scholarly journals Single-cell RNA-Sequencing uncovers transcriptional states and fate decisions in haematopoiesis

2017 ◽  
Author(s):  
Emmanouil I. Athanasiadis ◽  
Jan G. Botthof ◽  
Helena Andres ◽  
Lauren Ferreira ◽  
Pietro Lio ◽  
...  
Keyword(s):  
Cell Surface ◽  
Specific Cell ◽  
Surface Markers ◽  
Evolutionary Analysis ◽  
Cell Surface Markers ◽  
Lineage Differentiation ◽  
Lineage Tree ◽  
Stem And Progenitor Cells ◽  
A Cell ◽  
Fate Decision

ABSTRACTThe success of marker-based approaches for dissecting haematopoiesis in mouse and human is reliant on the presence of well-defined cell-surface markers specific for diverse progenitor populations. An inherent problem with this approach is that the presence of specific cell surface markers does not directly reflect the transcriptional state of a cell. Here we used a marker-free approach to computationally reconstruct the blood lineage tree in zebrafish and order cells along their differentiation trajectory, based on their global transcriptional differences. Within the population of transcriptionally similar stem and progenitor cells our analysis revealed considerable cell-to-cell differences in their probability to transition to another, committed state. Once fate decision was executed, the suppression of transcription of ribosomal genes and up-regulation of lineage specific factors coordinately controlled lineage differentiation. Evolutionary analysis further demonstrated that this haematopoietic program was highly conserved between zebrafish and higher vertebrates.

Towards an indirect screening technique facilitating detection of cellular populations bearing specific cell surface markers

2010 ◽  
Vol 26 (6) ◽  
pp. 1544-1550
Author(s):  
Sandeep K. Arora ◽  
Rohit Sharma ◽  
Gagandeep Kaur ◽  
Preeti Bhoria ◽  
Maryada Sharma ◽  
...  
Keyword(s):  
Cell Surface ◽  
Specific Cell ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Screening Technique ◽  
Specific Cell Surface

Metabolic glycan labeling-assisted discovery of cell-surface markers for primary neural stem and progenitor cells

2018 ◽  
Vol 54 (43) ◽  
pp. 5486-5489
Author(s):  
Qing-Ran Bai ◽  
Lu Dong ◽  
Yi Hao ◽  
Xing Chen ◽  
Qin Shen
Keyword(s):  
Mass Spectrometry ◽  
Stem Cell ◽  
Cell Surface ◽  
Progenitor Cells ◽  
Neural Stem Cell ◽  
Surface Markers ◽  
Metabolic Labeling ◽  
Cell Surface Markers ◽  
Stem And Progenitor Cells

Metabolic labeling with azidosugars in a neural stem cell (NSC)-enriched endothelial coculture followed by mass-spectrometry profiling identifies sialoglycoproteins on NSCs.

P5369Alpha-V integrin regulates the contribution of PW1+ cells to cardiac fibrosis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Bouvet ◽  
O Claude ◽  
M Roux ◽  
N Mougenot ◽  
V Duval ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Surface Proteins ◽  
Specific Cell ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Proteomic Profiling ◽  
The Matrix ◽  
Almost All

Abstract Background Activated cardiac fibroblasts produce extracellular matrix proteins that accumulate during cardiac fibrosis. We have recently shown that PW1 is expressed in a subset of cardiac stromal cells and that cardiac PW1+ cells represent a cellular source of fibroblasts in the ischemic hearts. Purpose We aimed to further identify new cell surface markers expressed by cardiac PW1+ cells and to investigate their role in the fibrogenic behavior of these cells. Methods and results We first performed transcriptomic and proteomic profiling of FACS-isolated cardiac PW1+ from normal and ischemic hearts. RNA-sequencing output files were processed with bioinformatics algorithms to identify 378 specific cell-surface markers for cardiac PW1+ cells. By comparing these candidates with the proteomic profile, we then cross-identified 9 cell surface proteins primarily involved in cell motility, adhesion to the matrix, inflammatory response and response to wounding. One of these candidates (i.e., aV-integrin or CD51) was expressed in almost all cardiac PW1+ cells (93±1%), and was predominantly found in cells expressing PW1 in the myocardium. Cardiac PW1+ cells showed a predominant expression of aVβ1 complex which is known to mediate fibrosis through TGF-beta activation in a number of tissues. The transfer of isolated cardiac PW1+CD51+ cells into ischemic hearts was associated with fibrosis development. We further demonstrated that inhibition of aV-integrin in cardiac PW1+ cells reduces their profibrotic gene expression profile and their ability to differentiate into fibroblasts. Lastly, a pharmacological blockade of aV-integrin improved cardiac function and animal survival following myocardial infarction coupled with a reduced infarct size and fibrotic lesion. Conclusions These data identify a targetable pathway that regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inhibition of aV-integrin leads to reduced pathological outcomes following cardiac ischemia. Acknowledgement/Funding Fondation Leducq (grant 13CVD01, CardioStemNet project), Fédération Française de Cardiologie and Era-CVD (ANR-16-ECVD-0011-03, Clarify project)

scholarly journals Hypothesis: differentiation of the human lymphoid system based on cell surface markers

