Telocytes/CD34+ Stromal Cells in Pathologically Affected White Adipose Tissue.

We studied telocytes/CD34+ stromal cells (TCs/CD34+SCs) in pathologically affected white adipose tissue after briefly examining them in normal fat. To this aim, we reviewed pathological processes, including original contributions, in which TCs/CD34+SCs are conserved, increased, and lost, or acquire a specific arrangement. The pathologic processes in which TCs/CD34+SCs are studied in adipose tissue include inflammation and repair through granulation tissue, iatrogenic insulin-amyloid type amyloidosis, non-adipose tissue components (nerve fascicles and fibres in neuromas and hyperplastic neurogenic processes) and tumours (signet ring carcinoma with Krukenberg tumour and colon carcinoma) growing in adipose tissue, adipose tissue tumours (spindle cell lipoma, dendritic fibromyxolipoma, pleomorphic lipoma, infiltrating angiolipoma of skeletal muscle and elastofibrolipoma), lipomatous hypertrophy of the interatrial septum, nevus lipomatosus cutaneous superficialis of Hoffman-Zurhelle and irradiated adipose tissue of the perirectal and thymic regions. Two highly interesting issues emerged: (1) whether the loss of CD34 expression in TCs/CD34+SCs is by changes in marker expression or the disappearance of these cells (the findings suggest the first possibility) and (2) whether in some invasive and metastatic malignant tumours, TCs/CD34+SCs that completely surround neoplastic cells act as nurse and/or isolating cells. Further studies are required on adipose tissue TCs/CD34+SCs, mainly in lipomatosis and obesity.

Presence/Absence and Specific Location of Resident CD34+ Stromal Cells/Telocytes Condition Stromal Cell Development in Repair and Tumors.

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.