The role of hormones and prostanoids in the in vitro proliferation and differentiation of human myoblasts

1987 ◽  
Vol 172 (2) ◽  
pp. 265-281 ◽  
Author(s):  
Rosalind J. Zalin
Keyword(s):  
In Vitro Proliferation ◽  
Proliferation And Differentiation

In Vitro Proliferation and Differentiation of Human Hair Follicle Stem Cells on Chitosan-Skin Regenerating Template

2015 ◽  
Vol 05 (999) ◽  
pp. 1-1
Author(s):  
Abu Bakar Mohd Hilmi ◽  
Mohd Noor Norhayati ◽  
Ahmad Sukari Halim ◽  
Chin Keong Lim ◽  
Zulkifli Mustafa ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hair Follicle ◽  
Human Hair ◽  
Human Hair Follicle ◽  
In Vitro Proliferation ◽  
Proliferation And Differentiation ◽  
Hair Follicle Stem Cells ◽  
Follicle Stem Cells

scholarly journals Increased Expression of Retinol-Binding Protein 4 in Ovarian Endometrioma and Its Possible Role in the Pathogenesis of Endometriosis

2021 ◽  
Vol 22 (11) ◽  
pp. 5827
Author(s):  
Jae Chul Lee ◽  
Sung Hoon Kim ◽  
Young Sang Oh ◽  
Ju Hee Kim ◽  
Sa Ra Lee ◽  
...  
Keyword(s):  
Retinol Binding Protein ◽  
Endometrial Stromal Cells ◽  
Endometrial Cells ◽  
Retinol Binding Protein 4 ◽  
Ovarian Endometrioma ◽  
Proliferation And Differentiation ◽  
In Vitro Effects ◽  
Ovarian Endometriomas

Although endometriosis is a benign disease characterized by the presence of endometrial tissues outside the uterus, ectopic endometrial cells can exhibit malignant biological behaviors. Retinol-binding protein4 (RBP4) is a novel adipocyte-derived cytokine, which has important roles in regulating insulin sensitivity and energy metabolism. RBP4 is a potent modulator of gene transcription, and acts by directly controlling cell growth, invasiveness, proliferation and differentiation. Here, we evaluated the possible role of RBP4 in the pathogenesis of endometriosis. We compared the levels of RBP4 in the tissues and peritoneal fluid (PF) of women with and without endometriosis and evaluated the in vitro effects of RBP4 on the viability, invasiveness, and proliferation of endometrial stromal cells (ESCs). RBP4 levels were significantly higher in the PF of the women in the endometriosis group than in the controls. RBP4 immunoreactivity was significantly higher in the ovarian endometriomas of women with advanced stage endometriosis than those of controls. In vitro treatment with human recombinant-RBP4 significantly increased the viability, bromodeoxyuridine expression, and invasiveness of ESCs. Transfection with RBP4 siRNA significantly reduced ESC viability and invasiveness. These findings suggest that RBP4 partakes in the pathogenesis of endometriosis by increasing the viability, proliferation and invasion of endometrial cells.

scholarly journals Critical role of integrin CD11c in splenic dendritic cell capture of missing-self CD47 cells to induce adaptive immunity

2018 ◽  
Vol 115 (26) ◽  
pp. 6786-6791 ◽  
Author(s):  
Jiaxi Wu ◽  
Huaizhu Wu ◽  
Jinping An ◽  
Christie M. Ballantyne ◽  
Jason G. Cyster
Keyword(s):  
Critical Role ◽  
T Cell Proliferation ◽  
Cell Capture ◽  
Antigen Uptake ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Missing Self

CD11c, also known as integrin alpha X, is the most widely used defining marker for dendritic cells (DCs). CD11c can bind complement iC3b and mediate phagocytosis in vitro, for which it is also referred to as complement receptor 4. However, the functions of this prominent marker protein in DCs, especially in vivo, remain poorly defined. Here, in the process of studying DC activation and immune responses induced by cells lacking self-CD47, we found that DC capture of CD47-deficient cells and DC activation was dependent on the integrin-signaling adaptor Talin1. Specifically, CD11c and its partner Itgb2 were required for DC capture of CD47-deficient cells. CD11b was not necessary for this process but could partially compensate in the absence of CD11c. Mice with DCs lacking Talin1, Itgb2, or CD11c were defective in supporting T-cell proliferation and differentiation induced by CD47-deficient cell associated antigen. These findings establish a critical role for CD11c in DC antigen uptake and activation in vivo. They may also contribute to understanding the functional mechanism of CD47-blockade therapies.

