The use of variable lactate/malic dehydrogenase ratios to distinguish between progenitor cells of cartilage and bone in the embryonic chick

Development ◽  
1976 ◽  
Vol 36 (2) ◽  
pp. 305-313
Author(s):  
P. V. Thorogood ◽  
Brian K. Hall
Keyword(s):  
Stem Cells ◽  
Progenitor Cells ◽  
Anaerobic Metabolism ◽  
Embryonic Chick ◽  
Malic Dehydrogenase ◽  
Membrane Bone ◽  
Chondrogenic Progenitor Cells ◽  
First Time

The activities of LDH and MDH have been studied, both in differentiated cartilage and bone from the embryonic chick, and in the pool of mixed osteogenic and chondrogenic stem cells found on the quadratojugal, a membrane bone. In confirmation of the model proposed by Reddi & Huggins (1971) we found that the LDH/MDH ratio was greater than 1 in cartilage and less than 1 in bone. Furthermore we established, for the first time, that ratios occurred in the chondrogenic and osteogenic stem cells, similar to the ratios in their differentiated counterparts. Alterations in LDH/MDH resulted from variations in the level of LDH/µg protein. MDH/µg protein remained constant, even when LDH/MDH was changing. We interpret these results in terms of adaptation of chondrogenic progenitor cells for anaerobic metabolism and anticipate that our model will be applicable to other skeletal systems where stem cells are being studied.

Human Hematopoietic Stem/Progenitor Cells (HSPCs) and Mesenchymal Stromal Cells (MSCs) Express Several Functional Pituitary and Gonadal Sex Hormone Receptors - Identification of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) As New Growth Factors for HSPCs and MSCs

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2393-2393
Author(s):  
Ahmed Abdelbaset-Ismail ◽  
Malwina Suszynska ◽  
Sylwia Julita Borkowska ◽  
Mateusz Adamiak ◽  
Janina Ratajczak ◽  
...  
Keyword(s):  
Stem Cells ◽  
Luteinizing Hormone ◽  
Progenitor Cells ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Follicle Stimulating Hormone ◽  
Hematopoietic Stem ◽  
First Time ◽  
Stimulating Hormone

Abstract Background . Evidence has accumulated that murine hematopoietic stem/progenitor cells (HSPCs) share several markers with the germline, a connection supported by our recent reports that pituitary and gonadal sex hormones (SexHs) regulate development of murine HSPCs (Stem Cells & Develop. 2015, 24, 927-937). In contrast to mice, relatively little is known about the role of SexHs in human hematopoiesis, except that androgens have been employed successfully to treat certain cases of bone marrow (BM) failure. In particular, no studies have been performed to study the roles of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in this process. It is known that the blood level of FSH increases with age and is high in older patients, which correlates with increased risk of hematopoietic malignancies. Aim of the study . To better address the effects of SexHs, and particularly pituitary SexHs, on human hematopoiesis, we tested human HSPCs purified from umbilical cord blood (UCB) and BM for expression of receptors for pituitary SexHs, including FSH, LH, and prolactin (PRL), as well as the receptors for gonadal SexHs, including progesterone, estrogens, and androgen. We then tested the functionality of these receptors in ex vivo signal transduction studies and in vitro clonogenic assays. In parallel, we tested the effect of SexHs on human mesenchymal stromal cells (MSCs). Finally, based on our observation that at least some of the UCB-derived, CD45- very small embryonic-like stem cells become specified into CD45+ HSPCs (Leukemia 2011;25,1278-1285), we also evaluated the expression of pituitary and gonadal SexH receptors on these cells. Results . We report for the first time that, like their murine counterparts, human HSPCs, small CD45- very small embryonic-like stem cells endowed with hematopoietic specification potential, and MSCs expressed functional pituitary and gonadal SexH receptors at the mRNA and protein level and responded by MAPKp42/44 and AKT phosphorylation to SexH stimulation. Most importantly, human HSPCs proliferated in vitro in response to SexH stimulation, as did MSCs. Finally, FSH and LH also chemoattracted MSCs in a Transwell migration assay and stimulated these cells to secrete several factors that enhanced in vitro angiogenesis. Conclusions . We report for the first time that FSH, LH, estrogens, and progesterone stimulate growth of human HSPCs and MSCs. In addition, we confirmed that androgens and prolactin stimulate proliferation of human HSPCs. These results are important for understanding the interplay of SexHs in the development and aging of BM, as plasma levels of some of these hormones change with age. Finally, these results further support a developmental link between hematopoiesis and the germline as previously proposed by us and others. Disclosures No relevant conflicts of interest to declare.

