Publications by authors named "Paula Ford"

During the intense neuronal activity in the retina, Müller cells are exposed to a hypotonic environment and activate a regulatory volume decrease (RVD) response, which depends on Aquaporin-4 (AQP4) and the calcium channel Transient Receptor Potential Vanilloid 4 (TRPV4). It was reported that Osteopontin (OPN), a cytokine and component of the extracellular matrix (ECM), may modulate the RVD of Müller cells. In other cell types, OPN participates in cell survival and migration, which Müller cells undergo to maintain retinal homeostasis.

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Article Synopsis
  • Aquaporin-4 (AQP4) is targeted by AQP4-IgG antibodies in NMOSD, leading to cell damage through binding to astrocytic AQP4.
  • Researchers studied the effects of AQP4-IgG on Müller cells in the retina, focusing on key functions like cell volume regulation and proliferation.
  • Binding of AQP4-IgG causes partial internalization of AQP4, reducing water permeability and disrupting normal cellular functions, which may play a role in retinal injury associated with NMOSD.
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Increasing evidence indicates that aquaporins (AQPs) exert an influence in cell signaling by the interplay with the transient receptor potential vanilloid 4 (TRPV4) channel. We previously found that TRPV4 physically and functionally interacts with AQP2 in cortical collecting ducts (CCD) cells, favoring cell volume regulation and cell migration. Because TRPV4 was implicated in ATP release in several tissues, we investigated the possibility that TRPV4/AQP2 interaction influences ATP release in CCD cells.

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We have previously shown in renal cells that expression of the water channel Aquaporin-2 increases cell proliferation by a regulatory volume mechanism involving Na/H exchanger isoform 2. Here, we investigated if Aquaporin-2 (AQP2) also modulates Na/H exchanger isoform 1-dependent cell proliferation. We use two AQP2-expressing cortical collecting duct models: one constitutive (WT or AQP2-transfected RCCD cell line) and one inducible (control or vasopressin-induced mpkCCD cell line).

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Aquaporin-2 (AQP2) promotes renal cell migration by the modulation of integrin β1 trafficking and the turnover of focal adhesions. The aim of this study was to investigate whether AQP2 also works in cooperation with Na /H exchanger isoform 1 (NHE1), another well-known protein involved in the regulation of cell migration. Our results showed that the lamellipodia of AQP2-expressing cells exhibit significantly smaller volumes and areas of focal adhesions and more alkaline intracellular pH due to increased NHE1 activity than AQP2-null cells.

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Neuronal activity in the retina generates osmotic gradients that lead to Müller cell swelling, followed by a regulatory volume decrease (RVD) response, partially due to the isoosmotic efflux of KCl and water. However, our previous studies in a human Müller cell line (MIO-M1) demonstrated that an important fraction of RVD may also involve the efflux of organic solutes. We also showed that RVD depends on the swelling-induced Ca release from intracellular stores.

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There is increasing evidence indicating that aquaporins (AQPs) exert an influence in cell signaling by the interplay with the TRPV4 Ca channel. Ca release from intracellular stores and plasma membrane hyperpolarization due to opening of Ca -activated potassium channels (KCa) are events that have been proposed to take place downstream of TRPV4 activation. A major mechanism for Ca entry, activated after depletion of intracellular Ca stores and driven by electrochemical forces, is the store-operated Ca entry (SOCE).

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Neural activity alters osmotic gradients favoring cell swelling in retinal Müller cells. This swelling is followed by a regulatory volume decrease (RVD), partially mediated by an efflux of KCl and water. The transient receptor potential channel 4 (TRPV4), a nonselective calcium channel, has been proposed as a candidate for mediating intracellular Ca elevation induced by swelling.

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We have previously shown in renal cells that expression of the water channel Aquaporin 2 (AQP2) increases the rate of cell proliferation by shortening the transit time through the S and G /M phases of the cell cycle. This acceleration is due, at least in part, to a down-regulation of regulatory volume decrease (RVD) mechanisms when volume needs to be increased in order to proceed into the S phase. We hypothesize that in order to increase cell volume, RVD mechanisms may be overtaken by regulatory volume increase mechanisms (RVI).

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Objective: To examine disparities in park availability, features, and characteristics by income and the percentage of foreign-born population within a predominately-Hispanic border community.

Methods: This study occurred in 2010-2011 in El Paso, Texas. All census tracts (n=112) were categorized as low, medium, or high income and percent foreign-born.

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Müller cells are mainly involved in controlling extracellular homeostasis in the retina, where intense neural activity alters ion concentrations and osmotic gradients, thus favoring cell swelling. This increase in cell volume is followed by a regulatory volume decrease response (RVD), which is known to be partially mediated by the activation of K(+) and anion channels. However, the precise mechanisms underlying osmotic swelling and subsequent cell volume regulation in Müller cells have been evaluated by only a few studies.

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We have previously demonstrated that in renal cortical collecting duct cells (RCCD(1)) the expression of the water channel Aquaporin 2 (AQP2) raises the rate of cell proliferation. In this study, we investigated the mechanisms involved in this process, focusing on the putative link between AQP2 expression, cell volume changes, and regulatory volume decrease activity (RVD). Two renal cell lines were used: WT-RCCD(1) (not expressing aquaporins) and AQP2-RCCD(1) (transfected with AQP2).

