scholarly journals Vessel wall signal enhancement on 3-T MRI in acute stroke patients after stent retriever thrombectomy

2017 ◽  
Vol 42 (4) ◽  
pp. E20 ◽  
Author(s):  
Peter Abraham ◽  
J. Scott Pannell ◽  
David R. Santiago-Dieppa ◽  
Vincent Cheung ◽  
Jeffrey Steinberg ◽  
...  
Keyword(s):  
Scale Score ◽  
Vessel Wall ◽  
Biological Effects ◽  
Endothelial Damage ◽  
Stent Retriever ◽  
Endothelial Injury ◽  
Control Group ◽  
Contrast Enhanced

OBJECTIVE In vivo and in vitro studies have demonstrated histological evidence of iatrogenic endothelial injury after stent retriever thrombectomy. However, noncontrast vessel wall (VW)–MRI is insufficient to demonstrate vessel injury. Authors of this study prospectively evaluated iatrogenic endothelial damage after stent retriever thrombectomy in humans by utilizing high-resolution contrast-enhanced VW-MRI. Characterization of VW-MRI changes in vessels subject to mechanical injury from thrombectomy may allow better understanding of the biological effects of this intervention. METHODS The authors prospectively recruited 11 patients for this study. The treatment group included 6 postthrombectomy patients and the control group included 5 subjects undergoing MRI for nonvascular indications. All subjects were evaluated on a Signa HD× 3.0-T MRI scanner with an 8-channel head coil. Both pre- and postcontrast T1-weighted Cube VW images as well as MR angiograms were acquired. Sequences obtained for evaluation of the brain parenchyma included diffusion-weighted, gradient echo, and T2-FLAIR imaging. Two independent neuroradiologists, who were blinded to the treatment status of each patient, determined the presence of VW enhancement. Patient age, National Institutes of Health Stroke Scale score on presentation, location of occlusion, stroke etiology, type of device used, number of device deployments, Thrombolysis in Cerebral Infarction (TICI) reperfusion score, stroke volume, and 90-day modified Rankin Scale score were also noted. RESULTS Postcontrast T1-weighted VW enhancement was detected in the M2 segment in 100% of the thrombectomy patients, in the M1 segment in 83%, and in the internal carotid artery in 50%. One patient also demonstrated A1 segment enhancement, which was attributable to thrombectomy treatment of that vessel segment during the same procedure. None of the control patients demonstrated VW enhancement of their intracranial vasculature on T1-weighted images. CONCLUSIONS The study findings suggest that VW injury incurred during stent retriever thrombectomy can be reliably detected utilizing contrast-enhanced 3-T VW-MRI. The results further demonstrate that endothelial injury is associated with oversizing of stent retrievers relative to the treated vessel. Further studies are needed to evaluate the clinical significance of endothelial injury and to characterize the differential effects of various devices.

Inhibition Effects of baicalin on Lymphoma Cell Line CA46 in Vitro and in Vivo

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5053-5053
Author(s):  
Jian Da Hu ◽  
Yi Huang ◽  
Yingyu Chen ◽  
Tiannan Wei ◽  
Tingbo Liu ◽  
...  
Keyword(s):  
Cell Line ◽  
Biological Effects ◽  
Annexin V ◽  
Lymphoma Cell ◽  
Control Group ◽  
Dependent Manner ◽  
Lymphoma Cell Line ◽  
Proliferation Inhibition

Abstract Baicalin is a traditional Chinese medicine with multiple biological effects. Some researches showed baicalin has anti-tumor effects in solid tumor, such as prostate cancer. In order to investigate its effects on proliferation inhibition and apoptosis induction in human lymphoma cell, we treated Burkitt lymphoma cell line CA46 with baicalin in vitro and in vivo of CA46 xenograft. Baicalin remarkably inhibited the cell proliferation, with an IC50 value of 10μM. Apoptosis was remarkably induced by baicalin in a dose-dependent manner, which was detected by Annexin V FITC/PI double staining analysis, TUNEL labeling method and DNA fragmentation respectively. Furthermore, RT-PCR showed that the mRNA expressions of c-myc and bcl-2 in treated CA46 cell decreased in a time-dependent manner. Western-Blot showed that the protein expressions of c-myc, bcl-2, procaspase-3 and PARP(116KD) in baicalin treated CA46 cell were down-regulated, while the expression of PARP(85KD) increased. Based on the results in vitro, we investigated in vivo efficacy of baicalin, alone or in combination with cytotoxic drug VP16, for treatment in CA46 nude mice xenograft. Baicalin with the dosage of 40mg/kg/d and 80kg/mg/d could remarkably inhibit the growth of the tumor compared with control group. Combination of baicalin and VP16 had better anti-tumor effects. Histological examination of tumor samples showed more necrotic cells in treated groups. And obvious apoptosis could be observed by electron microscope. No adverse events were found in treated groups. From above we could conclude that baicalin could efficiently induce proliferation inhibition and apoptosis of CA46 cells in vitro and in vivo, which may be related with the down-regulation of c-myc and bcl-2 expressions, as well as the up-regulation of caspase-3 activity.

