scholarly journals Regulation of Fc fragment-induced murine spleen cell proliferation.

1980 ◽  
Vol 151 (1) ◽  
pp. 1-11 ◽  
Author(s):  
E L Morgan ◽  
W O Weigle
Keyword(s):  
Cell Proliferation ◽  
Spleen Cell ◽  
Proliferative Response ◽  
Cleavage Product ◽  
Adherent Cell ◽  
Adherent Cells ◽  
Splenic Lymphocytes ◽  
Cell Type ◽  
Fc Fragment ◽  
Murine Spleen

Murine splenic lymphocytes proliferate in response to supernatant material derived from Fc fragment-pulsed splenic adherent cells. The stimulatory supernatant results from the interaction of Fc fragments with adherent cells or adherent cell supernate. Isolation of the stimulatory material in the supernate by Sephadex chromatography revealed that the mitogenic component was a cleavage product of Fc with a mol wt of approximately 14,000. The spleen cell type responsible for the generation of mitogenic Fc subfragments appears to be a macrophage. Unstimulated macrophages release an active supernate without being exposed to Fc fragments. The supernate of unstimulated macrophages apparently contain an enzyme which is capable of cleaving Fc fragments into the 14,000-mol wt mitogenic molecules. The spleen cell population induced to proliferate in response to the adherent cell supernate is present in T-cell depleted and Sephadex G-10 filtered cell preparations. Depletion of cells bearing immunoglobulin on their surfaces results in a reduced proliferative response to the mitogenic supernatant material indicating that it is probably a B cell.

scholarly journals The requirement for adherent cells in the Fc fragment-induced proliferative response of murine spleen cells.

1979 ◽  
Vol 150 (2) ◽  
pp. 256-266 ◽  
Author(s):  
E L Morgan ◽  
W O Weigle
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Population ◽  
Proliferative Response ◽  
Adherent Cell ◽  
Adherent Cells ◽  
Spleen Cells ◽  
Murine Spleen

The proliferative response of mouse B lymphocytes induced by Fc fragments was found to be dependent upon an adherent cell population. The adherent cell is esterase positive, irradiation resistant, and not susceptible to lysis by anti-thymus serum and complement. The mechanism(s) by which Fc fragments induce B-cell proliferation could be the result of the interaction of Fc with both B cells and adherent cells or with adherent cells which then release factors that trigger the B cells to proliferate. Spleen cells from the C3H/HeJ mouse were shown to be unable to respond to Fc fragments. The addition of adherent cells from either C3H/St or C3H/HeN mice to adherent cell depleted C3H/HeJ cells enabled them to respond to Fc, indicating the defect was in the adherent cell population.

scholarly journals Zebrafish Blunt-Force TBI Induces Heterogenous Injury Pathologies That Mimic Human TBI and Responds with Sonic Hedgehog-Dependent Cell Proliferation across the Neuroaxis

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 861
Author(s):  
James Hentig ◽  
Kaylee Cloghessy ◽  
Manuela Lahne ◽  
Yoo Jin Jung ◽  
Rebecca A. Petersen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Proliferative Response ◽  
Injury Severity ◽  
Granule Cell Layer ◽  
Dependent Manner ◽  
Adult Zebrafish ◽  
Post Injury ◽  
Blunt Force ◽  
Shh Pathway ◽  
Wide Range

Blunt-force traumatic brain injury (TBI) affects an increasing number of people worldwide as the range of injury severity and heterogeneity of injury pathologies have been recognized. Most current damage models utilize non-regenerative organisms, less common TBI mechanisms (penetrating, chemical, blast), and are limited in scalability of injury severity. We describe a scalable blunt-force TBI model that exhibits a wide range of human clinical pathologies and allows for the study of both injury pathology/progression and mechanisms of regenerative recovery. We modified the Marmarou weight drop model for adult zebrafish, which delivers a scalable injury spanning mild, moderate, and severe phenotypes. Following injury, zebrafish display a wide range of severity-dependent, injury-induced pathologies, including seizures, blood–brain barrier disruption, neuroinflammation, edema, vascular injury, decreased recovery rate, neuronal cell death, sensorimotor difficulties, and cognitive deficits. Injury-induced pathologies rapidly dissipate 4–7 days post-injury as robust cell proliferation is observed across the neuroaxis. In the cerebellum, proliferating nestin:GFP-positive cells originated from the cerebellar crest by 60 h post-injury, which then infiltrated into the granule cell layer and differentiated into neurons. Shh pathway genes increased in expression shortly following injury. Injection of the Shh agonist purmorphamine in undamaged fish induced a significant proliferative response, while the proliferative response was inhibited in injured fish treated with cyclopamine, a Shh antagonist. Collectively, these data demonstrate that a scalable blunt-force TBI to adult zebrafish results in many pathologies similar to human TBI, followed by recovery, and neuronal regeneration in a Shh-dependent manner.

