Hematopoietic Stem Cell Antigen CD34: Role in Adhesion or Homing

Gangenahalli, Gurudutta; Singh, Vimal Kishor; Verma, Yogesh Kumar; Gupta, Pallavi; Sharma, Rakesh Kumar; Chandra, Ramesh; Luthra, Pratibha Mehta

doi:10.1089/scd.2006.15.305

Cited by 74 publications

(50 citation statements)

References 63 publications

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“…They were also positive for surface markers such as CD13, CD44, CD59, CD73, CD90, CD105 and CD166 [Gronthos et al, 2001;Lee et al, 2004;Wagner et al, 2005;Dominici et al, 2006]. CD34, a haematopoietic marker described as a negative marker for MSCs [Dominici et al, 2006], was not expressed in bone marrow-derived MSCs, which is in keeping with the results obtained by other groups [Gangenahalli et al, 2006]. In adipose tissue-derived MSCs at P1, this marker was expressed in up to 15% of cells ( fig.…”

Section: Discussionsupporting

confidence: 87%

Differences in Surface Marker Expression and Chondrogenic Potential among Various Tissue-Derived Mesenchymal Cells from Elderly Patients with Osteoarthritis

Alegre-Aguarón

Desportes

García-Álvarez

et al. 2012

Cells Tissues Organs

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Mesenchymal stem cells (MSCs) are self-renewing, multipotent cells that could potentially be used to repair injured cartilage in diseases such as osteoarthritis (OA). In this study we used bone marrow, adipose tissue from articular and subcutaneous locations, and synovial fluid samples from 18 patients with knee OA to find a suitable alternative source for the isolation of MSCs with high chondrogenic potential. MSCs from all tissues analysed had a fibroblastic morphology, but their rates of proliferation varied. Subcutaneous fat-derived MSCs proliferated faster than bone marrow- and Hoffa’s fat pad-derived MSCs, while synovial fluid-derived MSCs grew more slowly. CD36 and CD54 expression was similar across all groups of MSCs with several minor differences. High expression of these surface markers in subcutaneous fat-derived MSCs was correlated with poor differentiation into hyaline cartilage. Synovial fluid-derived MSCs presented a relatively small chondrogenic differentiation capacity while Hoffa’s fat pad-derived MSCs had strong chondrogenic potential. In conclusion, MSCs from elderly patients with OA may still display significant chondrogenic potential, depending on their origin.

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Section: Discussionsupporting

confidence: 87%

Differences in Surface Marker Expression and Chondrogenic Potential among Various Tissue-Derived Mesenchymal Cells from Elderly Patients with Osteoarthritis

Alegre-Aguarón

Desportes

García-Álvarez

et al. 2012

Cells Tissues Organs

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“…The vast majority of studies on CD34 have focused on its presence in the hematopoietic system (for review, see Refs. 15,16,21,23), where this antigen is known to mark nonquiescent cells involved in migration or proliferation, but is absent in terminally differentiated lineages (8,19). Only a handful of studies have looked at vascular expression of CD34, where it has been reported to be widely expressed on the endothelium of blood vessels in normal human and mouse adult (3,14,18,24,37) and fetal (14,50,51) tissues, as well as on lymphatic endothelium in humans (13,41).…”

Section: Discussionmentioning

confidence: 99%

Immunotargeting and cloning of two CD34 variants exhibiting restricted expression in adult rat endothelia in vivo

