Retinoic acid and nitric oxide promote cell proliferation and differentially induce neuronal differentiation in vitro in the cnidarian Renilla koellikeri

2010 ◽  
Vol 70 (12) ◽  
pp. 842-852 ◽  
Author(s):  
Djoyce Estephane ◽  
Michel Anctil
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Promote Cell Proliferation ◽  
Renilla Koellikeri

Effects of retinoic acid steroidal analogs on human leukemic HL60 cell proliferation in vitro and on angiogenesis in vivo

2005 ◽  
Vol 16 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Evaggelia S. Arsenou ◽  
Evangelia P. Papadimitriou ◽  
Eleni Kliafa ◽  
Maria Hountala ◽  
Sotiris S. Nikolaropoulos
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Hl60 Cell ◽  
Proliferation In Vitro

scholarly journals In vitro anticancer activity of hydrogen sulfide and nitric oxide alongside nickel nanoparticle and novel mutations in their genes in CRC patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zjwan Housein ◽  
Tayeb Sabir Kareem ◽  
Abbas Salihi
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Hydrogen Sulfide ◽  
Direct Sequencing ◽  
Scorpion Venom ◽  
Enos Gene ◽  
Cytotoxic Activities ◽  
No Donors ◽  
The Impact

AbstractThis study was carried out to assess the impact of nickel nanoparticles (NiNPs) as well as scorpion venom on colorectal cancer (CRC) cells in the presence and/or absence of 5-fluorouracil (5-FU), hydrogen sulfide (H2S), and nitric oxide (NO) donors and to determine alterations in endothelial NO synthase (eNOS) and cystathionine γ-lyase (CSE) enzyme-producing genes in CRC patients. The IC50 of both H2S and NO donors, along with NiNPs, were determined. The CRC cells were treated for 24hrs, and the cytotoxic activities were assessed using the MTT test. Moreover, the apoptosis was determined after 24hrs and 48hrs using TUNEL assay. Furthermore, the mutations in the eNOS gene (intron 4, -786T>C and 894 G>T) and CSE gene (1364GT) were determined using direct sequencing. The IC50 values for sodium disulfide (Na2S) and sodium nitroprusside (SNP) at 24hrs treatment were found to be 5 mM and 10−6 M, respectively, while the IC50 value for 5-FU was reached after 5-days of treatment in CRC cell line. Both black and yellow scorpion venoms showed no inhibition of cell proliferation after 24hrs treatment. Furthermore, Na2S showed a significant decrease in cell proliferation and an increase in apoptosis. Moreover, a co-treatment of SNP and 5-FU resulted in inhibition of the cytotoxic effect of 5-FU, while a combination treatment of NiNPs with Na2S, SNP, and 5-FU caused highly significant cytotoxicity. Direct sequencing reveals new mutations, mainly intronic variation in eNOS gene that has not previously been described in the database. These findings indicate that H2S promotes the anticancer efficiency of 5-FU in the presence of NiNPs while NO has antiapoptotic activity in CRC cell lines.

scholarly journals HPV-18 E6 Oncoprotein and Its Spliced Isoform E6*I Regulate the Wnt/β-Catenin Cell Signaling Pathway through the TCF-4 Transcriptional Factor

2018 ◽  
Vol 19 (10) ◽  
pp. 3153 ◽  
Author(s):  
J. Muñoz-Bello ◽  
Leslie Olmedo-Nieva ◽  
Leonardo Castro-Muñoz ◽  
Joaquín Manzo-Merino ◽  
Adriana Contreras-Paredes ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Transcriptional Activation ◽  
Target Genes ◽  
Promote Cell Proliferation ◽  
E6 And E7 ◽  
Hpv 18

The Wnt/β-catenin signaling pathway regulates cell proliferation and differentiation and its aberrant activation in cervical cancer has been described. Persistent infection with high risk human papillomavirus (HR-HPV) is the most important factor for the development of this neoplasia, since E6 and E7 viral oncoproteins alter cellular processes, promoting cervical cancer development. A role of HPV-16 E6 in Wnt/β-catenin signaling has been proposed, although the participation of HPV-18 E6 has not been previously studied. The aim of this work was to investigate the participation of HPV-18 E6 and E6*I, in the regulation of the Wnt/β-catenin signaling pathway. Here, we show that E6 proteins up-regulate TCF-4 transcriptional activity and promote overexpression of Wnt target genes. In addition, it was demonstrated that E6 and E6*I bind to the TCF-4 (T cell factor 4) and β-catenin, impacting TCF-4 stabilization. We found that both E6 and E6*I proteins interact with the promoter of Sp5, in vitro and in vivo. Moreover, although differences in TCF-4 transcriptional activation were found among E6 intratype variants, no changes were observed in the levels of regulated genes. Furthermore, our data support that E6 proteins cooperate with β-catenin to promote cell proliferation.

scholarly journals Retinoic acid decreases fetal lung mesenchymal cell proliferation in vivo and in vitro

2004 ◽  
Vol 46 (3) ◽  
pp. 275-282 ◽  
Author(s):  
Sussie Dalvin ◽  
Katsumi Komatsuzaki ◽  
Mark A. Anselmo ◽  
David E. Kling ◽  
Jay J. Schnitzer ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Mesenchymal Cell ◽  
Fetal Lung

Retinoic acid modulation of the early development of the inner ear is associated with the control of c-fos expression

