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American Journal of Physiology. Cell Physiology

Cristina Matthewman, Tyne W Miller-Fleming, David M Miller, Laura Bianchi
Hyperactivated DEG/ENaC channels cause neuronal death mediated by intracellular Ca(2+) overload. Mammalian ASIC1a and C. elegans MEC-4(d) neurotoxic channels conduct both Na(+) and Ca(2+) raising the possibility that direct Ca(2+) influx through these channels contributes to the intracellular Ca(2+) overload. However, we showed that homologous C. elegans DEG/ENaC channel UNC-8(d) is not Ca(2+) permeable yet it is neurotoxic, suggesting that Na(+) influx is sufficient to induce cell death. Interestingly, UNC-8(d) shows small currents due to extracellular Ca(2+) block in the Xenopus oocytes expression system...
October 19, 2016: American Journal of Physiology. Cell Physiology
Feng Hao, Fuqiang Zhang, Daniel Dongwei Wu, Dong An, Jing Shi, Guohong Li, Xuemin Xu, Mei-Zhen Cui
Vascular smooth muscle cell (SMC) migration is an essential step involved in neointimal formation in restenosis and atherosclerosis. Lysophosphatidic acid (LPA) is a bioactive component of oxidized low density lipoprotein and is produced by activated platelets, implying that LPA influences vascular remodeling. Our previous study revealed that matricellular protein CCN1, a prominent extracellular matrix (ECM) protein, mediates LPA-induced SMC migration in vitro. Here we examined the role of CCN1 in LPA-induced neointimal formation...
October 19, 2016: American Journal of Physiology. Cell Physiology
Younggeon Jin, Anthony T Blikslager
Intestinal anoxia/reoxygenation (A/R) injury induces loss of barrier function followed by epithelial repair. Myosin light chain kinase (MLCK) has been shown to alter barrier function via regulation of interepithelial tight junctions (TJ), but has not been studied in intestinal A/R injury. We hypothesized that A/R injury would disrupt TJ barrier function via MLCK activation and MLC phosphorylation. Caco-2BBe1 monolayers were subjected to anoxia for 2 hours followed by reoxygenation in 21% O2, after which barrier function was determined by measuring transepithelial resistance (TER) and FITC-dextran flux...
October 19, 2016: American Journal of Physiology. Cell Physiology
Yan Xu, Jie Chen, Lan Xiao, Hee Kyoung Chung, Yuan Zhang, Joseph C Robinson, Jaladanki N Rao, Jian-Ying Wang
The RNA-binding protein HuR is crucial for normal intestinal mucosal regeneration by modulating the stability and translation of target mRNAs, but the exact mechanism underlying HuR trafficking between the cytoplasm and nucleus remains largely unknown. Here we report a novel function of transcription factor JunD in the regulation of HuR subcellular localization through the control of importin-α1 expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically inhibited importin-α1 at the transcription level, and this repression is mediated via interaction with CREB-binding site that was located at the proximal region of importin-α1 promoter...
October 12, 2016: American Journal of Physiology. Cell Physiology
Yao Li, Shengjie Li, Ping Jin, Liming Chen, Fei Ma
MicroRNAs play diverse roles in various physiological processes during Drosophila development. In the present study, we reported that miR-11 regulates pupal size during Drosophila metamorphosis via targeting Ras85D with following evidences: pupal size was increased in the miR-11 deletion mutant; restoration of miR-11 in the miR-11 deletion mutant rescued the increased pupal size phenotype observed in the miR-11 deletion mutant; ectopic expression of miR-11 in brain insulin-producing cells (IPCs) and whole body shows consistent alteration of pupal size; Dilps and Ras85D expressions were negatively regulated by miR-11 in vivo; miR-11 targets Ras85D through directly binding to Ras85D 3'UTR in vitro; removal of one copy of Ras85D in the miR-11 deletion mutant rescued the increased pupal size phenotype observed in the miR-11 deletion mutant...
October 12, 2016: American Journal of Physiology. Cell Physiology
Geoffrey E Ciarlone, Jay B Dean
Central CO2 chemoreceptive neurons in the caudal solitary complex (cSC) are stimulated by hyperoxia via a free radical mechanism. Hyperoxia has been shown to increase superoxide and nitric oxide in the cSC, but it remains unknown how changes in pCO2 during hyperoxia affect the production of O2-dependent reactive oxygen and nitrogen species (RONS) downstream that can lead to increased levels of oxidative and nitrosative stress, cellular excitability, and potentially, dysfunction. We used real time fluorescence microscopy in rat brain slices to determine how hyperoxia and hypercapnic acidosis (HA) modulate one another in the production of key RONS, as well as colorimetric assays to measure levels of oxidized and nitrated lipids and proteins...
