1 expression was localized to vascular smooth muscle cells in renal arteries, including the afferent and efferent arterioles. Additionally, we tested whether Panx1 channels expressed in renal epithelial cells facilitate luminal ATP release by measuring the ATP content of urine samples freshly collected from wild-type and Panx1(-/-) mice. Urinary ATP levels were reduced by 30% in Panx1(-/-) compared with wild-type mice. These results suggest that Panx1 channels in the kidney may regulate ATP release and via purinergic signaling may participate in the control of renal epithelial fluid and electrolyte transport and vascular functions.
MeSH term(s)	Adenosine Triphosphate/urine ; Animals ; Cell Membrane/metabolism ; Connexins/genetics ; Connexins/metabolism ; Epithelial Cells/metabolism ; Ion Channels/metabolism ; Kidney/metabolism ; Male ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Signal Transduction/physiology
Chemical Substances	Connexins ; Ion Channels ; Nerve Tissue Proteins ; Panx1 protein, mouse ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2012-09-05
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 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00206.2011
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Article ; Online: Paracellular epithelial sodium transport maximizes energy efficiency in the kidney.

Pei, Lei / Solis, Glenn / Nguyen, Mien T X / Kamat, Nikhil / Magenheimer, Lynn / Zhuo, Min / Li, Jiahua / Curry, Joshua / McDonough, Alicia A / Fields, Timothy A / Welch, William J / Yu, Alan S L

The Journal of clinical investigation

2016 Volume 126, Issue 7, Page(s) 2509–2518

Abstract: Efficient oxygen utilization in the kidney may be supported by paracellular epithelial transport, a form of passive diffusion that is driven by preexisting transepithelial electrochemical gradients. Claudins are tight-junction transmembrane proteins that ...

Abstract	Efficient oxygen utilization in the kidney may be supported by paracellular epithelial transport, a form of passive diffusion that is driven by preexisting transepithelial electrochemical gradients. Claudins are tight-junction transmembrane proteins that act as paracellular ion channels in epithelial cells. In the proximal tubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption. Here, we used murine models to investigate the role of claudin-2 in maintaining energy efficiency in the kidney. We found that claudin-2-null mice conserve sodium to the same extent as WT mice, even during profound dietary sodium depletion, as a result of the upregulation of transcellular Na-K-2Cl transport activity in the thick ascending limb of Henle. We hypothesized that shifting sodium transport to transcellular pathways would lead to increased whole-kidney oxygen consumption. Indeed, compared with control animals, oxygen consumption in the kidneys of claudin-2-null mice was markedly increased, resulting in medullary hypoxia. Furthermore, tubular injury in kidneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the absence of claudin-2. Our results indicate that paracellular transport in the PT is required for efficient utilization of oxygen in the service of sodium transport. We speculate that paracellular permeability may have evolved as a general strategy in epithelial tissues to maximize energy efficiency.
MeSH term(s)	Animals ; Claudin-2/metabolism ; Diet ; Epithelial Cells/metabolism ; Female ; Gene Expression Regulation ; Ion Transport ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Loop of Henle/metabolism ; Magnesium/metabolism ; Male ; Malondialdehyde/urine ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oxygen/metabolism ; Oxygen Consumption ; Permeability ; Reperfusion Injury/metabolism ; Sodium/metabolism ; Tight Junctions/metabolism
Chemical Substances	Claudin-2 ; Malondialdehyde (4Y8F71G49Q) ; Sodium (9NEZ333N27) ; Magnesium (I38ZP9992A) ; Oxygen (S88TT14065)
Language	English
Publishing date	2016--01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI83942
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Article ; Online: Effects of K+-deficient diets with and without NaCl supplementation on Na+, K+, and H2O transporters' abundance along the nephron.

Nguyen, Mien T X / Yang, Li E / Fletcher, Nicholas K / Lee, Donna H / Kocinsky, Hetal / Bachmann, Sebastian / Delpire, Eric / McDonough, Alicia A

American journal of physiology. Renal physiology

2012 Volume 303, Issue 1, Page(s) F92–104

Abstract: Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) ... ...

