Lead treatment in vitro at early developmental stage of bone marrow-derived macrophages enhances NO production through IL-1β and IL-6 but not TNF-α

Toxicology ◽  
2001 ◽  
Vol 162 (1) ◽  
pp. 61-68 ◽  
Author(s):  
J Song
Keyword(s):  
Bone Marrow ◽  
Developmental Stage ◽  
Early Developmental Stage ◽  
No Production ◽  
Tnf Α ◽  
Early Developmental

scholarly journals Ownership structure and performance in family businesses at early developmental stage: evidence from China

2009 ◽  
Vol 7 (1) ◽  
pp. 138-150 ◽  
Author(s):  
Zhong Qin ◽  
Xin Deng
Keyword(s):  
Developmental Stage ◽  
Ownership Structure ◽  
Family Firms ◽  
Family Businesses ◽  
Early Developmental Stage ◽  
Governance Mechanism ◽  
Professional Managers ◽  
And Performance ◽  
The Impact ◽  
Early Developmental

This paper explores the impact of ownership structure on performance of family businesses at its early developmental stage in a context of under-developed market environment. Using a survey data of 296 private family firms in Ningbo, China, we find both management and single largest shareholder’s ownership is positively related to firm’s performance. However, family’s shareholding does not have significant impact on performance. Further inquiry on firm’s willingness to give shares to managers who are not family members indicates that while nearly half of the firms are willing to provide shares to professional managers, weak corporate governance mechanism and under-developed market may discourage such practice.

scholarly journals Septin7 regulates inner ear formation at an early developmental stage

2016 ◽  
Vol 419 (2) ◽  
pp. 217-228 ◽  
Author(s):  
Hiroko Torii ◽  
Atsuhiro Yoshida ◽  
Tatsuya Katsuno ◽  
Takayuki Nakagawa ◽  
Juichi Ito ◽  
...  
Keyword(s):  
Developmental Stage ◽  
Inner Ear ◽  
Early Developmental Stage ◽  
Early Developmental

Abstract 3753: Critical Role of Scavenger Receptor-BI Expressing Bone Marrow-Derived Endothelial Progenitor Cells in the Attenuation of Allograft Vasculopathy by Human Apo A-I Transfer

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yingmei Feng ◽  
Miranda van Eck ◽  
Eline Van Craeyveld ◽  
Frank Jacobs ◽  
Sophie Van Linthout ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Critical Role ◽  
Scavenger Receptor ◽  
Hdl Cholesterol ◽  
Expression Cassette ◽  
No Production ◽  
Endothelial Progenitor ◽  
Allograft Vasculopathy ◽  
Endothelial Regeneration

Background: Accelerated endothelial regeneration mediated by enhanced endothelial progenitor cell (EPC) incorporation may attenuate the development of allograft vasculopathy. Hypothesis: We investigated the hypothesis that modulation of EPC biology and attenuation of allograft vasculopathy by increased HDL cholesterol following human apo A-I (AdA-I) transfer requires scavenger receptor (SR)-BI expression in bone marrow-derived EPCs. Methods: Bone marrow transplantations with SR-BI+/+ or SR-BI−/− bone marrow were performed 4 weeks before gene transfer or saline injection. E1E3E4-deleted vectors containing a hepatocyte-specific human apo A-I expression cassette or containing no expression cassette were injected via the tail vein. Two weeks later, a common carotid artery of a female Balb/c donor mouse was transplanted paratopically into male recipient C57BL/6 mice. To analyse EPC incorporation, sex mismatch bone marrow transplantations were performed in female C57BL/6 mice and incorporated EPCs were quantified by in situ hybridization for the murine Y-chromosome. Results: Following AdA-I transfer, the number of circulating EPCs increased 2.0-fold (p<0.0001) at different time-points in C57BL/6 mice transplanted with SR-BI+/+ bone marrow but was unaltered in mice with SR-BI−/− bone marrow. The effect of HDL on EPC migration in vitro requires signaling via SR-BI and extracellular signal-regulated kinases (ERK) and is dependent on increased NO production in EPCs. Human apo A-I transfer 2 weeks before paratopic artery transplantation reduced intimal area at day 21 3.7-fold (p<0.001) in mice with SR-BI+/+ bone marrow but had no effect in mice with SR-BI−/− bone marrow. The number of CD31 positive endothelial cells lining the lumen and the number of incorporated EPCs was increased 3.0-fold (p<0.001) and 9.7-fold (p<0.001), respectively, in AdA-I treated chimeric SR-BI+/+ mice compared to control mice with SR-BI+/+ bone marrow. Endothelial regeneration and EPC incorporation was not increased after AdA-I transfer in chimeric SR-BI−/−mice. Conclusion: Human apo A-I transfer-mediated endothelial regeneration to prevent allograft vasculopathy is strictly dependent on SR-BI expressing bone marrow-derived EPCs.

