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Dear Colleagues,

Cell motility and migration are fundamental in many physiological processes, such as embryogenesis, angiogenesis, wound healing, immune response, and several disease-related processes. The scientific interest in this topic has grown considerably in recent years, spanning a wide range of research fields. Cell movement represents a fundamental cellular function that integrates several cellular processes, including cell adhesion, cell signaling, cytoskeleton activity, and cell volume changes. It occurs thanks to multiple dynamic processes and is modulated by a wide range of biochemical and biophysical signals, either extracellular or intracellular. The research carried out in this field has allowed us to understand many aspects of cell movement; however, because of the inherent complexity of this function, several unanswered questions still need to be addressed.

This Special Issue of IJMS aims to cover more recent insights in the research on this field and on the molecular and cellular mechanisms and properties of this fundamental function, particularly the signaling networks underlying the motility and migration of individual cells as well as collective migrations.

Dr. Maria Giulia Lionetto
Guest Editor

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Keywords

cell motility
cell migration
cytoskeleton
adhesion
signaling
imaging
microscopy
molecular biology

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Research

13 pages, 1802 KiB

Open AccessArticle

Helicobacter pylori Eradication Reverses DNA Damage Response Pathway but Not Senescence in Human Gastric Epithelium

by Polyxeni Kalisperati, Evangelia Spanou, Ioannis S. Pateras, Konstantinos Evangelou, Irene Thymara, Penelope Korkolopoulou, Athanassios Kotsinas, Panayiotis G. Vlachoyiannopoulos, Athanasios G. Tzioufas, Christos Kanellopoulos, Vassilis G. Gorgoulis and Stavros Sougioultzis

Int. J. Mol. Sci. 2024, 25(7), 3888; https://doi.org/10.3390/ijms25073888 - 31 Mar 2024

Viewed by 691

Abstract

Helicobacter pylori (H. pylori) infection induces DNA Double-Strand Breaks (DSBs) and consequently activates the DNA Damage Response pathway (DDR) and senescence in gastric epithelium. We studied DDR activation and senescence before and after the eradication of the pathogen. Gastric antral and corpus biopsies of 61 patients with H. pylori infection, prior to and after eradication treatment, were analyzed by means of immunohistochemistry/immunofluorescence for DDR marker (γH2AΧ, phosporylated ataxia telangiectasia-mutated (pATM), p53-binding protein (53BP1) and p53) expression. Samples were also evaluated for Ki67 (proliferation index), cleaved caspase-3 (apoptotic index) and GL13 staining (cellular senescence). Ten H. pylori (−) dyspeptic patients served as controls. All patients were re-endoscoped in 72-1361 days (mean value 434 days), and tissue samples were processed in the same manner. The eradication of the microorganism, in human gastric mucosa, downregulates γH2AΧ expression in both the antrum and corpus (p = 0.00019 and p = 0.00081 respectively). The expression of pATM, p53 and 53BP1 is also reduced after eradication. Proliferation and apoptotic indices were reduced, albeit not significantly, after pathogen clearance. Moreover, cellular senescence is increased in H. pylori-infected mucosa and remains unaffected after eradication. Interestingly, senescence was statistically increased in areas of intestinal metaplasia (IM) compared with adjacent non-metaplastic mucosa (p < 0.001). In conclusion, H. pylori infection triggers DSBs, DDR and senescence in the gastric epithelium. Pathogen eradication reverses the DDR activation but not senescence. Increased senescent cells may favor IM persistence, thus potentially contributing to gastric carcinogenesis. Full article

(This article belongs to the Special Issue Cell Motility and Its Underlying Cellular and Molecular Mechanisms)

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