Swelling-Induced, Cftr-Independent Atp Release from a Human Epithelial Cell Line

Hazama, Akihiro; Shimizu, Takahiro; Ando‐Akatsuka, Yuhko; Hayashi, Seiji; Tanaka, Shoko; Maeno, Emi; Okada, Yasunobu

doi:10.1085/jgp.114.4.525

Cited by 121 publications

(132 citation statements)

References 42 publications

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“…A similar principle of ATP biosensing uses P2X receptor-expressing cells and patch clamp recordings to measure ATP-induced inward currents either in the whole-cell configuration or in outside-out excised patches [43,46]. It was coined the ATP 'patch sniffing' method [47].…”

Section: P2x 2 Receptor-mediated Ion Currents As Biosensors For Extramentioning

confidence: 99%

“…However, a significant number of studies failed to detect differences in extracellular ATP in normal and CFTR-deficient epithelial tissues [78][79][80]. It was also shown that swelling-induced ATP release was independent from CFTR [32,46,81]. Furthermore, more indirect approaches using CFTR blocking drugs failed to link agonist-stimulated ATP release to CFTR [26].…”

Section: The Link To Cftrmentioning

confidence: 99%

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ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

204

229

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All cells release nucleotides and are in one way or another involved in local autocrine and paracrine regulation of organ function via stimulation of purinergic receptors. Significant technical advances have been made in recent years to quantify more precisely resting and stimulated adenosine triphosphate (ATP) concentrations in close proximity to the plasma membrane. These technical advances are reviewed here. However, the mechanisms by which cells release ATP continue to be enigmatic. The current state of knowledge on different suggested mechanisms is also reviewed. Current evidence suggests that two separate regulated modes of ATP release co-exist in nonexcitable cells: (1) a conductive pore which in several systems has been found to be the channel pannexin 1 and (2) vesicular release. Modes of stimulation of ATP release are reviewed and indicate that both subtle mechanical stimulation and agonist-triggered release play pivotal roles. The mechano-sensor for ATP release is not yet defined.

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Section: P2x 2 Receptor-mediated Ion Currents As Biosensors For Extramentioning

confidence: 99%

Section: The Link To Cftrmentioning

confidence: 99%

ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

204

229

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“…Therefore, an administration of extracellular ATP to the CF cells should restore RVD as shown in CF mouse renal cells (47,48). However, no clear cause-and-effect relationship was observed with the ATP release and the VACC activation in the human intestinal epithelial cell line lacking CFTR (49) or in the murine mammary carcinoma cell line (50). Thus, further studies are needed to determine the precise underlying mechanisms of RVD in CF cholangiocytes and the role of extracellular ATP in RVD and its effect on VACC in CF cholangiocytes.…”

Section: Discussionmentioning

confidence: 98%

Impaired Regulatory Volume Decrease in Freshly Isolated Cholangiocytes from Cystic Fibrosis Mice

