Acid incubation reverses the polarity of intercalated cell transporters, an effect mediated by hensin

Schwartz, George J.; Tsuruoka, Shuichi; Vijayakumar, Soundarapandian; Petrovic, Snezana; Mian, Ayesa; Al‐Awqati, Qais

doi:10.1172/jci200213292

Cited by 26 publications

(58 citation statements)

References 30 publications

(45 reference statements)

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“…It has been shown that the majority of cells in clone C11 have characteristics of type b-intercalated cells, although the cells are not homogenous, as expected for a cloned cell line [16]. Moreover, it is known that bintercalated cells may differentiate to type a-intercalated cells in culture [17][18][19][20]. Therefore, to evaluate whether the expression of the a-subunit of Na + ,K + -ATPase in C11 cells is restricted to type a or type b intercalated cells, the cells were labeled for the asubunit of Na + ,K + -ATPase and PNA, a marker of bintercalated cells.…”

Section: Resultsmentioning

confidence: 95%

Lack of Na+,K+-ATPase expression in intercalated cells may be compensated by Na+-ATPase: A study on MDCK – C11 cells

Sampaio

Bezerra

Peçanha

et al. 2008

Cell. Mol. Life Sci.

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The lack of Na(+),K(+)-ATPase expression in intercalated cells (IC) is an intriguing condition due to its fundamental role in cellular homeostasis. In order to better understand this question we compared the activities of Na(+),K(+)-ATPase and Na(+)-ATPase in two MDCK cell clones: the C11, with IC characteristics, and the C7, with principal cells (PC) characteristics. The Na(+),K(+)-ATPase activity found in C11 cells is far lower than in C7 cells and the expression of its beta-subunit is similar in both cells. On the other hand, a subset of C11 without alpha-subunit expression has been found. In C11 cells the Na(+)-ATPase activity is higher than that of the Na(+),K(+)-ATPase, and it is increased by medium alkalinization, suggesting that it could account for the cellular Na(+)-homeostasis. Although further studies are necessary for a better understanding of these findings, the presence of Na(+)-ATPase may explain the adequate survival of cells that lack Na(+),K(+)-ATPase.

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Section: Resultsmentioning

confidence: 95%

Lack of Na+,K+-ATPase expression in intercalated cells may be compensated by Na+-ATPase: A study on MDCK – C11 cells

Sampaio

Bezerra

Peçanha

et al. 2008

Cell. Mol. Life Sci.

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“…An analogous remodeling of the cell may occur in patients with mutations encoding for subunits of apical H + ATPase, in which the intracellular pH of a-intercalated cells (H + -secreting) may be low. In cell culture, Schwartz et al [15] found that the intracellular acidosis induces a reversal of cell polarity, so that a-intercalated cells (H + secreting) functionally resemble b-intercalated cells (HCO 3 secreting). In both these models, plasticity of the cell would induce high Cl /HCO 3 exchange across the apical membrane, resulting in both hyperchloremia and metabolic acidosis.…”

Section: Discussionmentioning

confidence: 99%

An analysis of renal tubular acidosis by the Stewart method

2005

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Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated distal RTA (dRTA) and compared the results with data obtained from 17 healthy control subjects. In patients, but not in controls, saline loading induced both hyperchloremia and metabolic acidosis. Hyperchloremia was associated with high total and high distal fractional reabsorption of chloride [C(H20)/(C(H20)+C(Cl))]. The increase in plasma chloride varied inversely with the fractional excretion of chloride (C(Cl)) and correlated with the decrease in blood pH. However, the urinary excretion of bicarbonate did not correlate with either changes in blood pH or plasma bicarbonate concentration. Our findings suggest that the mechanism of hyperchloremia was enhanced Cl(-)/HCO(3) (-) exchange by the distal tubule. The resulting metabolic acidosis is better explained by changes in the strong ion difference (the Stewart theory) than by changes in the urine bicarbonate excretion (the traditional theory).

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“…The intercalated cell exists in two functionally distinct subtypes in the cortical collecting duct: one secretes HCO 3 -, while the other absorbs it. Reabsorption of HCO 3 -(i.e., secretion of protons) is accomplished in α-intercalated cells by an apical H + -ATPase and a basolateral Cl -/HCO 3 -exchanger.…”

Section: Intercalated Cellsmentioning

confidence: 99%

“…Reabsorption of HCO 3 -(i.e., secretion of protons) is accomplished in α-intercalated cells by an apical H + -ATPase and a basolateral Cl -/HCO 3 -exchanger. Secretion of HCO 3 -by β-intercalated cells is mediated by the same kinds of transporters but located on the opposite cell membranes. We found that when animals were fed an acid diet, the β form converted to the α phenotype (2).…”

Section: Intercalated Cellsmentioning

confidence: 99%