Autophagy in Cell Survival and Growth—2nd Edition

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1141

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Guest Editor
Paul Albrechtsen Research Institute, CancerCare Manitoba, University of Manitoba, Winnipeg, MB, Canada
Interests: autophagy; cell death; cancer; signaling pathway; microbiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is a "self-digestion" process conserved in eukaryotic cells. During autophagy, intracellular materials (cargo), such as dysfunctional organelles, protein aggregates, lipid droplets, and microbial pathogens, are delivered to the lysosome to be degraded. Based on the transportation method, autophagy can be classified into three main types: macroautophagy, which is the most extensively studied; chaperone-mediated autophagy; and microautophagy.

Autophagy plays a critical role in cellular homeostasis and is associated with the progression of various diseases, such as cancer and neurodegenerative disorders. It primarily supports cell survival, whereby autophagic degradation generates small molecules for biosynthesis and energy production. Recent studies have shown that autophagy promotes cell growth, which refers to an increase in cell numbers, and is regulated by cell proliferation and cell survival.

This Special Issue aims to collect original research and review articles on the underlying mechanisms of the autophagy regulation of cell survival and growth in various eukaryotic cells. 

Dr. Yongqiang Chen
Guest Editor

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Keywords

  • autophagy
  • cell survival
  • cell death
  • cell growth
  • proliferation

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15 pages, 2894 KiB  
Article
Bitter Taste Receptor T2R14 and Autophagy Flux in Gingival Epithelial Cells
by Nisha Singh, Ben Ulmer, Manoj Reddy Medapati, Christine Zhang, Robert J. Schroth, Saeid Ghavami and Prashen Chelikani
Cells 2024, 13(6), 531; https://doi.org/10.3390/cells13060531 - 17 Mar 2024
Viewed by 919
Abstract
Macroautophagy (hereafter autophagy) is a lysosomal degradation pathway that functions in nutrient recycling and as a mechanism of innate immunity. Previously, we reported a novel host–bacteria interaction between cariogenic S. mutans and bitter taste receptor (T2R14) in gingival epithelial cells (GECs), leading to [...] Read more.
Macroautophagy (hereafter autophagy) is a lysosomal degradation pathway that functions in nutrient recycling and as a mechanism of innate immunity. Previously, we reported a novel host–bacteria interaction between cariogenic S. mutans and bitter taste receptor (T2R14) in gingival epithelial cells (GECs), leading to an innate immune response. Further, S. mutans might be using the host immune system to inhibit other Gram-positive bacteria, such as S. aureus. To determine whether these bacteria exploit the autophagic machinery of GEC, it is first necessary to evaluate the role of T2R14 in modulating autophagic flux. So far, the role of T2R14 in the regulation of autophagy is not well characterized. Therefore, in this study, for the first time, we report that T2R14 downregulates autophagy flux in GECs, and T2R14 knockout increases acidic vacuoles. However, the treatments of GEC WT with a T2R14 agonist and antagonist did not lead to a significant change in acidic vacuole formation. Transmission electron microscopy morphometric results also suggested an increased number of autophagic vesicles in T2R14-knockout GEC. Further, our results suggest that S. mutans competence stimulating peptide CSP-1 showed robust intracellular calcium release and this effect is both T2R14- and autophagy protein 7-dependent. In this study, we provide the first evidence that T2R14 modulates autophagy flux in GEC. The results of the current study could help in identifying the impact of T2R in regulation of the immuno-microenvironment of GEC and subsequently oral health. Full article
(This article belongs to the Special Issue Autophagy in Cell Survival and Growth—2nd Edition)
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