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Molecular Mechanism of pH Regulation: From Physiology to Pathology 2.0
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Molecular Mechanism of pH Regulation: From Physiology to Pathology 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 December 2024 | Viewed by 3680

Special Issue Editor

Dr. Inyeong Choi

E-Mail Website
Guest Editor
Department of Cell Biology, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: pH regulation; acid/base disturbance; metabolic acidosis; sodium-bicarbonate transporter; brain acidosis; acidosis in cancer; structure-function of acid/base transporter
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

pH is an important biological factor that regulates cell function. Hydrogen ions interact with proteins and change their structure and function, resulting in modified cellular processes. Maintaining a normal pH is frequently challenged under both physiological and pathological conditions. For example, pH decreases when metabolic activity increases during heavy exercise or when blood supply is inefficient in ischemia. Typically, acidification inhibits cellular activity, such that severe acidification is deleterious to normal cells and causes cell death. On the other hand, acidification can be adversely beneficial under some pathological conditions. Cancer cells thrive in acidic microenvironments and undergo adaptations to promote survival and proliferation. The effects of pH abnormalities on physiology and relevant diseases have been studied over the past decades. This Special Issue focuses on the current understanding of pH regulation in various model systems and/or its involvement in diseases. The topic is open to original studies, reviews, and new methodologies, ranging from the molecular and cellular level to integrated organ systems.

You may choose our Joint Special Issue in CIMB.

Dr. Inyeong Choi
Guest Editor

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Keywords

  • pH regulation
  • acid base transporter
  • acid base disturbance
  • acidosis
  • intracellular pH
  • NBC
  • NHE
  • cancer

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Published Papers (3 papers)

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Research

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20 pages, 3168 KiB  
Article
Left Ventricular Systolic Dysfunction in NBCe1-B/C-Knockout Mice
by Clayton T. Brady, Aniko Marshall, Lisa A. Eagler, Thomas M. Pon, Michael E. Duffey, Brian R. Weil, Jennifer K. Lang and Mark D. Parker
Int. J. Mol. Sci. 2024, 25(17), 9610; https://doi.org/10.3390/ijms25179610 - 5 Sep 2024
Viewed by 670
Abstract
Congenital proximal renal tubular acidosis (pRTA) is a rare systemic disease caused by mutations in the SLC4A4 gene that encodes the electrogenic sodium bicarbonate cotransporter, NBCe1. The major NBCe1 protein variants are designated NBCe1-A, NBCe1-B, and NBCe1-C. NBCe1-A expression is kidney-specific, NBCe1-B is [...] Read more.
Congenital proximal renal tubular acidosis (pRTA) is a rare systemic disease caused by mutations in the SLC4A4 gene that encodes the electrogenic sodium bicarbonate cotransporter, NBCe1. The major NBCe1 protein variants are designated NBCe1-A, NBCe1-B, and NBCe1-C. NBCe1-A expression is kidney-specific, NBCe1-B is broadly expressed and is the only NBCe1 variant expressed in the heart, and NBCe1-C is a splice variant of NBCe1-B that is expressed in the brain. No cardiac manifestations have been reported from patients with pRTA, but studies in adult rats with virally induced reduction in cardiac NBCe1-B expression indicate that NBCe1-B loss leads to cardiac hypertrophy and prolonged QT intervals in rodents. NBCe1-null mice die shortly after weaning, so the consequence of congenital, global NBCe1 loss on the heart is unknown. To circumvent this issue, we characterized the cardiac function of NBCe1-B/C-null (KOb/c) mice that survive up to 2 months of age and which, due to the uninterrupted expression of NBCe1-A, do not exhibit the confounding acidemia of the globally null mice. In contrast to the viral knockdown model, cardiac hypertrophy was not present in KOb/c mice as assessed by heart-weight-to-body-weight ratios and cardiomyocyte cross-sectional area. However, echocardiographic analysis revealed reduced left ventricular ejection fraction, and intraventricular pressure–volume measurements demonstrated reduced load-independent contractility. We also observed increased QT length variation in KOb/c mice. Finally, using the calcium indicator Fura-2 AM, we observed a significant reduction in the amplitude of Ca2+ transients in paced KOb/c cardiomyocytes. These data indicate that congenital, global absence of NBCe1-B/C leads to impaired cardiac contractility and increased QT length variation in juvenile mice. It remains to be determined whether the cardiac phenotype in KOb/c mice is influenced by the absence of NBCe1-B/C from neuronal and endocrine tissues. Full article
(This article belongs to the Special Issue Molecular Mechanism of pH Regulation: From Physiology to Pathology 2.0)
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14 pages, 2500 KiB  
Article
Sodium Bicarbonate Decreases Alcohol Consumption in Mice
by Jason Lin, Ana P. Rivadeneira, Yani Ye, Clara Ryu, Shangrila Parvin, Kyeongran Jang, Sandra M. Garraway and Inyeong Choi
Int. J. Mol. Sci. 2024, 25(9), 5006; https://doi.org/10.3390/ijms25095006 - 3 May 2024
Cited by 1 | Viewed by 1114
Abstract
We previously reported that mice with low neuronal pH drink more alcohol, demonstrating the importance of pH for alcohol reward and motivation. In this study, we tested whether systemic pH affects alcohol consumption and if so, whether it occurs by changing the alcohol [...] Read more.
We previously reported that mice with low neuronal pH drink more alcohol, demonstrating the importance of pH for alcohol reward and motivation. In this study, we tested whether systemic pH affects alcohol consumption and if so, whether it occurs by changing the alcohol reward. C57BL/6J mice were given NaHCO3 to raise their blood pH, and the animals’ alcohol consumption was measured in the drinking-in-the-dark and two-bottle free choice paradigms. Alcohol consumption was also assessed after suppressing the bitterness of NaHCO3 with sucrose. Alcohol reward was evaluated using a conditioned place preference. In addition, taste sensitivity was assessed by determining quinine and sucrose preference. The results revealed that a pH increase by NaHCO3 caused mice to decrease their alcohol consumption. The decrease in high alcohol contents (20%) was significant and observed at different ages, as well as in both males and females. Alcohol consumption was also decreased after suppressing NaHCO3 bitterness. Oral gavage of NaHCO3 did not alter quinine and sucrose preference. In the conditioned place preference, NaHCO3-treated mice spent less time in the alcohol-injected chamber. Conclusively, the results show that raising systemic pH with NaHCO3 decreases alcohol consumption, as it decreases the alcohol reward value. Full article
(This article belongs to the Special Issue Molecular Mechanism of pH Regulation: From Physiology to Pathology 2.0)
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Review