Inactivation of Surface-adherent Listeria monocytogenes Hypochlorite and Heat

1991 ◽  
Vol 54 (1) ◽  
pp. 4-6 ◽  
Author(s):  
SHIN-HO LEE ◽  
JOSEPH F. FRANK
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Cell Population ◽  
Incubation Time ◽  
Cell Populations ◽  
Adherent Cell ◽  
Adherent Cells ◽  
D Cells

Inactivation by hypochlorite of Listeria monocytogenes cells adherent to stainless steel was determined. Adherent cell populations were prepared by incubating stainless steel slides with a 24 h culture of L. monocytogenes for 4 h at 21°C. Adherent microcolonies were prepared by growing L. monocytogenes on stainless steel slides submerged in a 1:15 dilution of tryptic soy broth at 21°C. The slides were then rinsed and transferred to fresh sterile broth every 2 d with a total incubation time of 8 d. Although the 4 h and 8 d adherent populations were at similar levels, 8 d adherent cells were over 100 times more resistant than the 4 h adherent cell population when exposed to 200 ppm hypochlorite for 30 s. When stainless steel slides containing adherent cells were heated at 72°C both adherent cell populations were inactivated after 1 min. Detectable numbers of L. monocytogenes remained on stainless steel slides after treatment at 65°C for 3 min when adherent 8 d cells were tested but not when adherent 4 h cells were used.

Ex VivoDetermination of the Effect of Whole-Body Exposure to Fast Neutrons on Murine Spleen Cell Viability and Apoptosis

2000 ◽  
Vol 154 (3) ◽  
pp. 301-306 ◽  
Author(s):  
V. Holl ◽  
D. Coelho ◽  
D. Weltin ◽  
J. M. Denis ◽  
P. Dufour ◽  
...  
Keyword(s):  
Cell Viability ◽  
Spleen Cell ◽  
Whole Body ◽  
Fast Neutrons ◽  
Murine Spleen

Is polyamine synthesis involved in the proliferative response of the intestinal epithelium to urogastrone-epidermal growth factor?

1989 ◽  
Vol 76 (6) ◽  
pp. 595-598 ◽  
Author(s):  
R. A. Goodlad ◽  
H. Gregory ◽  
N. A. Wright
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Proliferative Response ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Polyamine Synthesis ◽  
Proliferative Effect ◽  
Epidermal Growth

1. Intestinal epithelial cell proliferation was measured in rats maintained on total parenteral nutriton (TPN), in TPN rats given 300 μg of recombinant human epidermal growth factor (urogastrone-epidermal growth factor, URO-EGF) day−1 kg−1, and in further groups given URO-EGF and difluoromethylornithine (DFMO), an inhibitor of the enzyme ornithine decarboxylase (ODC). 2. URO-EGF significantly increased intestinal cell proliferation throughout the gastrointestinal tract. The proliferative response of the colon was particularly pronounced. 3. DFMO reduced the proliferative effect of urogastrone in the stomach and small intestine. DFMO also reduced URO-EGF-stimulated intestinal cell proliferation in the colon, but to a lesser extent. 4. It is concluded that ODC is essential for effecting the proliferative response of the stomach and small intestine to URO-EGF, but this role may be less important in the colon.

Macrophages as Regulatory Cells in Mitogen Induced Spleen Cell Proliferation. 1. Macrophages as Suppressor Cells

Immunobiology ◽  
1984 ◽  
Vol 168 (3-5) ◽  
pp. 260-273 ◽  
Author(s):  
E. Travniczek ◽  
G. Boltz-Nitulescu ◽  
C. Holzinger ◽  
O. Förster
Keyword(s):  
Cell Proliferation ◽  
Spleen Cell ◽  
Suppressor Cells ◽  
Regulatory Cells

scholarly journals Establishment of an adherent cell layer from human umbilical cord blood

