Cellular and molecular events of inflammation induced transdifferentiation (EMT) and regeneration (MET) in mesenteric me
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Inflammation Research
REVIEW
Cellular and molecular events of inflammation induced transdifferentiation (EMT) and regeneration (MET) in mesenteric mesothelial cells Viktória Zsiros1 · Anna L. Kiss1 Received: 29 June 2020 / Revised: 2 September 2020 / Accepted: 3 September 2020 © The Author(s) 2020
Abstract In this review we summarize the cellular and molecular events of inflammation induced epithelial-to-mesenchymal (EMT) and mesothelial-to-macrophage transition (MET) during regeneration. Since the receptor transmits the environmental stimulus, downregulating or upregulating the process on an epigenetic level, the intracellular localization of receptors (signaling organelles: early endosomes or lysosomal degradation: late endosomes) plays a crucial role in the signaling events regulating inflammation and regeneration. Therefore, we focused on the internalization of the receptors as well as the intracellular compartmentalization of signaling molecules during EMT and MET. The review draws the reader’s attention to the plasticity of mesothelial cells and supports the idea that during inflammation an ambient macrophage population might derive from mesothelial cells. Keywords Mesenteric mesothelial cells · Inflammation · Epithelial-to-mesenchymal transition · Mesenchymal-to-epithelial transition · Regeneration
Introduction Mesothelial cells covering the surface of the mesentery are simple squamous cells originating from the embryonic splanchnopleura. Under inflammatory stimuli these cells undergo a series of morphological and biochemical changes during which they lose their epithelial character, and transdifferentiate into mesenchymal cells [1]. They become cuboidal in shape, the volume of the cytoplasm and the number of the cytoplasmic organelles (rough ER, mitochondria, and Golgi vesicles) are dramatically increasing. They lose their polarity, the cell junctions are disassembling by E-cadherin and ß-catenin down-regulation [2, 3], the basement membrane is degrading [4], and the cytoskeleton becomes rearranged. The mesothelial cells start to express mesenchymal markers (N-cadherin, vimentin, α-smooth muscle Responsible Editor: John Di Battista. * Anna L. Kiss [email protected]‑univ.hu 1
Department of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó u. 58, Budapest 1094, Hungary
actin) and become highly mobile cells. Besides expressing mesenchymal markers, epithelial cells acquire the ability to produce extracellular matrix components, inflammatory cytokines, fibrogenic and angiogenic factors [5]. All these morphological and biochemical changes are characteristic of epithelial-to-mesenchymal transition (EMT). EMT is an important, reversible biological process, when polarized epithelial cells undergo a complex proteomic remodeling to assume mesenchymal characteristics [6]. Three types of EMT have been distinguished so far: type I EMT during embryogenesis; type II EMT associated with inflammation, wound healing, tissue regeneration and organ fibrosis and type III occurring during tumorig
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