scholarly journals Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

2017 ◽  
Vol 44 (6) ◽  
pp. 2395-2406 ◽  
Author(s):  
Li-yun Pan ◽  
Ya-feng Chen ◽  
Hong-chang Li ◽  
Li-ming Bi ◽  
Wen-jie Sun ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Serum Amylase ◽  
Endothelial Damage ◽  
Intestinal Injury ◽  
Control Group ◽  
Rt Pcr ◽  
Intestinal Tissue ◽  
Tnf Α

Background/Aims: Dachengqi decoction (DCQD) is a well-known traditional Chinese herbal drug with strong anti-inflammatory effects. Angiopoietin-1 (Ang-1) plays a vital role in maintaining the stability and integrity of the vascular wall and prevents vascular leakage due to inflammatory mediators. Our previous work found that DCQD protects against pancreatic injury in rats with severe acute pancreatitis (SAP). This study aims to investigate the effects of DCQD on intestinal endothelial damage in both damaged human umbilical vein endothelial cells (HUVECs) and SAP rats. Methods: HUVECs were randomly divided into four groups: control group, TNF-α group, TNF-α plus Ang-1 group (Ang-1 group), and TNF-α plus DCQD group (DCQD group). Cells were incubated for 6 h, 12 h, and 24 h, before collection. The treatment concentration of DCQD was decided based on a Cell Counting Kit-8 (CCK-8) assay. The monolayer permeability of the HUVECs was assessed by measuring the transendothelial electrical resistance (TEER). Apoptosis was analyzed by flow cytometry. mRNA and protein expression of aquaporin 1 (AQP-1), matrix metalloproteinase 9 (MMP9), and junctional adhesion molecule-C (JAM-C) was evaluated by RT-PCR, immunocytofluorescence, and western blot. Forty male Sprague-Dawley rats were randomized into a control group, SAP group, SAP plus Ang-1 group (Ang-1 group), and SAP plus DCQD group (DCQD group). SAP was induced by intraperitoneal injection of cerulein and lipopolysaccharide (LPS), while the control group received 0.9% saline solution. Evans blue was injected through the penile vein and the rats were then sacrificed 12 h after modeling. Levels of serum amylase, TNF-α, IL-1β, IL-2, and IL-6 were determined by using ELISA. Intestinal tissue was analysed by histology, and capillary permeability in the tissues was evaluated by Evans blue extravasation assay. Protein and mRNA expression of AQP-1, MMP9, and JAM-C were assessed by immunohistofluorescence, western blot, and RT-PCR. Results: DCQD reduced the permeability of HUVEC induced by TNF-α in vitro. Furthermore, DCQD altered the mRNA and protein levels of JAM-C, MMP9, and AQP-1 in HUVECs after TNF-α induction. SAP intestinal injury induced by cerulein combined with lipopolysaccharides was concomitant with increased expression of JAM-C and MMP9, and reduced expression of AQP-1 in intestinal tissue. Pretreatment with DCQD attenuated SAP intestinal injury and lowered the levels of serum amylase, TNF–α, IL-1β, IL-2, and IL-6 effectively. Our study demonstrated that DCQD decreased the expression of JAM-C and MMP9 and increased the expression of AQP-1 both in vitro and in vivo. Conclusion: DCQD can reduce capillary endothelial damage in acute pancreatitis-associated intestinal injury and the mechanism may be associated with the regulation of endothelial barrier function-associated proteins AQP-1, MMP9, and JAM-C.

scholarly journals Insightful Valorization of the Biological Activities of Pani Heloch Leaves through Experimental and Computer-Aided Mechanisms