Abstract	Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) and H(2)O transporters' pool size regulation in response to removing K(+) from a diet containing 0.74% NaCl, as well as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet electrolytes. Sprague-Dawley rats (n = 5-6) were fed for 6 days with one of these diets: 2% KCl, 0.74% NaCl (2K1Na, control chow) compared with 0.03% KCl, 0.74% NaCl (0K1Na); or 2% KCl, 2%NaCl (2K2Na) compared with 0.03% KCl, 2% NaCl (0K2Na, Na(+) replete). In both 0K1Na and 0K2Na there were significant decreases in: 1) plasma [K(+)] (<2.5 mM); 2) urinary K(+) excretion (<5% of control); 3) urine osmolality and plasma [aldosterone], as well as 4) an increase in urine volume and medullary hypertrophy. The 0K2Na group had the lowest [aldosterone] (172.0 ± 17.4 pg/ml) and lower blood pressure (93.2 ± 4.9 vs. 112.0 ± 3.1 mmHg in 2K2Na). Transporter pool size regulation was determined by quantitative immunoblotting of renal cortex and medulla homogenates. The only differences measured in both 0K1Na and 0K2Na groups were a 20-30% decrease in cortical β-ENaC, 30-40% increases in kidney-specific Ste20/SPS1-related proline/alanine-rich kinase, and a 40% increase in medullary sodium pump abundance. The following proteins were not significantly changed in both the 0 K groups: Na(+)/H(+) exchanger isoform 3; Na(+)-K(+)-Cl(-) cotransporter; Na(+)-Cl(-) cotransporter, oxidative stress response kinase-1; renal outer medullary K(+) channel; autosomal recessive hypercholesterolemia; c-Src, aquaporin 2 isoform; or renin. Thus, despite profound hypokalemia and renal K(+) conservation, we did not confirm many of the changes that were previously reported. We predict that changes in transporter distribution and activity are likely more important for conserving K(+) than changes in total abundance.
MeSH term(s)	Animals ; Epithelial Sodium Channels/metabolism ; Male ; Nephrons/drug effects ; Nephrons/metabolism ; Phosphorylation/drug effects ; Potassium Deficiency/metabolism ; Potassium, Dietary/pharmacology ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary/pharmacology ; Sodium-Hydrogen Exchangers/metabolism ; Sodium-Potassium-Chloride Symporters/metabolism
Chemical Substances	Epithelial Sodium Channels ; Potassium, Dietary ; Sodium Chloride, Dietary ; Sodium-Hydrogen Exchangers ; Sodium-Potassium-Chloride Symporters
Language	English
Publishing date	2012-04-11
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 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00032.2012
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Article ; Online: A systematic approach to the development of a safe live attenuated Zika vaccine.

Kwek, Swee Sen / Watanabe, Satoru / Chan, Kuan Rong / Ong, Eugenia Z / Tan, Hwee Cheng / Ng, Wy Ching / Nguyen, Mien T X / Gan, Esther S / Zhang, Summer L / Chan, Kitti W K / Tan, Jun Hao / Sessions, October M / Manuel, Menchie / Pompon, Julien / Chua, Camillus / Hazirah, Sharifah / Tryggvason, Karl / Vasudevan, Subhash G / Ooi, Eng Eong

Nature communications

2018 Volume 9, Issue 1, Page(s) 1031

Abstract: Zika virus (ZIKV) is a flavivirus that can cause congenital disease and requires development of an effective long-term preventative strategy. A replicative ZIKV vaccine with properties similar to the yellow fever 17D (YF17D) live-attenuated vaccine (LAV) ...

Abstract	Zika virus (ZIKV) is a flavivirus that can cause congenital disease and requires development of an effective long-term preventative strategy. A replicative ZIKV vaccine with properties similar to the yellow fever 17D (YF17D) live-attenuated vaccine (LAV) would be advantageous, as a single dose of YF17D produces lifelong immunity. However, a replicative ZIKV vaccine must also be safe from causing persistent organ infections. Here we report an approach to ZIKV LAV development. We identify a ZIKV variant that produces small plaques due to interferon (IFN)-restricted viral propagation and displays attenuated infection of endothelial cells. We show that these properties collectively reduce the risk of organ infections and vertical transmission in a mouse model but remain sufficiently immunogenic to prevent wild-type ZIKV infection. Our findings suggest a strategy for the development of a safe but efficacious ZIKV LAV.
MeSH term(s)	Aedes/immunology ; Aedes/virology ; Animals ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Humans ; Immunologic Techniques ; Mice ; Vaccines, Attenuated/administration & dosage ; Vaccines, Attenuated/genetics ; Vaccines, Attenuated/immunology ; Viral Vaccines/administration & dosage ; Viral Vaccines/genetics ; Viral Vaccines/immunology ; Zika Virus/genetics ; Zika Virus/growth & development ; Zika Virus/immunology ; Zika Virus Infection/immunology ; Zika Virus Infection/prevention & control ; Zika Virus Infection/virology
Chemical Substances	Vaccines, Attenuated ; Viral Vaccines
Language	English
Publishing date	2018-03-12
Publishing country	England
Document type	Evaluation Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-03337-2
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