Macula densa cell signaling involves ATP release through a maxi anion channel

Bell, P. Darwin; Lapointe, Jean‐Yves; Sabirov, Ravshan Z.; Hayashi, Seiji; Peti‐Peterdi, Janos; Manabe, Ken‐ichi; Kovács, Gergely; Okada, Yasunobu

doi:10.1073/pnas.0736323100

Cited by 256 publications

(298 citation statements)

References 39 publications

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“…ATP release was stimulated via an elevation of the luminal NaCl concentration without changing the environment of the biosensor cell. These findings were confirmed by PC12 cells [44]. Thus, little doubt is left that the release of ATP from the macula densa cells after exposure to high NaCl in the luminal perfusate is a key component of the tubulo-glomerular feedback mechanism [11].…”

Section: Biosensor Cells and Atp Detection Via An Increase Of Cytosolmentioning

confidence: 64%

“…This technique enables the researcher to answer in a convincing way the temporo-spatial characteristics of ATP release in different cells. Cultured mouse mesangial smooth muscle cells have been used as biosensors to detect ATP release from the basolateral side of rabbit renal macula densa cells [11,17,44]. ATP release was stimulated via an elevation of the luminal NaCl concentration without changing the environment of the biosensor cell.…”

Section: Biosensor Cells and Atp Detection Via An Increase Of Cytosolmentioning

confidence: 99%

“…taurine) and the methylamine betaine [69]. Okada has presented evidence that the maxi anion conductance (VDAC-like-VDACL) is a plasma membrane ATP-conductive pore in mammary cancer cells [70] and in macula densa cells [44], and follow-up work shows that this conductance is inhibited by internal arachidonic acid [71]. VDAC is a mitochondrial ATPpermeable membrane pore, but has been suggested also to be present in the plasma membrane as a specific splice variant (pl-VDAC-1) [72].…”

Section: Cell Swelling-activated Anion Conductancementioning

confidence: 99%

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ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

207

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: Biosensor Cells and Atp Detection Via An Increase Of Cytosolmentioning

confidence: 64%

Section: Biosensor Cells and Atp Detection Via An Increase Of Cytosolmentioning

confidence: 99%

Section: Cell Swelling-activated Anion Conductancementioning

confidence: 99%

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ATP release from non-excitable cells

Praetorius

Leipziger

2009

Purinergic Signalling

207

229

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“…Among the anion channels, there are two types that show properties similar to P2X 7 receptor-associated pore. The first one is the maxi anion channel, an ATP (6,21) and glutamate (47) permeable channel that depends on the increase in intracellular Ca 2ϩ (40,46) and it possesses a high unitary conductance (6, 21) (ϳ400 pS) (9,47). Moreover, this channel can be activated by ischemia or hypoxia (21), where raising intracellular Ca 2ϩ is also important (13).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological properties of a pore induced by raising intracellular Ca²⁺

Faria¹,

Reis²,

Casabulho³

et al. 2009

American Journal of Physiology-Cell Physiology

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-Recent studies on the P2X 7 receptor in 2BH4 cells and peritoneal macrophages have demonstrated that the raise in intracellular Ca 2ϩ concentration induces a pore opening similar to P2X 7 receptor pore. Herein, we have investigated whether the pore activated by the elevation of intracellular Ca 2ϩ concentration is associated to P2X 7 receptor. Using patch clamp in cell attached, whole cell configuration, and dye uptake, we measured the pore opening in cell types that express the P2X 7 receptor (2BH4 cells and peritoneal macrophages) and in cells that do not express this receptor . In 2BH4 cells, the stimulation with ionomycin (5-10 M) increased intracellular free Ca 2ϩ concentration and induced pore formation with conductance of 421 Ϯ 14 pS, half-time (t 1 ⁄2) for ethidium bromide uptake of 118 Ϯ 17 s, and t 1 ⁄2 for Lucifer yellow of 122 Ϯ 11 s. P2X 7 receptor antagonists did not block these effects. Stimulation of HEK-293 and IT45-RI cells resulted in pore formation with properties similar to those found for 2BH4 cells. Connexin hemichannel inhibitors (carbenoxolone and heptanol) also did not inhibit the pore-induced effect following the increase in intracellular Ca 2ϩ concentration. However, 5-(N,N-hexamethylene)-amiloride, a P2X 7 receptor pore blocker, inhibited the induced pore. Moreover, intracellular signaling modulators, such as calmodulin, phospholipase C, mitogen-activated protein kinase, and cytoskeleton components were important for the pore formation. Additionally, we confirmed the results obtained for electrophysiology by using the flow cytometry, and we discarded the possibility of cellular death induced by raising intracellular Ca 2ϩ at the doses used by using lactate dehydrogenase release assay. In conclusion, increased concentration in intracellular Ca ϩ2 induces a novel membrane pore pharmacologically different from the P2X 7 associated pore and hemigap-junction pore.P2X 7 receptor; pore formation; second messenger P2X RECEPTORS are members of a family of P2 receptors with seven subtypes (P2X 1 -P2X 7 ) that induce an increase in intracellular Ca 2ϩ concentration when activated. Among the P2X receptors, P2X 7 subtype is the most divergent component of this family in terms of pharmacological properties, molecular structure, and function (54). This receptor forms a nonselective cation channel upon low ATP concentration, whereas at high ATP concentration, this receptor induces a pore formation that allows the flux of molecules of up to 900 Da and may lead to cell death. Although P2X 7 receptor is associated with expression of both functional channels and large pores, the structure of the large pore-forming subunits and whether the channel and the large pore are the same structure are still not known.From a physiological point of view, P2X 7 is mainly expressed in the immune system found in all cells of this system studied so far. The activation of P2X 7 receptor has several effects in the immune system such as release of mature interleukin-␤ and other pro-inflammatory cytokines (interleukin-18,...