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 5153
Author(s):  
Naureen Banu ◽  
Najmul Alam ◽  
Mohammad Nazmul Islam ◽  
Sanjida Islam ◽  
Shahenur Alam Sakib ◽  
...  
Keyword(s):  
Secondary Metabolites ◽  
Methanol Extract ◽  
Biological Activities ◽  
Biological Effects ◽  
Experimental Models ◽  
Clot Lysis ◽  
Control Group ◽  
Anti Inflammatory

Pani heloch (Antidesma montanum) is traditionally used to treat innumerable diseases and is a source of wild vegetables for the management of different pathological conditions. The present study explored the qualitative phytochemicals; quantitative phenol and flavonoid contents; in vitro antioxidant, anti-inflammatory, and thrombolytic effects; and in vivo antipyretic and analgesic properties of the methanol extract of A. montanum leaves in different experimental models. The extract exhibited secondary metabolites including alkaloids, flavonoids, flavanols, phytosterols, cholesterols, phenols, terpenoids, glycosides, fixed oils, emodines, coumarins, resins, and tannins. Besides, Pani heloch showed strong antioxidant activity (IC50 = 99.00 µg/mL), while a moderate percentage of clot lysis (31.56%) in human blood and significant anti-inflammatory activity (p < 0.001) was achieved with the standard. Moreover, the analgesic and antipyretic properties appeared to trigger a significant response (p < 0.001) relative to in the control group. Besides, an in silico study of carpusin revealed favorable protein-binding affinities. Furthermore, the absorption, distribution, metabolism, excretion, and toxicity analysis and toxicological properties of all isolated compounds adopted Lipinski’s rule of five for drug-like potential and level of toxicity. Our research unveiled that the methanol extract of A. montanum leaves exhibited secondary metabolites that are a good source for managing inflammation, pyrexia, pain, and cellular toxicity. Computational approaches and further studies are required to identify the possible mechanism which responsible for the biological effects.

Abstract 1122‐000112: In Vitro Investigation of Endothelial Injury During Mechanical Thrombectomy for Ischemic Stroke

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Maxim Mokin ◽  
Ana Martinez ◽  
Zackary Lorton ◽  
Julia Kretz ◽  
Chris Bashur ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Mechanical Thrombectomy ◽  
Endothelial Damage ◽  
Stent Retriever ◽  
Endothelial Injury ◽  
Immunofluorescent Staining ◽  
Lumen Diameter ◽  
Stent Retrievers

Introduction : Ischemic stroke (IS) makes up a significant proportion of all strokes, of which large vessel occlusions (LVO) are the most debilitating type. The current clinical standard‐of‐care for IS includes mechanical thrombectomy with stent retrievers. One of the impediments to the success of SR intervention is endothelial injury (EI), which can occur in approximately 30% of cases and impedes vessel reperfusion. Since successful reperfusion of the occluded vessel is instrumental in survival and patient recovery, it is imperative to reduce device injury‐based complications such as vasospasm, and to improve patient outcomes. Methods : In this work, our hypothesis is that EI can be reduced by investigating the mechanisms of stent retriever‐induced injury in vitro using live cell 3D cerebrovascular models. Using true‐scale cerebrovascular phantoms with lumen diameter approximately 4 mm created using 3D printing and PDMS casting, Human Umbilical Vein Endothelial Cells (HUVECs) were seeded on the luminal surface. The in vitro models were coated with fibronectin (density 4 µgrams/cm2) to encourage cell adhesion, and were divided into control and treated samples (n = 3 each). Mechanical thrombectomy was performed using two different clinically used SR (Trevo XP PROVUE 3 × 20 mm and Trevo XP PROVUE 6 × 30 mm) to investigate the extent of stent retriever size on EI on the same diameter lumen. Following thrombectomy, the cerebrovascular models were fixed and stained with immunofluorescent dyes (DAPI, Phalloidin and VE cadherin antibody) and imaged using transmitted light, confocal microscopy and scanning electron microscopy. For quantitative assessment, real time PCR was performed on both control and treated samples. Results : All models were initially confluent and functional, as assessed by immunofluorescent staining (Figure 1 A and B). All treated samples demonstrated EI and endothelial damage, as evidenced by loss of endothelial cell coverage, denuding of the models, stripping / clumping of endothelial cells into non‐physiological three dimensional structures and physical scratching of the in vitro model (Figure 1 C and D). Sizing of stent retriever had a strong influence on the effects on the endothelium, with larger sizes causing more damage. Conclusions : A significant knowledge gap exists in understanding the factors responsible for disruption of the endothelium during mechanical thrombectomy. Using a 3D in vitro platform of cerebrovasculature, we demonstrated that endothelial damage occurs during thrombectomy using stent retrievers. A parameteric investigation is currently ongoing that characterizes the influence of vessel lumen diameter, stent retriever size, number of passes and patient specific vasculature. This work can provide guidelines for optimal stent retriever devices to be used where possible, ultimately reducing EI and improving outcomes of ischemic stroke treatment.