scholarly journals Existence of a pool of T-lymphocyte colony-forming cells (T-CFC) in human bone marrow and their place in the differentiation of the T- lymphocyte lineage

Blood ◽  
1981 ◽  
Vol 58 (5) ◽  
pp. 911-915 ◽  
Author(s):  
F Triebel ◽  
WA Robinson ◽  
AR Hayward ◽  
PG Goube de Laforest
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
T Lymphocyte ◽  
Cell Lineage ◽  
Marrow Graft ◽  
In Vitro Proliferation ◽  
Complement Dependent Cytotoxicity ◽  
Self Tolerance ◽  
Proliferation And Differentiation

Abstract The existence and characteristics of bone marrow T-cell progenitors have not yet been established in man. Several pieces of evidence such as the reconstitution of certain immunodeficiencies by bone marrow graft suggest that T-cell precursors are present in the bone marrow. We report the growth of T-cell colonies from bone marrow populations using PHA-stimulated lymphocyte-conditioned medium containing T-cell growth factor (TCGF). Rosetting experiments and complement-dependent cytotoxicity assays with monoclonal antibodies indicate that the bone marrow T colony-forming cells (T-CFC) are E- OKT 3- and la+, i.e., immature progenitors. The colonies derived from these cells have the phenotype of mature T cells: E + OKT 3 + la- with either helper (OKT 4+) and suppressor (OKT 8 +) antigens. These results suggest that a thymic microenvironment may not be necessary for the in vitro proliferation and differentiation of the T-cell lineage in adult humans. These methodologies may permit direct investigation of early phenomena concerning the T-cell lineage, such as the acquisition of self-tolerance, the formation of a repertoire of specificities, and the HLA restriction phenomena that we believe takes place before the thymic maturation.

scholarly journals Common and pre-B acute lymphoblastic leukemia cells express interleukin 2 receptors, and interleukin 2 stimulates in vitro colony formation

Blood ◽  
1985 ◽  
Vol 66 (3) ◽  
pp. 556-561 ◽  
Author(s):  
I Touw ◽  
R Delwel ◽  
R Bolhuis ◽  
G van Zanen ◽  
B Lowenberg
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Colony Formation ◽  
B Lymphocyte ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Colony Growth ◽  
Leukemic Cells ◽  
In Vitro Proliferation ◽  
Proliferation And Differentiation

Abstract The role of interleukin 2 (IL 2) as a possible regulator of in vitro proliferation and differentiation of non-T acute lymphoblastic leukemia (ALL) cells was investigated. For this purpose, leukemic cells from the blood or bone marrow of eight untreated patients with common or pre-B ALL were analyzed using the anti-Tac monoclonal antibody (reactive with the IL 2 receptor) in indirect immunofluorescence. The receptors for IL 2, which were initially absent from the cell surface, were induced on high percentages of the ALL cells after the in vitro exposure to the lectin phytohemagglutinin or the phorbol ester 12-O- tetradecanoylphorbol-13-acetate in six patients, suggesting that the cells had become sensitive to IL 2. In colony cultures to which feeder leukocytes and IL 2 had been added, colony growth was obtained in five of eight cases. Whereas the cells from one patient formed colonies in the absence of exogenous stimuli, the cells from others were dependent on the addition of feeder leukocytes plus IL 2. In the latter cases, feeder leukocytes alone, releasing some IL 2, stimulated growth suboptimally at different cell concentrations. Their stimulative effect was significantly enhanced when leukocyte-derived IL 2 or pure recombinant IL 2 was supplemented. Alone, IL 2 (up to 500 U/mL) did not support colony formation. Apparently, IL 2 and feeder leukocytes are both required for the induction of colonies in these cases of ALL. From cell sorting of fluorescent anti-common ALL antigen (CALLA) stained cells it appeared that colonies descended from cells with high as well as low or negative CALLA expression. Immunophenotyping demonstrated the presence of the original leukemia markers on colony cells, but was not indicative of maturation of ALL toward more differentiated B cells. We suggest that IL 2 can stimulate the in vitro proliferation of certain neoplastic B lymphocyte progenitors.