Leishmania donovani infection of bone marrow stromal macrophages selectively enhances myelopoiesis, by a mechanism involving GM-CSF and TNF-α

Blood ◽  
2000 ◽  
Vol 95 (5) ◽  
pp. 1642-1651 ◽  
Author(s):  
Sara E. J. Cotterell ◽  
Christian R. Engwerda ◽  
Paul M. Kaye
Keyword(s):  
Infectious Disease ◽  
Bone Marrow ◽  
Stromal Cell ◽  
Leishmania Donovani ◽  
Protozoan Parasite ◽  
Gm Csf ◽  
Tnf Α ◽  
Macrophage Colony

Alterations in hematopoiesis are common in experimental infectious disease. However, few studies have addressed the mechanisms underlying changes in hematopoietic function or assessed the direct impact of infectious agents on the cells that regulate these processes. In experimental visceral leishmaniasis, caused by infection with the protozoan parasite Leishmania donovani, parasites persist in the spleen and bone marrow, and their expansion in these sites is associated with increases in local hematopoietic activity. The results of this study show that L donovani targets bone marrow stromal macrophages in vivo and can infect and multiply in stromal cell lines of macrophage, but not other lineages in vitro. Infection of stromal macrophages increases their capacity to support myelopoiesis in vitro, an effect mediated mainly through the induction of granulocyte macrophage-colony stimulating factor and tumor necrosis factor-. These data are the first to directly demonstrate that intracellular parasitism of a stromal cell population may modify its capacity to regulate hematopoiesis during infectious disease.

scholarly journals Phylloseptin-1 is Leishmanicidal for Amastigotes of Leishmania amazonensis Inside Infected Macrophages

2020 ◽  
Vol 17 (13) ◽  
pp. 4856
Author(s):  
Selma A. S. Kückelhaus ◽  
Daniela Sant’Ana de Aquino ◽  
Tatiana K. Borges ◽  
Daniel C. Moreira ◽  
Luciana de Magalhães Leite ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Leishmania Amazonensis ◽  
In Vivo Studies ◽  
Public Health Issue ◽  
Neglected Diseases ◽  
No Production ◽  
Tnf Α ◽  
Production Of Hydrogen

Leishmania protozoans are the causal agents of neglected diseases that represent an important public health issue worldwide. The growing occurrence of drug-resistant strains of Leishmania and severe side effects of available treatments represent an important challenge for the leishmaniases treatment. We have previously reported the leishmanicidal activity of phylloseptin-1 (PSN-1), a peptide found in the skin secretion of Phyllomedusa azurea (=Pithecopus azureus), against Leishmania amazonensis promastigotes. However, its impact on the amastigote form of L. amazonensis and its impact on infected macrophages are unknown. In this work, we evaluated the effects of PSN-1 on amastigotes of L. amazonensis inside macrophages infected in vitro. We assessed the production of hydrogen peroxide and nitric oxide, as well as the levels of inflammatory and immunomodulatory markers (TGF-β, TNF-α and IL-12), in infected and non-infected macrophages treated with PSN-1. Treatment with PSN-1 decreased the number of infected cells and the number of ingested amastigotes per cell when compared with the untreated cells. At 32 µM (64 µg/mL), PSN-1 reduced hydrogen peroxide levels in both infected and uninfected macrophages, whereas it had little effect on NO production or TGF-β release. The effect of PSN-1 on IL-12 and TNF-α secretion depended on its concentration, but, in general, their levels tended to increase as PSN-1 concentration increased. Further in vitro and in vivo studies are needed to clarify the mechanisms of action of PSN-1 and its interaction with the immune system aiming to develop pharmacological applications.

scholarly journals Development of Gonadotropin-Releasing Hormone-1 Secretion in Mouse Nasal Explants