scholarly journals Biological Effects and Biodistribution of Bufotenine on Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Hugo Vigerelli ◽  
Juliana Mozer Sciani ◽  
Maria Andrea Camarano Eula ◽  
Luciana Almeida Sato ◽  
Marta M. Antoniazzi ◽  
...  
Keyword(s):  
Biological Effects ◽  
Cellular Damage ◽  
Control Group ◽  
Behavioral Alterations ◽  
Incurable Disease ◽  
Neurological Effects ◽  
High Doses ◽  
Higher Doses

Bufotenine is an alkaloid derived from serotonin, structurally similar to LSD and psilocin. This molecule is able to inhibit the rabies virus infection in in vitro and in vivo models, increasing the survival rate of infected animals. Being a very promising molecule for an incurable disease and because of the fact that there is no consensus regarding its neurological effects, this study aimed to evaluate chronic treatment of bufotenine on behavior, pathophysiology, and pharmacokinetics of mice. Animals were daily treated for 21 consecutive days with 0.63, 1.05, and 2.1 mg/animal/day bufotenine and evaluated by open field test and physiological parameters during all the experiment. After this period, organs were collected for histopathological and biodistribution analysis. Animals treated with bufotenine had mild behavioral alterations compared to the control group, being dose-response relationship. On the other hand, animals showed normal physiological functions and no histological alterations in the organs. With high doses, an inflammatory reaction was observed in the site of injection, but with no cellular damage. The alkaloid could be found in the heart and kidney with all doses and in the lungs and brain with higher doses. These results show that the effective dose, 0.63 mg/day, is safe to be administered in mice, since it did not cause significant effects on the animals’ physiology and on the CNS. Higher doses were well tolerated, causing only mild behavioral effects. Thus, bufotenine might be a drug prototype for rabies treatment, an incurable disease.

scholarly journals Influence of Porous Dressings Based on Butyric-Acetic Chitin Co-Polymer on Biological Processes In Vitro and In Vivo

Materials ◽  
2019 ◽  
Vol 12 (6) ◽  
pp. 970 ◽  
Author(s):  
Witold Sujka ◽  
Zbigniew Draczynski ◽  
Beata Kolesinska ◽  
Ilona Latanska ◽  
Zenon Jastrzebski ◽  
...  
Keyword(s):  
Wound Healing ◽  
Subcutaneous Tissue ◽  
Biological Effects ◽  
Skin Irritation ◽  
Early Period ◽  
In Vivo Studies ◽  
Control Group ◽  
Dressing Materials

In spite of intensively conducted research allowing for the development of more and more advanced wound dressing materials, there is still a need for dressings that stimulate not only reparative and regenerative processes, but also have a positive effect on infected and/or difficult-to-heal wounds. Porous dressing materials based on butyric-acetic chitin co-polyester containing 90% of butyryl and 10% of acetyl groups (BAC 90/10) can also be included in the group mentioned above. Two types of dressings were obtained by the salt leaching method, i.e. a porous sponge Medisorb R and Medisorb Ag with an antibacterial additive. The aim of the study was to evaluate biological effects of porous Medisorb R and Medisorb Ag dressings under in vitro and in vivo conditions. In an in vitro biodegradation test, no mass loss of Medisorb R dressing was observed within 14 days of incubation in physiological fluids at 37 °C. However, on the basis of the FTIR (Fourier Transform Infrared Spectroscopy) tests, surface degradation of Medisorb R dressing was observed. Additionally, the antibacterial activity of the porous Medisorb Ag dressing containing microsilver as an antibacterial additive was confirmed. The in vivo studies included inflammatory activity, skin irritation and sensitisation tests, as well an assessment of local effect after contact with subcutaneous tissue up to 6 months and skin wounds up to 21 days. In the in vivo tests, the dressings exhibited neither effects of skin irritation nor sensitisation. Under macroscopic examination, in full thickness defects of subcutaneous tissue and skin, the dressings caused wound healing with no inflammation, undergoing the most gradual biodegradation between weeks 4 and 8, and the observed differences were statistically significant. In the histological assessment, a weakened, limited inflammatory process associated with degradation of the material has been observed. The process of skin wound healing under Medisorb R dressing in the early period was accelerated compared to that observed in the control group with a gauze dressing.

