International Journal of Molecular Sciences

Journal Browser

► Journal Browser

Calcium Homeostasis of Cells in Health and Disease 2.0

Share This Special Issue

Special Issue Editors

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Calcium Homeostasis of Cells in Health and Disease”.

Whether in health or in disease, calcium ion (Ca²⁺) plays a very important role in stimulus–answers processes of cells as a second messenger. This works by retaining intracellular Ca²⁺ concentration low at rest and by mobilizing Ca²⁺ in answer to stimuli, which activates cellular functions. This second messenger role of Ca²⁺ was first discovered in excitation–contraction coupling of skeletal muscle. Later on, the characteristics of Ca²⁺ as a second messenger, the variety of targets, its ability to achieve quick and enormous transient and also oscillatory mobilization, and the capability of causing localized and also generalized cell responses were studied widely.

Although calcium is extensively studied in a variety of cells, there are a lot of features which are still uncertain: what is its role in physiological and in pathological circumstances? Quite a few studies have shown that the Ca²⁺ homeostasis of cells is modified during development and while they are getting old. The latter becomes more and more important as the Earth’s population reaches an increasingly old age. Thus, aging is one of the hot topics in human research. However, alteration in calcium homeostasis can occur not only in old age but in several diseases. In addition, new technological challenges and innovations on the use of calcium sensors appear from time to time and open new possibilities to deepen our knowledge in studying calcium concentration outside and inside of the cells or even in cell organelles.

The aim of the present Special Issue is to collect novel data regarding the role of calcium in the functions of cells. We specifically encourage the submission of manuscripts presenting innovative approaches to identify novel strategies to maintain and/or improve cell functions in aging and in diseases.

Dr. Péter Szentesi
Prof. Dr. László Csernoch
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Related Special Issue

Published Papers (2 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

14 pages, 3938 KiB

Open AccessArticle

The Rise in Tubular pH during Hypercalciuria Exacerbates Calcium Stone Formation

by Farai C. Gombedza, Samuel Shin, Jaclyn Sadiua, George B. Stackhouse and Bidhan C. Bandyopadhyay

Int. J. Mol. Sci. 2024, 25(9), 4787; https://doi.org/10.3390/ijms25094787 (registering DOI) - 27 Apr 2024

Viewed by 198

Abstract

In calcium nephrolithiasis (CaNL), most calcium kidney stones are identified as calcium oxalate (CaOx) with variable amounts of calcium phosphate (CaP), where CaP is found as the core component. The nucleation of CaP could be the first step of CaP+CaOx (mixed) stone formation. High urinary supersaturation of CaP due to hypercalciuria and an elevated urine pH have been described as the two main factors in the nucleation of CaP crystals. Our previous in vivo findings (in mice) show that transient receptor potential canonical type 3 (TRPC3)-mediated Ca²⁺ entry triggers a transepithelial Ca²⁺ flux to regulate proximal tubular (PT) luminal [Ca²⁺], and TRPC3-knockout (KO; -/-) mice exhibited moderate hypercalciuria and microcrystal formation at the loop of Henle (LOH). Therefore, we utilized TRPC3 KO mice and exposed them to both hypercalciuric [2% calcium gluconate (CaG) treatment] and alkalineuric conditions [0.08% acetazolamide (ACZ) treatment] to generate a CaNL phenotype. Our results revealed a significant CaP and mixed crystal formation in those treated KO mice (KOT) compared to their WT counterparts (WTT). Importantly, prolonged exposure to CaG and ACZ resulted in a further increase in crystal size for both treated groups (WTT and KOT), but the KOT mice crystal sizes were markedly larger. Moreover, kidney tissue sections of the KOT mice displayed a greater CaP and mixed microcrystal formation than the kidney sections of the WTT group, specifically in the outer and inner medullary and calyceal region; thus, a higher degree of calcifications and mixed calcium lithiasis in the kidneys of the KOT group was displayed. In our effort to find the Ca²⁺ signaling pathophysiology of PT cells, we found that PT cells from both treated groups (WTT and KOT) elicited a larger Ca²⁺ entry compared to the WT counterparts because of significant inhibition by the store-operated Ca²⁺ entry (SOCE) inhibitor, Pyr6. In the presence of both SOCE (Pyr6) and ROCE (receptor-operated Ca²⁺ entry) inhibitors (Pyr10), Ca²⁺ entry by WTT cells was moderately inhibited, suggesting that the Ca²⁺ and pH levels exerted sensitivity changes in response to ROCE and SOCE. An assessment of the gene expression profiles in the PT cells of WTT and KOT mice revealed a safeguarding effect of TRPC3 against detrimental processes (calcification, fibrosis, inflammation, and apoptosis) in the presence of higher pH and hypercalciuric conditions in mice. Together, these findings show that compromise in both the ROCE and SOCE mechanisms in the absence of TRPC3 under hypercalciuric plus higher tubular pH conditions results in higher CaP and mixed crystal formation and that TRPC3 is protective against those adverse effects. Full article

(This article belongs to the Special Issue Calcium Homeostasis of Cells in Health and Disease 2.0)

► Show Figures

Figure 1

12 pages, 2443 KiB

Open AccessArticle

Vaping-Dependent Pulmonary Inflammation Is Ca²⁺ Mediated and Potentially Sex Specific

by Jeffrey G. Shipman, Rob U. Onyenwoke and Vijay Sivaraman

Int. J. Mol. Sci. 2024, 25(3), 1785; https://doi.org/10.3390/ijms25031785 - 01 Feb 2024

Viewed by 931

Abstract

Here we use the SCIREQ InExpose system to simulate a biologically relevant vaping model in mice to investigate the role of calcium signaling in vape-dependent pulmonary disease as well as to investigate if there is a gender-based difference of disease. Male and female mice were vaped with JUUL Menthol (3% nicotine) using the SCIREQ InExpose system for 2 weeks. Additionally, 2-APB, a known calcium signaling inhibitor, was administered as a prophylactic for lung disease and damage caused by vaping. After 2 weeks, mice were exposed to lipopolysaccharide (LPS) to mimic a bacterial infection. Post-infection (24 h), mice were sacrificed, and bronchoalveolar lavage fluid (BALF) and lungs were taken. Vaping primed the lungs for worsened disease burden after microbial challenge (LPS) for both males and females, though females presented increased neutrophilia and inflammatory cytokines post-vape compared to males, which was assessed by flow cytometry, and cytokine and histopathological analysis. This increased inflammatory burden was controlled by calcium signaling inhibition, suggesting that calcium dysregulation may play a role in lung injury caused by vaping in a gender-dependent manner. Full article

(This article belongs to the Special Issue Calcium Homeostasis of Cells in Health and Disease 2.0)

► Show Figures

Journal Menu

Journal Browser

Calcium Homeostasis of Cells in Health and Disease 2.0

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Related Special Issue

Published Papers (2 papers)

Research

Further Information

Guidelines

MDPI Initiatives

Follow MDPI