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“…The exact source of adenosine still remains to be identified. Reportedly, ATP is released from macula densa cells into the interstitium of the extraglomerular mesangium, where it is broken down by nucleoside triphosphate diphosphohydrolases to adenosine monophosphate (AMP) [21,22] and is further hydrolyzed to adenosine by the ecto-5′-nucleotidase [10]. In ecto-5′-nucleotidase/CD73-deficient mice [23] as well as in rats or rabbits, when the e-5′-NT/D73 inhibitor β,γ-methylene adenosine diphosphate was used, TGF response was found to be markedly impaired [18,24].…”

mentioning

confidence: 99%

Cross-talk between arterioles and tubules in the kidney

et al. 2009

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In hypertension the pressure natriuresis set point is shifted to a higher pressure due to an increase in both renal vascular resistance and sodium (Na) reabsorption. The afferent arterioles (Af-Arts) and efferent arterioles (Ef-Arts) account for most renal vascular resistance; they control glomerular filtration rate (GFR) and peritubular pressure, and, consequently, renal function. Af-Art and Ef-Art resistance is regulated by factors similar to those in other arterioles and also by tubuloglomerular feedback (TGF). TGF operates via the macula densa, which senses increases in sodium chloride (NaCl) and sends a signal that constricts the Af-Art and dilates the Ef-Art. In the outer renal cortex, the connecting tubule (CNT) returns to the glomerular hilus and contacts the Af-Art. This morphology is compatible with cross-talk between the CNT and Af-Art, so-called connecting tubule glomerular feedback (CTGF). Our studies show that increasing NaCl delivery to the CNT results in Af-Art dilatation that can be blocked by inhibitors of Na transport. We believe cross-talk between the CNT and Af-Art is a novel mechanism that may contribute to regulation of renal blood flow and GFR. KeywordsAfferent arteriole; Macula densa; Connecting tubule; Tubuloglomerular feedback; Na transporterThe afferent arteriole (Af-Art) accounts for most renal vascular resistance. It controls glomerular filtration rate (GFR) and peritubular pressure, and consequently renal function. The hormonal and neural influences on vascular resistance that participate in the control of blood flow and GFR have been fairly well defined. Anatomical contact between the end of the thick ascending limb of the loop of Henle and its own glomerulus was described for the first time more than 100 years ago. In each nephron of the mammalian kidney, the tubule returns to the hilus of the parent glomerulus, forming the juxtaglomerular apparatus (JGA). The JGA is made up of (a) a plaque of specialized tubular epithelial cells called the macula densa; (b) the extraglomerular mesangium; and (c) the glomerular Af-Art and efferent arteriole (Ef-Art). This anatomical connection is thought to be crucial for tubuloglomerular feedback (TGF) control of GFR [1][2][3]. Therefore, Af-Art resistance is regulated not only by factors similar to those in other arterioles but also by the macula densa. TGF describes a functional connection between the tubular epithelium at the site of the macula densa and the underlying smooth muscle cells of the Af-Art and Ef-Art. An increase or decrease in sodium chloride (NaCl) concentration in the luminal fluid at the macula densa cells activates arteriolar constriction or dilation, respectively, and hence alters single-nephron GFR (SNGFR).Experimental studies of TGF began with the microinjection experiment designed and initiated by Klaus Thurau [4]. After the proximal segments belonging to the same nephron had been © IPNA 2008 Correspondence to: YiLin Ren, yren1@hfhs.org. Thomson and Blantz [9] evaluated the ability of TGF to stabilize tubula...

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Macula densa cell signaling involves ATP release through a maxi anion channel

Abstract: Macula densa cells are unique renal biosensor cells that detect changes in luminal NaCl concentration ([NaCl]

Cited by 256 publications

References 39 publications

ATP release from non-excitable cells

ATP release from non-excitable cells

Pharmacological properties of a pore induced by raising intracellular Ca²⁺

Cross-talk between arterioles and tubules in the kidney

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Macula densa cell signaling involves ATP release through a maxi anion channel

Abstract: Macula densa cells are unique renal biosensor cells that detect changes in luminal NaCl concentration ([NaCl]

Cited by 256 publications

References 39 publications

ATP release from non-excitable cells

ATP release from non-excitable cells

Pharmacological properties of a pore induced by raising intracellular Ca2+

Cross-talk between arterioles and tubules in the kidney

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Product

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Pharmacological properties of a pore induced by raising intracellular Ca²⁺