Objective: CD133 may be the most specific marker of endothelial progenitor cells (EPCs), which are thought to be largely confined to the bone marrow milieu. This study reports on the phenotypic characterization and functional analysis of human CD133+ cells and their generation from cells in the peripheral circulation.
Methods: Adult human CD133+ and CD133- cells were isolated from peripheral blood mononuclear cells, and the generation of CD133+ cells in culture was attempted using different culture combinations. The phenotypic, migratory, adhesive, and angiogenic properties of the native and generated populations were investigated.
Results: In adherent and in suspension culture systems, CD133+ cells also expressing CD34 and VEGFR-2 were successfully derived from a previously CD133- population. The migratory potential of CD133+ cells was enhanced by the presence of the CD133- cells. Also, the CD133+ cells derived from the CD133- cells demonstrated improved adhesion to extracellular matrix and endothelial monolayer substrates, and their contribution to in vitro angiogenesis was enhanced compared to freshly isolated CD133+ cells.
Conclusions: These results demonstrate a source of blood CD133+ cells other than direct mobilization from the bone marrow. Cellular interaction was observed between fractions, with CD133+ cells showing better in vitro function in the presence of CD133- cells. These findings provide a novel source for CD133+ cells and a rationale for the investigation of angiogenic cell recruitment or delivery strategies involving more than one cell type at ischemic sites.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.cardiores.2006.01.014 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The endonuclease activity of MCPIP1 controls the neoplastic transformation of epithelial cells via the c-Met/CD44 axis.
Cell Commun Signal
January 2025
Department of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
The RNase activity of MCPIP1 is essential for regulating cellular homeostasis, proliferation, and tumorigenesis. Our study elucidates the effects of downregulation of MCPIP1 expression and an RNase-inactivating mutation (D141N) on normal epithelial kidney cells, indicating that MCPIP1 expression is a key factor that suppresses neoplastic transformation. We observed that either expression downregulation or mutation of MCPIP1 significantly increased its clonogenicity and altered the expression of cancer stem cell (CSC) markers and factors involved in epithelial-to-mesenchymal transition (EMT).
View Article and Find Full Text PDFISG15-LFA1 interactions in latent HIV clearance: mechanistic implications in designing antiviral therapies.
Front Cell Dev Biol
December 2024
Biomedical Research Institute of Southern California, Oceanside, CA, United States.
Interferon types-I/II (IFN-αβ/γ) secretions are well-established antiviral host defenses. The human immunodeficiency virus (HIV) particles are known to prevail following targeted cellular interferon secretion. CD4 T-lymphocytes are the primary receptor targets for HIV entry, but the virus has been observed to hide (be latent) successfully in these cells through an alternate entry route via interactions with LFA1.
View Article and Find Full Text PDFHBx Facilitates Drug Resistance in Hepatocellular Carcinoma via CD133-regulated Self-renewal of Liver Cancer Stem Cells.
J Clin Transl Hepatol
January 2025
Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Background And Aims: Hepatitis B virus (HBV) infection contributes to hepatocellular carcinoma (HCC) tumorigenesis, drug resistance, and recurrence, although the underlying molecular mechanisms remain unclear. Recent studies suggest that HBV infection may be associated with liver cancer stem cells (LCSCs), but the exact mechanisms are yet to be resolved. In this study, we aimed to analyze the role of HBV infection in regulating the stemness of HCCs, which is closely linked to drug resistance.
View Article and Find Full Text PDFHuman parietal epithelial cells as Trojan horses in albumin overload.
Sci Rep
January 2025
Kidney Histomorphology and Molecular Biology Laboratory, Nephrology Unit, Department of Medicine - DIMED, University of Padua, Via Giustiniani 2, 35128, Padua, Italy.
Parietal Epithelial Cells (PECs) activation and proliferation are common to several distinct forms of glomerulopathies. Due to several stimuli, PECs can change to a progenitor (CD24 and CD133/2) or a pro-sclerotic (CD44) phenotype. In addition, PECs, which are constantly exposed to filtered albumin, are known to be involved in albumin internalization, but how this mechanism occurs is unknown.
View Article and Find Full Text PDFFOXA1 activates NOLC1 transcription through NOTCH pathway to promote cell stemness in lung adenocarcinoma.
Kaohsiung J Med Sci
January 2025
Department of Respiratory and Critical Care Medicine of Affiliated Yueqing Hospital, Wenzhou Medical University, Yueqing, China.
Tumor cell stemness plays a pivotal role in generating functional heterogeneity within tumors and is implicated in essential processes such as drug resistance, metastasis, and cell proliferation. Therefore, creating novel tumor diagnostic techniques and therapeutic plans requires a knowledge of the possible processes that preserve the stem cell-like qualities of cancers. Bioinformatics analysis of NOLC1 expression in lung adenocarcinoma (LUAD) and prediction of its upstream transcription factors and their binding sites were completed.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!