Microvesicles of osteoblasts modulate bone marrow mesenchymal stem cell‐induced apoptosis to curcumin in myeloid leukemia cells

Abstract

Microvesicles (MVs) derived from bone marrow niche components have an important role in genetic reprogramming and subsequent drugs induce apoptosis in leukemic cells. Here, we have found that undertreatment of curcumin or daunorubicin, the cross‐talk through MVs of KG‐1‐bone marrow mesenchymal stem cells (BMSCs), significantly downregulates the expression of the survival gene osteopontin (OPN), CXCL‐12, IL‐6 (interleukin‐6), STAT‐3, and VCAM‐1 (vascular cell adhesion molecule 1) in treated‐KG‐1 cells as well as exclusively upregulates CXCL‐12 in BMSCs. Drug treated‐cell populations’ MVs of both single cultured osteoblasts (OBs) and cocultured KG‐1 + BMSCs + OBs similarly upregulate survival mediators’ OPN, CXCL‐12, IL‐6, STAT‐3, and VCAM‐1 in treated‐KG‐1 cells. Likewise, isolated MVs from KG‐1 cells or communication between KG‐1, BMSCs, and OBs treated by drugs increase the expression of genes OPN, CXCL‐12, IL‐6, STAT3, and VCAM‐1 by OBs. MVs derived from KG‐1 + BMSCs + OBs reduce drug‐induced apoptosis in KG‐1 cells. This suggests MVs‐mediated information transfer is a procedure whereby OBs could overcome BMSCs‐induced apoptosis in drug‐treated‐KG‐1 cells.

Extracellular Vesicles Derived from Human Bone Marrow Stem Cells Inhibit Acute Lymphoblastic Leukemia Cell Growth by Inhibiting MAPK Pathway via the miR-29b-3p/GDF15 Axis

“…A recent study reported that BMSCs-EVs could enhance Imatin-induced apoptosis in human leukemia cells [7]. In this study, BMSCs-EVs could potentiate ALL cell apoptosis and repress proliferation, which verified the reported latent capacity of BMSCs-EVs to partially induce apoptosis of leukemia cells and to be applied in the supportive treatment of leukemia [27,28]. Similar to the previous studies, our results confirmed that MSCs-EVs had anti-proliferative and pro-apoptotic properties in leukemia cells despite the varied origin of EVs and techniques used [9,29,30].…”

Gadus morhua Eggs Sialoglycoprotein Prevent Estrogen Deficiency-Induced High Bone Turnover by Controlling OPG/RANKL/TRAF6 Pathway and Serum Metabolism

“…Osteoprotegerin (OPG) is secreted out of the cell by osteoblast and antagonizes the osteoclast development induced by RANKL ( 10 ). Mesenchymal stem cells in bone marrow proliferate and differentiate to form osteoblasts ( 13 ). Osteoblasts secrete various osteogenic active substances, regulate extracellular matrix maturation, and promote bone formation.…”