Testa¹,

Chrastina²,

Oh³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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ping protein expression of endothelial cells (EC) in vivo is fundamental to understanding cellular function and may yield new tissueselective targets. We have developed a monoclonal antibody, MAb J120, to a protein expressed primarily in rat lung and heart endothelium. The antigen was identified as CD34, a marker of hematopoietic stem cells and global marker of endothelial cells in human and mouse tissues. PCR-based cloning identified two CD34 variant proteins, full length and truncated, both of which are expressed on luminal endothelial cell plasma membranes (P) isolated from lung. Truncated CD34 predominated in heart P, and neither variant was detected in P from kidney or liver. CD34 in lung was readily accessible to 125 I-J120 inoculated intravenously, and immunohistochemistry showed strong CD34 expression in lung EC. Few microvessels stained in heart and kidney, and no CD34 was detected in vessels of other organs or in lymphatics. We present herein the first complete sequence of a rat CD34 variant and show for the first time that the encoded truncated variant is endogenously expressed on EC in vivo. We also demonstrate that CD34 expression in rat EC, unlike mouse and human, is restricted in its distribution enabling quite specific lung targeting in vivo.immunohistochemistry; immunofluorescence; PCR; SPECT imaging; biodistribution THE COHORT OF PROTEINS EXPRESSED in each particular cell type helps define the cell's function. The molecular fingerprint exhibited by different cells and tissues can provide insights into protein function within a given phenotypic setting. In vitro protein expression, even in cells freshly isolated from tissues and/or grown in culture, can vary considerably from in vivo expression under native conditions found in tissues. Creation of a well-defined molecular atlas is crucial to efforts to identify cell type-specific markers, including disease biomarkers, to use as diagnostic tools and as specific targets for treatment.The proteomic signature of blood vessels, and especially endothelial cells (EC), has gained a great deal of attention in the search for specific vascular targets as a means of delivering drugs, nanomedicines, and imaging agents to blood vessels (11,25,42). Specific delivery of these agents, however, relies on identification of unique targets whose expression is restricted to the desired tissue. While the majority of studies have focused on tumor vessels (for a review see Ref. 6), there is also a need to identify and characterize molecules expressed on normal endothelia, to find reliable endothelial cell markers and to develop good, specific antibodies with which to detect these proteins. While most studies rely on antibodies to proteins such as CD31 and CD34 to detect endothelial cells in vivo and in vitro, not all have been fully characterized in rodent tissues.Accurately defining the endogenous expression of a given protein is critical to understanding the function of a given protein in vivo. We have used a silica nanoparticle-coating method to isolate the luminal p...

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“…Another study showed that only 5.5 ± 2.3% (mean ± SD) of CD34+ cells homed to the myocardium after intracoronary injection in 6 patients [41]. Although its precise structure and function remain poorly understood [42], these data suggest that CD34 might be involved in the migration of stem cells. Specific selection of this CD34+ cell type might turn out to be beneficial for stem cell therapy [43].…”

Section: Stem Cell Therapymentioning

confidence: 99%

“…Specific selection of this CD34+ cell type might turn out to be beneficial for stem cell therapy [43]. Some have even suggested manipulating CD34 or its interactions to enhance therapy efficiency [42]. …”

Section: Stem Cell Therapymentioning

confidence: 99%

Stem Cell Therapy for Myocardial Infarction: Are We Missing Time?

Horst

2010

Cardiology

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The success of stem cell therapy in myocardial infarction (MI) is modest, and for stem cell therapy to be clinically effective fine-tuning in regard to timing, dosing, and the route of administration is required. Experimental studies suggest the existence of a temporal window of opportunity bound by the acute inflammatory response on one hand and by scar formation on the other. In the meantime, microenvironmental factors must favor stem cell homing, survival, differentiation, and integration for stem cell therapy to be effective. Clinical data on the optimal timing of treatment are scarce. Experimental studies and clinical subgroup analyses can provide a clue and useful guidance for further research. In this review, the fundamental mechanisms as well as trial results important for the determination of the optimal timing of stem cell therapy following MI are summarized and discussed. We conclude that optimization of stem cell therapy requires further research on the fundamental mechanisms responsible for stem cell homing, survival, differentiation, and integration. Clinically, randomized trials with bone-marrow-derived stem cells should be conducted timing therapy at different points within the first month after MI, which seems to be the most promising period for this cell type.

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Hematopoietic Stem Cell Antigen CD34: Role in Adhesion or Homing

Cited by 74 publications

References 63 publications

Differences in Surface Marker Expression and Chondrogenic Potential among Various Tissue-Derived Mesenchymal Cells from Elderly Patients with Osteoarthritis

Differences in Surface Marker Expression and Chondrogenic Potential among Various Tissue-Derived Mesenchymal Cells from Elderly Patients with Osteoarthritis

Immunotargeting and cloning of two CD34 variants exhibiting restricted expression in adult rat endothelia in vivo

Stem Cell Therapy for Myocardial Infarction: Are We Missing Time?

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