scholarly journals Neohesperidin Protects Hypertension-induced Endothelial Injury by Intervening Oxidative Stress

2021 ◽  
Author(s):  
Jingsi Zhang ◽  
Yuanshu Hui ◽  
Fengyi Liu ◽  
Qian Yang ◽  
Yi Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Inflammation ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Vascular Endothelial ◽  
Ang Ii ◽  
Induced Hypertension ◽  
And Oxidative Stress

Abstract Background: Currently, vascular endothelial damage caused by hypertension is one of the major health challenges facing countries around the world. Neohesperidin has been shown to play an important role in tumorigenesis and tumorigenesis, cardiac hypertrophy and remodeling, and oxidative stress. However, whether Nehesperidin plays an important role in endothelial injury induced by hypertension has not been clarified.Results: In this study, Angiotensin II was used to induce hypertension in mice. Blood pressure and vasoconstrictor function were measured, vascular thickness and fibrosis were detected by H&E and Masson tricolor staining, vascular inflammation was detected by immunofluorescence, oxidative stress was detected by DHE staining, and markers such as fibrosis, hypertrophy and oxidative stress were detected by qPCR. At the same time, we observed the effect of Nehesperidin on Ang II-induced HUVECs. The results showed that neohesperidin can significantly inhibit Ang II-induced hypertension, vascular thickness, fibrosis, oxidative stress and inflammation in vivo and in vitro. Conclusions: The results suggested that Nehesperidin could act as an antioxidant to significantly inhibit Ang II-induced hypertension and endothelial injury in HUVECs in mice by inhibiting oxidative stress response.

Models Of Granulocyte-Mediated Endothelial Injury In Vitro

1981 ◽  
Author(s):  
G Vercellotti ◽  
P Flynn ◽  
D Weisdorf ◽  
C J Lammi-Keefe ◽  
H Jacob ◽  
...  
Keyword(s):  
Lipid A ◽  
Umbilical Vein ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Free Radical Scavengers ◽  
Methyl Prednisolone ◽  
Vitro Model ◽  
Umbilical Vein Endothelial Cells

To determine the role of neutrophil (PMN) induced vascular injury during inflammation an in vitro model of endothelial damage was investigated. Injury to human umbilical vein endothelial cells (EC) labeled with 51Cr or 14c sodium arachidonate was monitored by specific release of these labels or their products. Several agents were capable of triggering PMN to induce significant EC injury: these include activated serum complement (C') opsonized particles, serotonin , phorbol myristate acetate, and the lipid A moiety of endotoxin. PMN must adhere closely to the EC for effective cytotoxicity, since agents which retard PMN adherence (cytochalasin B, methyl prednisolone) inhibit 51Cr release.Lyscsorcal proteases did not mediate PMN induced endothelial injury since there was no correlation between release and injury, and soluble stimuli which did not release lysosomal contents induced injury. Free radical scavengers such as SOD/catalase, and a-tocopherol significantly reduced PMN mediated endothelial injury implying that PMN generated reactive oxygen species were responsible for this damage.To further study PMN mediated endothelial injury, other inflammatory agents were also utilized. C' activated PMN’s exposed to Ibuprofen (I) (50 μg/ml) but not Aspirin (ASA) (200 μg/ml) induced no EC injury (51cr releasey Furthermore, it was shown that I inhibits O- 2 production, blocks release of PMN lysozyme and glucuronidase, and inhibits aggregation of C' stimulated PMN’s. ASA at doses of 500 μg/ml (clinically toxic), failed to inhibit these in vitro activities. This data suggests that I’s anti-inflammatory affect may be expressed through inhibition of PMN functions. Since I and ASA both inhibit cyclooxygenase, but only I modulated PMN induced endothelial injury, these agents may provide useful probes to elucidate PMN-endothelial interactions in vivo.