Cho

Siegrist

Zinzow

2004

Journal of Biological Chemistry

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Various K ؉ and Cl ؊ channels are important in cell volume regulation and biliary secretion, but the specific role of cystic fibrosis transmembrane conductance regulator in cholangiocyte cell volume regulation is not known. The goal of this research was to study regulatory volume decrease (RVD) in bile duct cell clusters (BDCCs) from normal and cystic fibrosis (CF) mouse livers. Mouse BDCCs without an enclosed lumen were prepared as described (Cho, W. K. (2002) Am. J. Physiol. 283, G1320 -G1327). The isotonic solution consisted of HEPES buffer with 40% of the NaCl replaced with isomolar amounts of sucrose, whereas hypotonic solution was the same as isotonic solution without sucrose. The cell volume changes were indirectly assessed by measuring cross-sectional area (CSA) changes of the BDCCs using quantitative videomicroscopy. Exposure to hypotonic solutions increased relative CSAs of normal BDCCs to 1.20 ؎ 0.01 (mean ؎ S.E., n ‫؍‬ 50) in 10 min, followed by RVD to 1.07 ؎ 0.01 by 40 min. Hypotonic challenge in CF mouse BDCCs also increased relative CSA to 1.20 ؎ 0.01 (n ‫؍‬ 53) in 10 min but without significant recovery. Coadministration of the K ؉ -selective ionophore valinomycin restored RVD in CF mouse BDCCs, suggesting that the impaired RVD was likely from a defect in K ؉ conductance. Moreover, this valinomycin-induced RVD in CF mice was inhibited by 5-nitro-2 -(3-phenylpropylamino)-benzoate, indicating that it is not from nonspecific effects. Neither cAMP nor calcium agonists could reverse the impaired RVD seen in CF cholangiocytes. Our conclusion is that CF mouse cholangiocytes have defective RVD from an impaired K ؉ efflux pathway, which could not be reversed by cAMP nor calcium agonists.Under physiological conditions, osmoregulation plays a crucial role in cholangiocytes, which are exposed to various osmotic stresses from the uptake of solutes and electrolytes and bile secretion (1, 2). A recent study on a human cholangiocarcinoma cell line (3), as well as our results in a study on primary bile duct cell clusters (BDCCs) 1 from normal mouse livers (4), indicates that cholangiocytes can regulate their cell volumes back to base line from hypotonicity-induced swelling. As in other cell types, these adaptive mechanisms of regulatory volume decrease (RVD) in cholangiocytes are mediated by certain K ϩ and Cl Ϫ conductances (3, 4).Cystic fibrosis (CF) is the most common inherited multisystem disease in the Caucasian population and is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR). Many CF patients develop a spectrum of hepatobiliary diseases that are thought to be due to secretory dysfunctions from the CFTR Cl Ϫ channel defects. In recent years, CF liver diseases have become the second most common cause of mortality in CF patients as they live longer, but the underlying pathophysiological mechanisms are not well understood. Recent immunocytochemical studies of the liver have shown that CFTR is expressed only on the bile duct epithelium but not on hepatocytes (5). The CFTR is...

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“…In addition, we used the patch-clamp technique to directly measure functional P2X 7 R activity at the plasma membrane and carried out spectrofluoremetric measurements of ROS production as well as of ethidium uptake to evaluate downstream responses resulting from the activation of receptors by ATP released during the hypotonic shock [21] since we also failed to observe purinergic-dependent currents or P2X 7 R protein in neutrophils isolated in the presence of apyrase. Finally, we have previously shown that P2X 7 R Na + current is sustained during an ATP application lasting more than 30 s, suggesting that this receptor do not desensitise [7] as has been previously shown by others (see [33] for a review).…”

Section: Discussionmentioning

confidence: 99%

Human neutrophils do not express purinergic P2X7 receptors

Martel-Gallegos

Rosales-Saavedra

Reyes

et al. 2010

Purinergic Signalling

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It has been reported that in human neutrophils, external ATP activates plasma membrane purinergic P2X 7 receptors (P2X 7 R) to elicit Ca 2+ entry, production of reactive oxygen species (ROS), processing and release of pro-inflammatory cytokines, shedding of adhesion molecules and uptake of large molecules. However, the expression of P2X 7 R at the plasma membrane of neutrophils has also been questioned since these putative responses are not always reproduced. In this work, we used electrophysiological recordings to measure functional responses associated with the activation of membrane receptors, spectrofluorometric measurements of ROS production and ethidium bromide uptake to asses coupling of P2X 7 R activation to downstream effectors, immunelabelling of P2X 7 R using a fluorescein isothiocyanateconjugated antibody to detect the receptors at the plasma membrane, RT-PCR to determine mRNA expression of P2X 7 R and Western blot to determine protein expression in neutrophils and HL-60 cells. None of these assays reported the presence of P2X 7 R in the plasma membrane of neutrophils and non-differentiated or differentiated HL-60 cells-a model cell for human neutrophils. We concluded that P2X 7 R are not present at plasma membrane of human neutrophils and that the putative physiological responses triggered by external ATP should be reconsidered.

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Swelling-Induced, Cftr-Independent Atp Release from a Human Epithelial Cell Line

Cited by 121 publications

References 42 publications

ATP release from non-excitable cells

ATP release from non-excitable cells

Impaired Regulatory Volume Decrease in Freshly Isolated Cholangiocytes from Cystic Fibrosis Mice

Human neutrophils do not express purinergic P2X7 receptors

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