scholarly journals Cell-cell interaction between vocal fold fibroblasts and bone marrow mesenchymal stromal cells in three-dimensional hyaluronan hydrogel

2013 ◽  
Vol 10 (5) ◽  
pp. 437-446 ◽  
Author(s):  
Xia Chen ◽  
Susan L. Thibeault
Keyword(s):  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Vocal Fold ◽  
Three Dimensional ◽  
Cell Interaction ◽  
Cell Cell

scholarly journals Chondrogenic differentiation of human bone marrow‐derived mesenchymal stromal cells in a three‐dimensional environment

2019 ◽  
Vol 235 (4) ◽  
pp. 3497-3507
Author(s):  
Eve Salonius ◽  
Leena Kontturi ◽  
Anita Laitinen ◽  
Anne‐Marie Haaparanta ◽  
Matti Korhonen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Chondrogenic Differentiation ◽  
Three Dimensional ◽  
Human Bone ◽  
Human Bone Marrow

Targeting mesenchymal stromal cells plasticity to reroute acute myeloid leukemia course

Blood ◽  
2021 ◽  
Author(s):  
Giulia Borella ◽  
Ambra Da Ros ◽  
Giulia Borile ◽  
Elena Porcù ◽  
Claudia Tregnago ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Myeloid Leukemia ◽  
Synergistic Effects ◽  
Three Dimensional ◽  
Cell Interaction ◽  
Acute Myeloid

Bone marrow (BM) microenvironment contributes to the regulation of normal hematopoiesis through a finely tuned balance of self-renewal and differentiation processes, cell-cell interaction and secretion of cytokines that during leukemogenesis are altered and favor tumor cell growth. In pediatric acute myeloid leukemia (AML), chemotherapy is the standard of care, but still >30% of patients relapse. The need to accelerate the evaluation of innovative medicines prompted us to investigate the mesenchymal stromal cells (MSCs) role in the leukemic niche to define its contribution to the mechanisms of leukemia escape. We generated humanized three-dimensional (3D) niche with AML cells and MSCs derived from either patients (AML-MSCs) or healthy donors. We observed that AML cells establish physical connections with MSCs, mediating a reprogrammed transcriptome inducing aberrant cell proliferation and differentiation, and severely compromising their immunomodulatory capability. We confirmed that AML cells modulate h-MSCs transcriptional profile promoting functions similar to the AML-MSCs when co-cultured in vitro, thus facilitating leukemia progression. Conversely, MSCs derived from BM of patients at time of disease remission showed recovered healthy features, at transcriptional and functional levels, including the secretome. We proved that AML blasts alter MSCs activities in the BM niche, favoring disease development and progression. We discovered that a novel AML-MSCs selective CaV1.2 channel blocker drug, Lercanidipine, is able to impair leukemia progression in 3D niche both in vitro and when implanted in vivo, if used in combination with chemotherapy, supporting the hypothesis that synergistic effects can be obtained by dual targeting approaches.

N-Cadherin and Cadherin-11 Play Vital Roles in the Cell-Cell Contact between Hematopoietic Progenitor Cells and Mesenchymal Stromal Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1406-1406
Author(s):  
Wolfgang Wagner ◽  
Frederik Wein ◽  
Anke Diehlmann ◽  
Rainer Saffrich ◽  
Patrick Wuchter ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Cell Interaction ◽  
Hematopoietic Progenitor Cells ◽  
Feeder Layer ◽  
Primitive Function ◽  
Hematopoietic Progenitor ◽  
Cd34 Cells ◽  
Direct Cell ◽  
Cell Cell

Abstract Self renewal and differentiation of hematopoietic progenitor cells (HPC) are regulated by the microenvironment of the bone marrow. As an in vitro model system, mesenchymal stromal cells (MSC) provide a supportive cellular microenvironment for maintaining primitive function of HPC. It has been postulated that direct cell-cell interaction is crucial for maintenance of “stemness”. Human HPC were co-cultured with MSC from human bone marrow and subsequently separated into an adherent and a non-adherent fraction. HPC subsets with higher self-renewing capacity demonstrated significantly higher adhesion to MSC (CD34+vs. CD34−, CD34+/CD38−vs. CD34+/CD38+, slow dividing fraction vs. fast dividing fraction). Long-term culture-initiating cell (LTC-IC) frequency was higher in the adherent fraction than in the non-adherent fraction of CD34+ cells. Microarray analysis (Affymetrix, U133_Plus_2.0) revealed that differentially expressed genes coding for adhesion proteins were highly up-regulated in the adherent fraction of CD34+ cells. These genes included VCAM1, connexin 43 and cadherin-11. Furthermore, we have compared the supportive potential of different feeder layer preparations. Human MSC were isolated from bone marrow (BM), from adipose tissue (AT) and umbilical cord blood (CB). The ability to maintain LTC-IC and a primitive CD34+CD38− immunophenotype was significantly higher for MSC derived from BM and CB compared to those from AT. These results were in line with higher adhesion of HPC to BM-MSC and CB-MSC in comparison to AT-MSC. Analysis of the cytokine production of MSC preparations by antibody arrays, ELISA and by a cytometric bead array showed that albeit there were significant differences in the chemokine secretion profiles of the aforementioned MSC preparations, there was no relationship to their potentials in maintaining primitive function of HPC. Global gene expression profiles of MSC preparations showed that adhesion proteins including N-cadherin, cadherin-11, VCAM1, NCAM1 and integrins were highly expressed in MSC preparations derived from BM and CB. Western blot analysis confirmed higher protein expression of N-cadherin and cadherin-11 in BM-MSC compared to AT-MSC and CB-MSC. Fluorescent microscopic analysis revealed that N-cadherin is located at the cell-cell contacts between HPC and MSC. Expression of N-cadherin or cadherin-11 was efficiently knocked down in MSC feeder layer using siRNA. This effect was verified by Western blot analysis and it lasted for up to seven days. Adhesion of HPC was significantly reduced on MSC that have been treated by siRNAs for N-cadherin and cadherin-11 whereas siRNA for MAPK did not affect cell-cell interaction. Similarly, a blocking functional antibody for N-cadherin reduced significantly the adhesion of HPC to MSC. MSC provide a microenvironment which supports the maintenance of primitive function of HPC. Our results indicated that direct cell-cell interaction mediated by N-cadherin and cadherin-11 plays a central role in this interaction of HPC with their cellular microenvironment.

scholarly journals Direct cell-cell interaction of cardiomyocytes is key for bone marrow stromal cells to go into cardiac lineage in vitro

2003 ◽  
Vol 125 (6) ◽  
pp. 1470-1479 ◽  
Author(s):  
Shinya Fukuhara ◽  
Shinji Tomita ◽  
Seiji Yamashiro ◽  
Takayuki Morisaki ◽  
Chikao Yutani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Cell Interaction ◽  
Marrow Stromal Cells ◽  
Direct Cell ◽  
Cardiac Lineage ◽  
Cell Cell
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