Improved dialytic removal of protein-bound uremic toxins by intravenous lipid emulsion in chronic kidney disease rats

2019 ◽  
Vol 34 (11) ◽  
pp. 1842-1852 ◽  
Author(s):  
Yuanyuan Shi ◽  
Yumei Zhang ◽  
Huajun Tian ◽  
Yifeng Wang ◽  
Yue Shen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Emulsion ◽  
Biological Effects ◽  
Inhibitory Effect ◽  
Uremic Toxins ◽  
Control Group ◽  
Rat Serum ◽  
Intravenous Lipid Emulsion

AbstractBackgroundProtein-bound uremic toxins (PBUTs) have received extensive attention, as their accumulation leads to pleiotropic toxic biological effects, while the removal of these solutes by conventional dialysis therapies is severely hampered. This study aimed to examine whether increased removal of PBUTs could be achieved with intravenous lipid emulsion (ILE).MethodsPBUTs such as 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid (CMPF), p-cresyl sulfate (PCS) and indoxyl sulfate (IS) were spiked with human serum albumin (HSA) solution and the inhibitory effects of free fatty acid (FFA) on the binding of CMPF, PCS and IS to HSA were examined separately in vitro by ultrafiltration. In vitro dialysis of albumin solution was then performed to investigate the effects of fatty acid (FAs) mixtures infusion on the fractional removal of PBUTs. Finally, the inhibitory effect of FFA on the binding of PBUTs to albumin was examined in uremic rats, and blood purification therapy was conducted to calculate the reduction ratio (RR) and the total solute removal (TSR) of solutes.ResultsThe percentage protein binding of CMPF, PCS and IS decreased significantly with increasing FFAs concentrations, and the inhibitory effect was more remarkable with the addition of oleic acid or linoleic acid than that of eicosapentaenoic acid and docosahexaenoic acid. In vitro infusion of FAs increased the fractional removal of CMPF to 14.40 ± 2.38%. PCS, IS and indole-3-acetic acid removal increased from 8.00 ± 2.43%, 11.68 ± 1.54% and 15.38 ± 3.97%, respectively, at baseline to 28.21 ± 5.99%, 35.42 ± 5.27% and 40.18 ± 5.05%, respectively, when FAs were present. In vivo, rat serum concentrations of free PBUTs were significantly higher in the ILE group than in the control group, and administration of ILE resulted in higher RRs and more TSR for PBUTs after 3 h of hemodialysis (HD) therapy compared with the control group.ConclusionsAdministration of ILE effectively increased the dialytic removal of PBUTs. This method could be applied to current HD therapy.

In-vitro- und In-vivo-Wirkung von Schilddrüsenhormon auf das Wachstum von Neuroblastomzellen

1990 ◽  
Vol 29 (03) ◽  
pp. 120-124
Author(s):  
R. P. Baum ◽  
E. Rohrbach ◽  
G. Hör ◽  
B. Kornhuber ◽  
E. Busse
Keyword(s):  
Cell Differentiation ◽  
Neuroblastoma Cells ◽  
Control Group ◽  
Initial Value ◽  
Initial Rise ◽  
Biphasic Effect ◽  
Contrast Microscopy ◽  
Morphological Sign

The effect of triiodothyronine (T3) on the differentiation of cultured neuroblastoma (NB) cells was studied after 9 days of treatment with a dose of 10-4 M/106 cells per day. Using phase contrast microscopy, 30-50% of NB cells showed formation of neurites as a morphological sign of cellular differentiation. The initial rise of the mitosis rate was followed by a plateau. Changes in cyclic nucleotide content, in the triphosphates and in the activity of the enzyme ornithine decarboxylase (ODC) were assessed in 2 human and 2 murine cell lines to serve as biochemical parameters of the cell differentiation induced by T3. Whereas the cAMP level increased significantly (3 to 7 fold compared with its initial value), the cGMP value dropped to 30 to 50% of that of the control group. ATP and GTP increased about 200%, the ODC showed a decrease of about 50%. The present studies show a biphasic effect of T3 on neuroblastoma cells: the initial rise of mitotic activity is followed by increased cell differentiation starting from day 4 of the treatment.

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