October 12, 2016: American Journal of Physiology. Cell Physiology
Geoffrey E Ciarlone, Jay B Dean
Central CO2 chemosensitive neurons in the caudal solitary complex (cSC) are stimulated not only by hypercapnic acidosis (HA), but by hyperoxia as well. While a cellular mechanism for the CO2 response has yet to be isolated, previous data show that a redox-sensitive mechanism underlies neuronal excitability to hyperoxia. However, it remains unknown how changes in pO2 affect the production of reactive oxygen and nitrogen species (RONS) in the cSC that can lead to increased cellular excitability and with larger doses, cellular dysfunction and death...
October 12, 2016: American Journal of Physiology. Cell Physiology
Bruce D Schultz
Not applicable.
October 5, 2016: American Journal of Physiology. Cell Physiology
Adam Kassan, Uyen Pham, Quynhmy Nguyen, Melissa E Reichelt, Eunbyul Cho, Piyush M Patel, David M Roth, Brian P Head, Hemal H Patel
Autophagy is a dynamic recycling process responsible for the breakdown of misfolded proteins and damaged organelles, providing nutrients and energy for cellular renovation and homeostasis. Loss of autophagy is associated with cardiovascular diseases. Caveolin-3 (Cav-3), a muscle-specific isoform, is a structural protein within caveolae and is critical to stress adaptation in the heart. Whether Cav-3 plays a role in regulating autophagy to modulate cardiac stress responses remains unknown. In the present study, we used HL-1 cells, a cardiac muscle cell line, with stable Cav-3 knockdown (Cav-3 KD) and Cav-3 over-expression (Cav-3 OE) to study the impact of Cav-3 in regulation of autophagy...
October 5, 2016: American Journal of Physiology. Cell Physiology
Matthew A Dragovich, Daniel Chester, Bingmei M Fu, Chenyu Wu, Yan Xu, Michael S Goligorsky, X Frank Zhang
The endothelial surface glycocalyx (ESG) is a carbohydrate-rich layer found on the vascular endothelium, serving critical functions in the mechanotransduction of blood flow induced forces. One of the most important protective functions of the ESG is to mediate the production of nitric oxide (NO) in response to blood flow. However, the detailed mechanism underlying ESG's mechanotransduction of the production of NO has not been completely identified. Herein, using the cultured rat brain microvascular endothelial cells (bEnd...
September 28, 2016: American Journal of Physiology. Cell Physiology
Evan J Myers, Aniko Marshall, Michael L Jennings, Mark D Parker
The SLC4A11 gene encodes the bicarbonate-transporter-related protein BTR1, which is mutated in syndromes characterized by vision and hearing loss. Signs of these diseases (congenital hereditary endothelial dystrophy (CHED) and Harboyan Syndrome) are evident in mouse models of Slc4a11 disruption. However, the intrinsic activity of Slc4a11 remains controversial, complicating assignment of its (patho)physiological role. Most studies concur that Slc4a11 transports H(+) (or the thermodynamically equivalent species OH(-)) rather than HCO3 (-) but disparities have arisen as to whether the transport is coupled to another species such as Na(+) or NH3/NH4 (+) Here for the first time, we examine the action of mouse Slc4a11 in Xenopus oocytes...
September 28, 2016: American Journal of Physiology. Cell Physiology
Julieta Diaz-Juarez, Jorge Suarez, Federico Cividini, Brian T Scott, Tanja Diemer, Anzhi Dai, Wolfgang H Dillmann
Diabetic cardiomyopathy is associated with metabolic changes including decreased glucose oxidation (Gox) and increased fatty acid oxidation (FAox), which result in cardiac energetic deficiency. Diabetic hyperglycemia is a pathophysiological mechanism that triggers multiple maladaptive phenomena. The mitochondrial calcium uniporter (MCU) is the channel responsible for Ca(2+) uptake in mitochondria and free mitochondrial calcium concentration ([Ca(2+)]m) regulates mitochondrial metabolism. Experiments with cardiac myocytes (CM) exposed to simulated hyperglycemia revealed both reduced [Ca(2+)]m and MCU protein levels...
September 28, 2016: American Journal of Physiology. Cell Physiology
R Brent Thomson, Claire L Thomson, Peter S Aronson
The brush border Cl-oxalate exchanger SLC26A6 plays an essential role in mediating intestinal secretion of oxalate, and is crucial for the maintenance of oxalate homeostasis and the prevention of hyperoxaluria and calcium oxalate nephrolithiasis. Previous in vitro studies have suggested that SLC26A6 is heavily N-glycosylated. N-linked glycosylation is known to critically affect folding, trafficking and function in a wide variety of integral membrane proteins and could therefore potentially have a critical impact on SLC26A6 function and subsequent oxalate homeostasis...