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1081-1090 ◽  
Author(s):  
J. Represa ◽  
A. Sanchez ◽  
C. Miner ◽  
J. Lewis ◽  
F. Giraldez
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Inner Ear ◽  
Early Development ◽  
Otic Vesicle ◽  
Low Concentrations ◽  
Full Effect ◽  
20 Nm ◽  
Otic Vesicles

The effects of retinoic acid (RA) on the early development of the inner ear were studied in vitro using isolated chick embryo vesicles. Low concentrations of RA (1–50 nM) inhibited vesicular growth in stage 18 otic vesicles that were made quiescent and then reactivated by either serum or bombesin. Growth inhibition was concentration-dependent and was paralleled by a reduction in the rate of DNA synthesis as measured by [3H]thymidine incorporation. Half-inhibition occurred between 1 and 10 nM RA, and the full effect at 20 nM. Retinoic acid, in the presence of serum, induced the precocious differentiation of (1) secretory epithelium, the tegmentum vasculosum and endolymphatic sac and (2) early sensory and supporting epithelia. These structures were positioned in their corresponding normal presumptive areas. The overall direction of growth was reversed by RA and the ratio of the internal to the external vesicular surface area increased with RA concentration. The expression of the nuclear proto-oncogene c-fos in the developing otic vesicle was transient and stage-dependent. High levels of c-fos mRNA were positively correlated with cell proliferation. Incubation of growth-arrested otic vesicles with bombesin plus insulin at concentrations that induced cell proliferation produced a strong induction of c-fos. This mitogen-induced expression was suppressed by 25 nM RA. The results suggest (1) a role for retinoic acid in controlling the early development of the inner ear and (2) that this control is effected through the regulation of the proto-oncogene c-fos.

scholarly journals Preparation and Characterization of Coaxial Electrospinning rhBMP2-Loaded Nanofiber Membranes

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
He Zhao ◽  
Yali Ma ◽  
Dahui Sun ◽  
Wendi Ma ◽  
Jihang Yao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Drug Release ◽  
Osteogenic Differentiation ◽  
Release Behavior ◽  
Promote Cell Proliferation ◽  
Drug Release Behavior ◽  
One Step ◽  
Nanofiber Membranes ◽  
Dual Release

DEX and rhBMP2-loaded core-shell nanofiber membranes were synthesized by electrospinning method in one step. Zein/PLLA, Zein-DEX/PLLA, Zein/PLLA-rhBMP2, and Zein-DEX/PLLA-rhBMP2 were fabricated; and morphology, hydrophilicity, mechanics properties, in vitro drug release behavior, cell proliferation, and osteogenic differentiation were investigated. The results showed that the dual-release system containing rhBMP2 and DEX prepared by electrospinning had rough surface, constant drug release behavior, and could also significantly promote cell proliferation and osteogenic differentiation of RMSCs, indicating that the scaffolds we fabricated might be suitable for bone tissue engineering.

scholarly journals Actions and Potential Therapeutic Applications of Growth Hormone–Releasing Hormone Agonists

Endocrinology ◽  
2019 ◽  
Vol 160 (7) ◽  
pp. 1600-1612 ◽  
Author(s):  
Andrew V Schally ◽  
Xianyang Zhang ◽  
Renzhi Cai ◽  
Joshua M Hare ◽  
Riccarda Granata ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cardiac Tissue ◽  
Human Cancer ◽  
Large Body ◽  
Neuroprotective Effects ◽  
Promote Cell Proliferation ◽  
Therapeutic Applications ◽  
Human Cancer Cells

Abstract In this article, we briefly review the identification of GHRH, provide an abridged overview of GHRH antagonists, and focus on studies with GHRH agonists. Potent GHRH agonists of JI and MR class were synthesized and evaluated biologically. Besides the induction of the release of pituitary GH, GHRH analogs promote cell proliferation and exert stimulatory effects on various tissues, which express GHRH receptors (GHRH-Rs). A large body of work shows that GHRH agonists, such as MR-409, improve pancreatic β-cell proliferation and metabolic functions and facilitate engraftment of islets after transplantation in rodents. Accordingly, GHRH agonists offer a new therapeutic approach to treating diabetes. Various studies demonstrate that GHRH agonists promote repair of cardiac tissue, producing improvement of ejection fraction and reduction of infarct size in rats, reduction of infarct scar in swine, and attenuation of cardiac hypertrophy in mice, suggesting clinical applications. The presence of GHRH-Rs in ocular tissues and neuroprotective effects of GHRH analogs in experimental diabetic retinopathy indicates their possible therapeutic applications for eye diseases. Other effects of GHRH agonists, include acceleration of wound healing, activation of immune cells, and action on the central nervous system. As GHRH might function as a growth factor, we examined effects of GHRH agonists on tumors. In vitro, GHRH agonists stimulate growth of human cancer cells and upregulate GHRH-Rs. However, in vivo, GHRH agonists inhibit growth of human cancers xenografted into nude mice and downregulate pituitary and tumoral GHRH-Rs. Therapeutic applications of GHRH analogs are discussed. The development of GHRH analogs should lead to their clinical use.

NRF2 Mediates Neuroblastoma Proliferation and Resistance to Retinoic Acid Cytotoxicity in a Model of In Vitro Neuronal Differentiation

2015 ◽  
Vol 53 (9) ◽  
pp. 6124-6135 ◽  
Author(s):  
Vitor de Miranda Ramos ◽  
Alfeu Zanotto-Filho ◽  
Matheus Augusto de Bittencourt Pasquali ◽  
Karina Klafke ◽  
Juciano Gasparotto ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation
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