In vitro proliferation and differentiation of erythroid progenitors from patients with myelodysplastic syndromes: evidence for Fas-dependent apoptosis

Blood ◽  
2002 ◽  
Vol 99 (5) ◽  
pp. 1594-1601 ◽  
Author(s):  
Yann-Erick Claessens ◽  
Didier Bouscary ◽  
Jean-Michel Dupont ◽  
Françoise Picard ◽  
Josiane Melle ◽  
...  
Keyword(s):  
Myelodysplastic Syndromes ◽  
Liquid Culture ◽  
Fas Ligand ◽  
Chimeric Protein ◽  
Refractory Anemia ◽  
Erythroid Progenitors ◽  
In Vitro Proliferation ◽  
Cd34 Cells ◽  
Proliferation And Differentiation

Erythropoiesis results from the proliferation and differentiation of pluripotent stem cells into immature erythroid progenitors (ie, erythroid burst-forming units (BFU-Es), whose growth, survival, and terminal differentiation depends on erythropoietin (Epo). Ineffective erythropoiesis is a common feature of myelodysplastic syndromes (MDS). We used a 2-step liquid-culture procedure to study erythropoiesis in MDS. CD34+ cells from the marrow of patients with MDS were cultured for 10 days in serum-containing medium with Epo, stem cell factor, insulinlike growth factor 1, and steroid hormones until they reached the proerythroblast stage. The cells were then placed in medium containing Epo and insulin for terminal erythroid differentiation. Numbers of both MDS and normal control cells increased 103fold by day 15. However, in semisolid culture, cells from patients with refractory anemia (RA) with ringed sideroblasts and RA or RA with excess of blasts produced significantly fewer BFU-Es than cells from controls. Fluorescence in situ hybridization analysis of interphase nuclei from patients with chromosomal defects indicated that abnormal clones were expanded in vitro. Epo-signaling pathways (STAT5, Akt, and ERK 1/2) were normally activated in MDS erythroid progenitors. In contrast, apoptosis was significantly increased in MDS cells once they differentiated, whereas it remained low in normal cells. Fas was overexpressed on freshly isolated MDS CD34+ cells and on MDS erythroid cells throughout the culture. Apoptosis coincided with overproduction of Fas ligand during the differentiation stage and was inhibited by Fas-Fc chimeric protein. Thus, MDS CD34+-derived erythroid progenitors proliferated normally in our 2-step liquid culture with Epo but underwent abnormal Fas-dependent apoptosis during differentiation that could be responsible for the impaired erythropoiesis.

scholarly journals Smad4 is critical for self-renewal of hematopoietic stem cells

2007 ◽  
Vol 204 (3) ◽  
pp. 467-474 ◽  
Author(s):  
Göran Karlsson ◽  
Ulrika Blank ◽  
Jennifer L. Moody ◽  
Mats Ehinger ◽  
Sofie Singbrant ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
In Vitro Proliferation ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Early Embryonic Lethality

Members of the transforming growth factor β (TGF-β) superfamily of growth factors have been shown to regulate the in vitro proliferation and maintenance of hematopoietic stem cells (HSCs). Working at a common level of convergence for all TGF-β superfamily signals, Smad4 is key in orchestrating these effects. The role of Smad4 in HSC function has remained elusive because of the early embryonic lethality of the conventional knockout. We clarify its role by using an inducible model of Smad4 deletion coupled with transplantation experiments. Remarkably, systemic induction of Smad4 deletion through activation of MxCre was incompatible with survival 4 wk after induction because of anemia and histopathological changes in the colonic mucosa. Isolation of Smad4 deletion to the hematopoietic system via several transplantation approaches demonstrated a role for Smad4 in the maintenance of HSC self-renewal and reconstituting capacity, leaving homing potential, viability, and differentiation intact. Furthermore, the observed down-regulation of notch1 and c-myc in Smad4−/− primitive cells places Smad4 within a network of genes involved in the regulation HSC renewal.

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