Changes Induced by Inflammatory-Activated Immune Cell Microenvironment in the Paracrine Profile of MSC

Горностаева, А. Н.; Buravkova, Ludmila

doi:10.1007/s10517-023-05745-x

Cited by 1 publication

(1 citation statement)

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“…The downregulation of TGFα gene expression in cMSCs of IH at T0 and its upregulation after propranolol therapy are not consensual with their proangiogenic activity. However, very recently, it has been reported both an inflammatory environment in IH with multiple lesions [40] and a role of inflammation in defining the paracrine profile of MSCs, possibly altering the expression of angiogenic cytokines such as TGFα, in favor of a major reparative capacity [41]. In addition, propranolol and its isomers have been described in in vitro studies to promote the internalization of the MSC membrane receptors binding either EGF or TGFα; a similar mechanism may alter in vivo the TGFα gene expression [42].…”

Section: Discussionmentioning

confidence: 99%

Circulating Mesenchymal Stromal Cells in Patients with Infantile Hemangioma: Evaluation of Their Functional Capacity and Gene Expression Profile

Abbà,

Croce,

Valsecchi

et al. 2024

Cells

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We previously published that in patients with infantile hemangioma (IH) at the onset (T0) colony forming unit-fibroblasts (CFU-Fs) are present in in vitro cultures from PB. Herein, we characterize these CFU-Fs and investigate their potential role in IH pathogenesis, before and after propranolol therapy. The CFU-F phenotype (by flow cytometry), their differentiation capacity and ability to support angiogenesis (by in vitro cultures) and their gene expression (by RT-PCR) were evaluated. We found that CFU-Fs are actual circulating MSCs (cMSCs). In patients at T0, cMSCs had reduced adipogenic potential, supported the formation of tube-like structures in vitro and showed either inflammatory (IL1β and ESM1) or angiogenic (F3) gene expression higher than that of cMSCs from CTRLs. In patients receiving one-year propranolol therapy, the cMSC differentiation in adipocytes improved, while their support in in vitro tube-like formation was lost; no difference was found between patient and CTRL cMSC gene expressions. In conclusion, in patients with IH at T0 the cMSC reduced adipogenic potential, their support in angiogenic activity and the inflammatory/angiogenic gene expression may fuel the tumor growth. One-year propranolol therapy modifies this picture, suggesting cMSCs as one of the drug targets.

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Section: Discussionmentioning

confidence: 99%