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 871-880
Author(s):  
S Davis
Keyword(s):  
B Cells ◽  
Cell Surface ◽  
Developmental Stages ◽  
Human Lymphocytes ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Characteristic Surface ◽  
T And B Cells ◽  
Lymphoproliferative Diseases ◽  
A Cell

Human lymphocytes can be separated into distinct populations based upon receptors on their cell surface. Thymus-derived (T-cell) lymphocytes can be identified by their ability to form rosetts with sheep erythrocytes (SRBC); bone marrow-derived (B-cell) lymphocytes bear characteristic surface markers for immunoglobulin, complement, and the Fc portion of IgG. Recently, populations of lymphocytes having either multiple markers or no detectable markers (null cells) have been observed. Based on studies of cell surface markers, a scheme is proposed that expands the known differentiation of the lymphod cell to include subpopulations which represent developmental stages. It is suggested that lymphocyte maturation involves alloantigenic changes in a circulating stem cell-drived nill cell, leading to a cell bearing markers for both T- and B-cells. It is from this latter cell that the classic T- and B-cells ultimately arise. Maturational defects which may explain the origin of primary lymphoproliferative diseases are discussed.

scholarly journals Systemic surfaceome profiling identifies target antigens for immune-based therapy in subtypes of advanced prostate cancer

2018 ◽  
Vol 115 (19) ◽  
pp. E4473-E4482 ◽  
Author(s):  
John K. Lee ◽  
Nathanael J. Bangayan ◽  
Timothy Chai ◽  
Bryan A. Smith ◽  
Tiffany E. Pariva ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Surface ◽  
Cell Lines ◽  
Treatment Resistance ◽  
Specific Cell ◽  
Surface Markers ◽  
Mrna Levels ◽  
Cell Surface Markers ◽  
Cell Surface Antigens ◽  
Cancer Subtypes

Prostate cancer is a heterogeneous disease composed of divergent molecular and histologic subtypes, including prostate adenocarcinoma (PrAd) and neuroendocrine prostate cancer (NEPC). While PrAd is the major histology in prostate cancer, NEPC can evolve from PrAd as a mechanism of treatment resistance that involves a transition from an epithelial to a neurosecretory cancer phenotype. Cell surface markers are often associated with specific cell lineages and differentiation states in normal development and cancer. Here, we show that PrAd and NEPC can be broadly discriminated by cell-surface profiles based on the analysis of prostate cancer gene expression datasets. To overcome a dependence on predictions of human cell-surface genes and an assumed correlation between mRNA levels and protein expression, we integrated transcriptomic and cell-surface proteomic data generated from a panel of prostate cancer cell lines to nominate cell-surface markers associated with these cancer subtypes. FXYD3 and CEACAM5 were validated as cell-surface antigens enriched in PrAd and NEPC, respectively. Given the lack of effective treatments for NEPC, CEACAM5 appeared to be a promising target for cell-based immunotherapy. As a proof of concept, engineered chimeric antigen receptor T cells targeting CEACAM5 induced antigen-specific cytotoxicity in NEPC cell lines. Our findings demonstrate that the surfaceomes of PrAd and NEPC reflect unique cancer differentiation states and broadly represent vulnerabilities amenable to therapeutic targeting.

scholarly journals Hypothesis: differentiation of the human lymphoid system based on cell surface markers

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 871-880 ◽  
Author(s):  
S Davis
Keyword(s):  
B Cells ◽  
Cell Surface ◽  
Developmental Stages ◽  
Human Lymphocytes ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Characteristic Surface ◽  
T And B Cells ◽  
Lymphoproliferative Diseases ◽  
A Cell

Abstract Human lymphocytes can be separated into distinct populations based upon receptors on their cell surface. Thymus-derived (T-cell) lymphocytes can be identified by their ability to form rosetts with sheep erythrocytes (SRBC); bone marrow-derived (B-cell) lymphocytes bear characteristic surface markers for immunoglobulin, complement, and the Fc portion of IgG. Recently, populations of lymphocytes having either multiple markers or no detectable markers (null cells) have been observed. Based on studies of cell surface markers, a scheme is proposed that expands the known differentiation of the lymphod cell to include subpopulations which represent developmental stages. It is suggested that lymphocyte maturation involves alloantigenic changes in a circulating stem cell-drived nill cell, leading to a cell bearing markers for both T- and B-cells. It is from this latter cell that the classic T- and B-cells ultimately arise. Maturational defects which may explain the origin of primary lymphoproliferative diseases are discussed.

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