September 28, 2016: American Journal of Physiology. Cell Physiology
Samanta Gasco, Amaya Rando, Pilar Zaragoza, Alberto García-Redondo, Ana Cristina Calvo, Rosario Osta
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a difficult diagnosis and prognosis. In this regard, new and more reliable biomarkers for the disease are needed. We propose peripheral blood, and more specifically the Hematopoietic Stem and Progenitor Cells (HSPCs) as potential prognostic biomarkers in the SOD1G93A murine model of ALS. We accurately and serially studied three HSPCs, Hematopoietic Stem Cells (HSCs), Common Lymphoid Progenitors (CLPs) and Common Myeloid Progenitors (CMPs), in both control and SOD1G93A mice along the disease progression by RT-PCR and flow cytometry analysis...
September 28, 2016: American Journal of Physiology. Cell Physiology
Kevin P M Currie
This is a an editorial focus article - there is no abstract.
September 21, 2016: American Journal of Physiology. Cell Physiology
Qinghua Kong, Lan Gao, Yanfen Niu, Pianchou Gongpan, Yuhui Xu, Yan Li, Wenyong Xiong
Adipose tissue plays a critical role in metabolic diseases and the maintenance of energy homeostasis. RACK1 has been identified as an adaptor protein involved in multiple intracellular signal transduction pathways and diseases. However, whether it regulates adipogenesis remains unknown. Here, we reported that RACK1 is expressed in 3T3-L1 cells and murine white adipose tissue, and RACK1 knockdown by shRNA profoundly suppressed adipogenesis by reducing the expression of PPARγ and C/EBPβ. Depletion of RACK1 increased β-Catenin protein levels and activated Wnt signaling...
September 21, 2016: American Journal of Physiology. Cell Physiology
Christopher M Johnson, Weiwei Zhong, Ningren Cui, Yang Wu, Hao Xing, Shuang Zhang, Chun Jiang
Rett Syndrome (RTT) is an X-linked neurodevelopmental disorder caused mostly by disruption of the MECP2 gene. Among several RTT-like mouse models, one of them is a strain of mice that carries an R168X point mutation in Mecp2, and resembles one of the most common RTT-causing mutations in humans. Although several behavioral defects have previously been found in Mecp2(R168X/Y) mice, alterations in nerve cells remain unknown. Here we compare several behavioral and cellular outcomes between this Mecp2(R168X/Y) model and a widely used Mecp2Bird/Y mouse model...
September 21, 2016: American Journal of Physiology. Cell Physiology
Connor J Telles, Sarah E Decker, William W Motley, Alexander W Peters, Ali Poyan Mehr, Raymond A Frizzell, John N Forrest
In the shark rectal gland (SRG), apical chloride secretion is electrically coupled to a basolateral K(+) conductance whose type and molecular identity are unknown. We performed studies in the perfused SRG with 17 K(+) channel inhibitors to begin this search. Maximal chloride secretion was inhibited by low perfusate pH, quinine, bupivicaine, and anandamide, consistent with the properties of an acid sensitive four transmembrane, two-pore-domain K(+) channel (4TM-K2P). Using PCR with degenerate primers to this family, we identified a TASK-1 fragment in shark rectal gland, brain, gill, and kidney...
September 21, 2016: American Journal of Physiology. Cell Physiology
Pin Lv, Fan Zhang, Ya-Juan Yin, Yu-Can Wang, Min Gao, Xiao-Li Xie, Li-Li Zhao, Li-Hua Dong, Yan-Ling Lin, Ya-Nan Shu, Dan-Dan Zhang, Gui-Xia Liu, Mei Han
We previously demonstrated that smooth muscle (SM) 22α promotes the migration activity in contractile vascular smooth muscle cells (VSMCs). Based on the varied functions exhibited by SM22α in different VSMC phenotypes, we investigated the effect of SM22α on VSMC migration under pathological conditions. The results demonstrated that SM22α overexpression in synthetic VSMCs inhibited platelet-derived growth factor (PDGF)-BB-induced cell lamellipodium formation and migration, which was different from its action in contractile cells...
September 14, 2016: American Journal of Physiology. Cell Physiology
Megan C Moorer, Atum M Buo, Karla P Garcia-Pelagio, Joseph P Stains, Robert J Bloch
While the type IV intermediate filament protein, synemin, has been shown to play a role in striated muscle and neuronal tissue, its presence and function has not been described in skeletal tissue. Here, we report that genetic ablation of synemin in 14-week old male mice results in osteopenia that includes a more than a 2-fold reduction in the trabecular bone fraction in the distal femur and a reduction in the cross sectional area at the femoral mid-diaphysis due to an attendant reduction in both the periosteal and endosteal perimeter...
September 7, 2016: American Journal of Physiology. Cell Physiology
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