Polyurethane/Polylactide-Based Electrospun Nonwovens as Carriers for Human Adipose-Derived Stromal Stem Cells and Chondrogenic Progenitor Cells

2016 ◽  
Vol 55 (18) ◽  
pp. 1897-1907 ◽  
Author(s):  
Krzysztof Marycz ◽  
Monika Marędziak ◽  
Jakub Grzesiak ◽  
Ryszard Fryczkowski ◽  
Jadwiga Laska
Keyword(s):  
Stem Cells ◽  
Progenitor Cells ◽  
Chondrogenic Progenitor Cells ◽  
Stromal Stem Cells

Breakthrough Regenerative Cardiopoietic Stem Cells and Related Technologies in the Field of Cardiovascular Medicine – From Bench to Bedside

2012 ◽  
Vol 7 (1) ◽  
pp. 14
Author(s):  
Christian Homsy ◽  
Keyword(s):  
Stem Cells ◽  
Cell Therapy ◽  
Progenitor Cells ◽  
Cardiac Disease ◽  
Cardiac Tissue ◽  
Cardiac Repair ◽  
Cardiac Diseases ◽  
Cardiac Progenitor Cells ◽  
Biotechnology Company ◽  
Cardiovascular Medicine

The scale of cardiac diseases, and in particular heart failure and acute myocardial infarction, emphasises the need for radically new approaches, such as cell therapy, to address the underlying cause of the disease, the loss of functional myocardium. Stem cell-based therapies, whether through transplanted cells or directing innate repair, may provide regenerative approaches to cardiac diseases by halting, or even reversing, the events responsible for progression of organ failure. Cardio3 BioSciences, a leading Belgian biotechnology company focused on the discovery and development of regenerative and protective therapies for the treatment of cardiac disease, was founded in this context in 2004. The company is developing a highly innovative cell therapy approach based on a platform designed to reprogramme the patient’s own stem cells into cardiac progenitor cells. The underlying rationale behind this approach is that, in order to reconstruct cardiac tissue, stem cells need to be specific to cardiac tissue. The key is therefore to provide cardiac-specific progenitor cells to the failing heart to induce cardiac repair.

Elevated Inflammatory Parameter Levels Negatively Impact Populations of Circulating Stem Cells (CD133+), Early Endothelial Progenitor Cells (CD133+/VEGFR2+), and Fibroblast Growth Factor in Stroke Patients

2019 ◽  
Vol 16 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Monika Golab-Janowska ◽  
Edyta Paczkowska ◽  
Boguslaw Machalinski ◽  
Dariusz Kotlega ◽  
Agnieszka Meller ◽  
...  
Keyword(s):  
Risk Factors ◽  
Stem Cells ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Plasma Levels ◽  
Fibroblast Growth ◽  
Vascular Risk ◽  
Endothelial Progenitor ◽  
Inflammatory Parameters

Background: Endothelial Progenitor Cells (EPCs) are important players in neovascularization, mobilized through signalling by Angiogenic Growth Factors (AGFs) such as Vascular Endothelial Growth Factor (VEGF) and fibroblast growth factor (FGF). In vitro, inflammatory parameters impair the function and influence of EPCs on AGFs. However, this connection is not clear in vivo. To understand the mechanisms of augmented arteriogenesis and angiogenesis in acute ischemic stroke (AIS) patients, we investigated whether circulating stem cells (CD133+), early endothelial progenitor cells (CD133+/VEGFR2+), and endothelial cells (ECs; CD34¯/CD133¯/VEGFR2+) were increasingly mobilized during AIS, and whether there were correlations between EPC levels, growth factor levels and inflammatory parameters. Methods: Data on demographics, classical vascular risk factors, neurological deficit information (assessed using the National Institutes of Health Stroke Scale), and treatment were collected from 43 consecutive AIS patients (group I). Risk factor control patients (group II) included 22 nonstroke subjects matched by age, gender, and traditional vascular risk factors. EPCs were measured by flow cytometry and the populations of circulating stem cells (CD133+), early EPCs (CD133+/VEGFR2+), and ECs (CD34¯/CD133¯/VEGFR2+) were analysed. Correlations between EPC levels and VEGF and FGF vascular growth factor levels as well as the influence of inflammatory parameters on EPCs and AGFs were assessed. Results: Patient ages ranged from 54 to 92 years (mean age 75.2 ± 11.3 years). The number of circulating CD34¯/CD133¯/VEGF-R2+ cells was significantly higher in AIS patients than in control patients (p < 0.05). VEGF plasma levels were also significantly higher in AIS patients compared to control patients on day 7 (p < 0.05). FGF plasma levels in patients with AIS were significantly higher than those in the control group on day 3 (p < 0.05). There were no correlations between increased VEGF and FGF levels and the number of CD133+, CD133+/VEGFR2+, or CD34¯/CD133¯/VEGFR2+ cells. Leukocyte levels, FGF plasma levels, and the number of early EPCs were negatively correlated on day 3. High sensitivity C-reactive protein levels and the number of CD133+ and CD133+/VEGFR2+ cells were negatively correlated on day 7. In addition, there was a negative correlation between fibrinogen levels and FGF plasma levels as well as the number of early EPCs (CD133+/VEGFR2+). Conclusion: AIS patients exhibited increased numbers of early EPCs (CD133+/VEGFR2+) and AGF (VEGF and FGF) levels. A negative correlation between inflammatory parameters and AGFs and EPCs indicated the unfavourable influence of inflammatory factors on EPC differentiation and survival. Moreover, these correlations represented an important mechanism linking inflammation to vascular disease.

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