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NMO-IgG autoantibody selectively binds to aquaporin-4 (AQP4), the most abundant water channel in the central nervous system and is now considered a useful serum biomarker of neuromyelitis optica (NMO). A series of clinical and pathological observations suggests that NMO-IgG may play a central role in NMO physiopathology. The current study evaluated, in well-differentiated astrocytes cultures, the consequences of NMO-IgG binding on the expression pattern of AQP4 and on plasma membrane water permeability.

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Purpose: To investigate the effects of use of water from irrigation canals to flood residential yards on the risk of West Nile disease in El Paso, Texas.

Methods: West Nile disease confirmed cases in 2009 through 2010 were compared with a random sample of 50 residents of the county according to access to and use of water from irrigation canals by subjects or their neighbors, as well as geo-referenced closest distance between their home address and the nearest irrigation canal. A windshield survey of 600 m around the study subjects' home address recorded the presence of irrigation canals.

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Article Synopsis
  • The study shows that RCCD(1) cells activate volume regulation mechanisms in response to low osmotic stress, which requires both the water channel AQP2 and calcium influx.
  • It hypothesizes that the calcium entry might be facilitated by the TRPV4 channel, crucial for responding to changes in osmotic pressure.
  • Findings indicate that TRPV4 is activated primarily in the presence of AQP2, and blocking TRPV4 disrupts calcium influx and volume regulation, suggesting a significant interaction between TRPV4 and AQP2 in response to osmotic stress.
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High levels of neighborhood deprivation and lack of access to supermarkets have been associated with increased risk of obesity in women. This multilevel study used a statewide dataset (n = 21,166) of low-income women in the Special Supplemental Nutrition Program for Women, Infants, and Children to determine whether the association between neighborhood deprivation and BMI is mediated by the availability of retail food stores, and whether this relationship varied across the urban rural continuum. Residence in a high deprivation neighborhood was associated with a 0.

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Collecting ducts (CD) not only constitute the final site for regulating urine concentration by increasing apical membrane Aquaporin-2 (AQP2) expression, but are also essential for the control of acid-base status. The aim of this work was to examine, in renal cells, the effects of chronic alkalosis on cell growth/death as well as to define whether AQP2 expression plays any role during this adaptation. Two CD cell lines were used: WT- (not expressing AQPs) and AQP2-RCCD(1) (expressing apical AQP2).

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Socioecological theory and a growing body of research suggests that geographic, racial, ethnic, and socioeconomic disparities in the prevalence of obesity are linked to disparities in the availability of food retail outlets that provide healthy food options. We examined the availability of food stores for low-income women in Kansas and tested whether food store availability was associated with obesity using cross-sectional, geocoded data from women participating in the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) (n = 21,166) in Kansas. The availability and density of food stores within a 1, 3, and 5 mile radius of residence was determined, and multivariate logistic regression was used to examine the association of food store availability with obesity.

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Background Information: A major hallmark of apoptosis is cell shrinkage, termed apoptotic volume decrease, due to the cellular outflow of potassium and chloride ions, followed by osmotically obliged water. In many cells, the ionic pathways triggered during the apoptotic volume decrease may be similar to that observed during a regulatory volume decrease response under hypotonic conditions. However, the pathways involved in water loss during apoptosis have been largely ignored.

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Although the overall population in the United States has experienced a dramatic increase in obesity in the past 25 years, ethnic/racial minorities, and socioeconomically disadvantaged populations have a greater prevalence of obesity, as compared to white, and/or economically advantaged populations. Disparities in obesity are unlikely to be predominantly due to individual psychosocial or biological differences, and they may reflect differences in the built or social environment. The retail food environment is a critical aspect of the built environment that can contribute to observed disparities.

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Arginine-vasopressin (AVP) has been proposed to be involved in the modulation of acid-base transporters; however, the nature of the mechanisms underlying AVP direct action on intracellular pH (pH(i)) in the cortical collecting duct (CCD) is not yet clearly defined. The aim of the present study was to elucidate which are the proteins implicated in AVP modulation of pH(i), as well as the receptors involved in these responses using a CCD cell line (RCCD(1)); pH(i) was monitored with the fluorescent dye BCECF in basal conditions and after stimulation with basolateral 10(-8) M AVP. Specific V1- or V2-receptor antagonists were also used.

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The Cl(-)/HCO3- exchanger (AE) is one of the mechanisms that cells have developed to adjust pH Despite its importance, the role of AE isoforms in controlling steady-state pH during alkalosis has not been widely investigated. In the present study, we have evaluated whether conditions simulating acute and chronic metabolic alkalosis affected the transport activity and protein levels of Cl-/HCO3- exchangers in a rat cortical collecting duct cell line (RCCD1). pH(i) was monitored using the fluorescent dye BCECF in monolayers grown on permeable supports.

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Background Information: The renal CCD (cortical collecting duct) plays a role in final volume and concentration of urine by a process that is regulated by the antidiuretic hormone, [arginine]vasopressin. This hormone induces an increase in water permeability due to the translocation of AQP2 (aquaporin 2) from the intracellular vesicles to the apical membrane of principal cells. During the transition from antidiuresis to diuresis, CCD cells are exposed to changes in environmental osmolality, and cell-volume regulation may be especially important for the maintenance of intracellular homoeostasis.

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