Abstract
CD34+ stromal cells/telocytes (CD34+SCs/TCs) can have a role as mesenchymal precursor cells. Our objective is to assess whether the myofibroblastic stromal cell response in repair and in desmoplastic reactions in tumors depend on the presence or absence of resident CD34+SCs/TCs in specific regions/layers of an organ and on the location of their possible subpopulations. For this purpose, using conventional and immunohistochemical procedures, we studied specimens of (a) acute cholecystitis, with early repair phenomena (n: 6), (b) surgically resected segments of colon tattooed with India ink during previous endoscopic removal of malignant polyps, with macrophage infiltration and stromal cell reaction (n: 8) and (c) infiltrative adenocarcinomas of colon, with desmoplastic reaction (n: 8). The results demonstrated (a) stromal myofibroblastic reaction during repair and tumor desmoplasia in most regions in which resident CD34+SCs/TCs are present, (b) absence of stromal myofibroblastic reaction during repair in the mucosa of both organs in which resident CD34+SCs/TCs are absent and (c) permanence of CD34+SCs/TCs as such, without myofibroblastic response, in smooth muscle fascicles, nerves, and Meissner and Auerbach plexuses, in which the CD34+SCs/TCs mainly undergo reactive phenomena. Therefore, the development of activated αSMA+ myofibroblasts in these conditions requires the presence of resident CD34+SCs/TCs and depends on their location. In conclusion, the facts support the hypotheses that CD34+SCs/TCs participate in the origin of myofibroblasts during repair and tumor stroma formation, and that there is a heterogeneous population of resident CD34+SCs/TCs with different roles.
Highlights
CD34+ stromal cells are present in the connective tissue of multiple anatomical sites
Depending on the gallbladder layer (Figure 1A), the distribution of CD34+SCs/TCs was as follows: (1) absence in the lamina propria of the mucosa (Figure 1B), (2) presence in variable numbers in the other layers (Table 1), including the fibrovascular connective tissue that separates the muscle bundles of the muscularis propria (Figures 1C,D and insert), the perimuscular subserosal layer of connective tissue (Figure 1D and insert) and the serosa, in which CD34+SCs/TCs are generally arranged in strands parallel to the serosa surface (Figure 1E)
Depending on the intestinal layer, the CD34+SCs/TCs showed the following distribution: (1) Absence in the mucosa (Figure 4A), except in the areas underlying the tubular glands and the muscularis mucosae, where they were present in variable numbers (Figures 4B,C). (2) Presence in variable numbers (Table 1) in (a) the submucosa (Figure 4C), including perivascular niches, the adventitia of the largest vessels, the interstitium, the nerves and the Meissner plexus, (b) the muscularis propria, including the muscle fascicles (Figures 4D–F), nerves and the myenteric plexus (Figure 4G), close to the c-kit+ interstitial cells of Cajal, and (c) the serosa, including perivascular niches, adventitia of larger vessels, interstitium, nerves and adipose tissue
Summary
CD34+ stromal cells are present in the connective tissue of multiple anatomical sites. A new cellular type named telocyte was identified by electron microscopy and described in 2010 (Popescu and Faussone-Pellegrini, 2010; Faussone Pellegrini and Popescu, 2011; Popescu, 2011) This cell type largely corresponds to the CD34+ stromal cells observed in light microscopy. The vascular/perivascular niche (da Silva Meirelles et al, 2006, 2015, 2016; Díaz-Flores et al, 2015a,b; Corrêa Bellagamba et al, 2018) is one of the principal sources of mesenchymal precursor cells that participate in tissue repair Among these precursor cells are CD34+SCs/TCs, which are located around the abluminal surface of the pericytes and of the vascular smooth muscle cells. The CD34-stained vessels show a double-ring appearance (CD34+ endothelium and CD34+SCs/TCs), owing to two concentric circles “sandwiching” the unstained media layer (smooth muscle or pericytic layer) (Pusztaszeri et al, 2006; Lin et al, 2008, 2010; Díaz-Flores et al, 2015a,b)
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