2000 ◽  
Vol 23 (3) ◽  
pp. 519-522 ◽  
Author(s):  
Zeni Z.C. Alfonso ◽  
Eduardo D. Forneck ◽  
Waldir F. Allebrandt ◽  
Nance B. Nardi
Keyword(s):  
Bone Marrow ◽  
Cord Blood ◽  
Umbilical Cord Blood ◽  
Mononuclear Cells ◽  
Adherent Cell ◽  
Human Umbilical Cord Blood ◽  
Human Umbilical Cord ◽  
Adherent Cells ◽  
Bone Marrow Cultures ◽  
Marrow Cultures

In addition to bone marrow and peripheral blood, stem cells also occur in human umbilical cord blood (HUCB), and there is an increasing interest in the use of this material as an alternative source for bone marrow transplantation and gene therapy. In vitro hematopoiesis has been maintained for up to 16 weeks in HUCB cultures, but the establishment of an adherent, stromal layer has consistently failed. Adherent cell precursors among mononuclear cells from HUCB were sought for in long-term cultures. Mononuclear cells obtained from cord blood after full term, normal deliveries were cultivated at different concentrations in Iscove's modified Dulbecco's medium (IMDM) with weekly feeding. An adherent layer was detected in 16 of 30 cultures, 12 of which were plated at cell concentrations higher than 2 x 10(6) cells/ml. In contrast to bone marrow cultures, in which the stroma is detected early, in most (10/16) positive cultures from HUCB the adherent layer was identified only after the fourth week of culture. The cells never reached confluence and detached from the plate approximately four weeks after detection. May-Grünwald-Giemsa staining of positive cultures revealed fibroblast- or endothelial-like adherent cells in an arrangement different from that of bone marrow stroma in 13 samples. In two of these, the adherent cells were organized into characteristic, delimited cords of cells. Unlike bone marrow cultures, fat cells were never observed in the adherent layers. A rapid development of large myeloid cells in the first week of culture was characteristic of negative cultures and these cells were maintained for up to 12 weeks. HUCB contains adherent cell precursors which occur in lower numbers than in bone marrow and may be at a different (possibly less mature) stage of differentiation.

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

Cell type-specific requirement of the MAPK pathway for the growth factor action of gastrin

1999 ◽  
Vol 276 (6) ◽  
pp. G1363-G1372 ◽  
Author(s):  
Vinzenz M. Stepan ◽  
Chris J. Dickinson ◽  
John del Valle ◽  
Masashi Matsushima ◽  
Andrea Todisco
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Protein Kinase ◽  
Mapk Pathway ◽  
Cell Type ◽  
Ar42j Cells ◽  
Cell Type Specific ◽  
Ar42j Cell ◽  
Stimulation Of

Gastrin (G17) has a CCKBreceptor-mediated growth-promoting effect on the AR42J rat acinar cell line that is linked to induction of both mitogen-activated protein kinase (MAPK) and c- fos gene expression. We investigated the mechanisms that regulate the growth factor action of G17 on the rat pituitary adenoma cell line GH3. Both AR42J and GH3cells displayed equal levels of CCKBreceptor expression and similar binding kinetics of125I-labeled G17. G17 stimulation of cell proliferation was identical in both cell lines. G17 stimulation of GH3cell proliferation was completely blocked by the CCKBreceptor antagonist D2 but not by the MEK inhibitor PD-98059 or the protein kinase C inhibitor GF-109203X, which completely inhibited G17 induction of AR42J cell proliferation. G17 induced a c- fos SRE-luciferase reporter gene plasmid more than fourfold in the AR42J cells, whereas it had no effect in the GH3cells. In contrast to what we observed in the AR42J cells, G17 failed to stimulate MAPK activation and Shc tyrosyl phosphorylation and association with the adapter protein Grb2. Epidermal growth factor induced the MAPK pathway in the GH3cells, demonstrating the integrity of this signaling system. G17 induced Ca2+mobilization in both the GH3and AR42J cells. The calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide inhibited AR42J cell proliferation by 20%, whereas it completely blocked G17 induction of GH3cell growth. The Ca2+ionophore ionomycin stimulated GH3cell proliferation to a level similar to that observed in response to G17, but it had no effect on AR42J cell proliferation. Thus there are cell type specific differences in the requirement of the MAPK pathway for the growth factor action of G17. Whereas in the AR42J cells G17 stimulates cell growth through activation of MAPK and c- fos gene expression, in the GH3cells, G17 fails to activate MAPK, and it induces cell proliferation through Ca2+-dependent signaling pathways. Furthermore, induction of Ca2+mobilization in the AR42J cells appears not to be sufficient to sustain cell proliferation.

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