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16 pages, 1365 KiB  
Review
Chloride/Multiple Anion Exchanger SLC26A Family: Systemic Roles of SLC26A4 in Various Organs
by Dongun Lee and Jeong Hee Hong
Int. J. Mol. Sci. 2024, 25(8), 4190; https://doi.org/10.3390/ijms25084190 - 10 Apr 2024
Cited by 1 | Viewed by 1432
Abstract
Solute carrier family 26 member 4 (SLC26A4) is a member of the SLC26A transporter family and is expressed in various tissues, including the airway epithelium, kidney, thyroid, and tumors. It transports various ions, including bicarbonate, chloride, iodine, and oxalate. As a multiple-ion transporter, [...] Read more.
Solute carrier family 26 member 4 (SLC26A4) is a member of the SLC26A transporter family and is expressed in various tissues, including the airway epithelium, kidney, thyroid, and tumors. It transports various ions, including bicarbonate, chloride, iodine, and oxalate. As a multiple-ion transporter, SLC26A4 is involved in the maintenance of hearing function, renal function, blood pressure, and hormone and pH regulation. In this review, we have summarized the various functions of SLC26A4 in multiple tissues and organs. Moreover, the relationships between SLC26A4 and other channels, such as cystic fibrosis transmembrane conductance regulator, epithelial sodium channel, and sodium chloride cotransporter, are highlighted. Although the modulation of SLC26A4 is critical for recovery from malfunctions of various organs, development of specific inducers or agonists of SLC26A4 remains challenging. This review contributes to providing a better understanding of the role of SLC26A4 and development of therapeutic approaches for the SLC26A4-associated hearing loss and SLC26A4-related dysfunction of various organs. Full article
(This article belongs to the Special Issue Molecular Mechanism of pH Regulation: From Physiology to Pathology 2.0)
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