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3221-3227 ◽  
Author(s):  
Stephanie Constantin ◽  
Alain Caraty ◽  
Susan Wray ◽  
Anne H. Duittoz
Keyword(s):  
Pulse Generator ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Early Developmental Stage ◽  
Limiting Factor ◽  
Sequence Of Events ◽  
Natural Ligands ◽  
Early Developmental ◽  
Secretory Pattern

Pulsatile release of GnRH-1 is critical to stimulate gonadotropes of the anterior pituitary. This secretory pattern seems to be inherent to GnRH-1 neurons, however, the mechanisms underlying such episodical release remain unknown. In monkey nasal explants, the GnRH-1 population exhibits synchronized calcium events with the same periodicity as GnRH-1 release, suggesting a link, though the sequence of events was unclear. GnRH-1 neurons in mouse nasal explants also exhibit synchronized calcium events. In the present work, GnRH-1 release was assayed in mouse nasal explants using radioimmunology and its relationship with calcium signaling analyzed. GnRH-1 neurons generated episodical release as early as 3 d in vitro (div) and maintained such release throughout the period studied (3–21 div). The pulse frequency remained constant, suggesting that the pulse generator is operative at an early developmental stage. In contrast, pulse amplitude increased 2-fold between 3 and 7 div, and again between 7 and 14 div, suggesting maturation in synthesizing and/or secretory mechanisms. To evaluate these possibilities, total GnRH-1 content was measured. Only a small increase in GnRH-1 content was detected between 7 and 14 div, whereas a large increase occurred between 14 and 21 div. These data indicate that GnRH-1 content was not a limiting factor for the amplitude of the pulses at 7 div but that the secretory mechanisms mature between 3 and 14 div. The application of kisspeptin-10 revealed the ability of GnRH-1 neurons to integrate signals from natural ligands into a secretory response. Finally, simultaneous sampling of medium and calcium imaging recordings indicated that the synchronized calcium events and secretory events are congruent.

scholarly journals In Vitro Investigation of Host Resistance toToxoplasma gondii Infection in Microglia of BALB/c and CBA/Ca Mice

2001 ◽  
Vol 69 (2) ◽  
pp. 765-772 ◽  
Author(s):  
Yvonne R. Freund ◽  
Naunihal T. Zaveri ◽  
Harold S. Javitz
Keyword(s):  
Toxoplasmic Encephalitis ◽  
No Production ◽  
Partial Recovery ◽  
Newborn Mice ◽  
Tryptophan Degradation ◽  
Tnf Α ◽  
In Vitro Investigation ◽  
Dependent Inhibition ◽  
Ifn Γ

ABSTRACT Toxoplasmic encephalitis (TE) is a life-threatening disease of immunocompromised individuals and has increased in prevalence as a consequence of AIDS. TE has been modeled in inbred mice, with CBA/Ca mice being susceptible and BALB/c mice resistant to the development of TE. To better understand the innate mechanisms in the brain that play a role in resistance to TE, nitric oxide (NO)-dependent and NO-independent mechanisms were examined in microglia from BALB/c and CBA/Ca mice and correlated with the ability of these cells to inhibit Toxoplasma gondii replication. These parameters were measured 48 h after stimulation with lipopolysaccharide (LPS) gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), or combinations of these inducers in T. gondii-infected microglia isolated from newborn mice. CBA/Ca microglia consistently produced less NO than did BALB/c microglia after stimulation with LPS or with IFN-γ plus TNF-α, and they inhibitedT. gondii replication significantly less than did BALB/c microglia. Cells of both strains treated with IFN-γ alone significantly inhibited uracil incorporation by T. gondii, and N G-monomethyl-l-arginine (NMMA) treatment did not reverse this effect. In cells treated with IFN-γ in combination with other inducers, NMMA treatment resulted in only partial recovery of T. gondii replication. This IFN-γ-dependent inhibition of replication was not due to generation of reactive oxygen species or to increased tryptophan degradation. These data suggest that NO production and an IFN-γ-dependent mechanism contribute to the inhibition of T. gondii replication after in vitro stimulation with IFN-γ plus TNF-α or with LPS. Differences in NO production but not in IFN-γ-dependent inhibition of T. gondii replication were observed between CBA/Ca and BALB/c microglia.

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