scholarly journals Cinnamaldehyde enhances in vitro parameters of immunity and reduces in vivo infection against avian coccidiosis

2011 ◽  
Vol 106 (6) ◽  
pp. 862-869 ◽  
Author(s):  
Sung Hyen Lee ◽  
Hyun S. Lillehoj ◽  
Seung I. Jang ◽  
Kyung Woo Lee ◽  
Myeong Seon Park ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Interferon Γ ◽  
Antibody Responses ◽  
Chicken Spleen ◽  
Intestinal Lymphocytes ◽  
Avian Coccidiosis ◽  
Spleen Lymphocytes ◽  
Stimulation Of

The effects of cinnamaldehyde (CINN) on in vitro parameters of immunity and in vivo protection against avian coccidiosis were evaluated. In vitro stimulation of chicken spleen lymphocytes with CINN (25–400 ng/ml) induced greater cell proliferation compared with the medium control (P < 0·001). CINN activated cultured macrophages to produce higher levels of NO at 1·2–5·0 μg/ml (P < 0·001), inhibited the growth of chicken tumour cells at 0·6–2·5 μg/ml (P < 0·001) and reduced the viability of Eimeriatenella parasites at 10 and 100 μg/ml (P < 0·05 and P < 0·001, respectively), compared with media controls. In chickens fed a diet supplemented with CINN at 14·4 mg/kg, the levels of IL-1β, IL-6, IL-15 and interferon-γ transcripts in intestinal lymphocytes were 2- to 47-fold higher (P < 0·001) compared with chickens given a non-supplemented diet. To determine the effect of CINN diets on avian coccidiosis, chickens were fed diets supplemented with CINN at 14·4 mg/kg (E. maxima or E. tenella) or 125 mg/kg (E. acervulina) from hatch for 24 d, and orally infected with 2·0 × 104 sporulated oocysts at age 14 d. CINN-fed chickens showed 16·5 and 41·6 % increased body-weight gains between 0–9 d post-infection (DPI) with E. acervulina or E. maxima, reduced E. acervulina oocyst shedding between 5–9 DPI and increased E. tenella-stimulated parasite antibody responses at 9 DPI compared with controls.

scholarly journals Interferon-γ Induced by In Vitro Re-Stimulation of CD4+ T-Cells Correlates with In Vivo FMD Vaccine Induced Protection of Cattle against Disease and Persistent Infection

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e44365 ◽  
Author(s):  
Yooni Oh ◽  
Lucy Fleming ◽  
Bob Statham ◽  
Pip Hamblin ◽  
Paul Barnett ◽  
...  
Keyword(s):  
T Cells ◽  
Persistent Infection ◽  
Cd4 T Cells ◽  
Interferon Γ ◽  
Stimulation Of

scholarly journals A peptide that inhibits the mitogenic stimulation of Swiss 3T3 cells by bombesin or vasopressin

1985 ◽  
Vol 231 (3) ◽  
pp. 781-784 ◽  
Author(s):  
A N Corps ◽  
L H Rees ◽  
K D Brown
Keyword(s):  
Cell Proliferation ◽  
Synthetic Peptide ◽  
3T3 Cells ◽  
Wide Range ◽  
Vasopressin Receptors ◽  
Bombesin Receptor ◽  
Swiss 3T3 ◽  
Stimulation Of

The synthetic peptide [D-Arg1,D-Pro2,D-Trp7,9,Leu1]substance P inhibits the stimulation of DNA synthesis induced in Swiss 3T3 cells by bombesin or vasopressin, but not that induced by a wide range of other growth factors and mitogens. The stimulation induced by 10 pM-3 nM-bombesin is inhibited by 1-30 microM-antagonist in a manner consistent with competition at the bombesin receptor. The inhibition by the antagonist of the stimulation induced by vasopressin suggests a previously unrecognized interaction of the antagonist with vasopressin receptors. The antagonist should be useful in studies of cell proliferation both in vivo and in vitro.

scholarly journals IL-21 is the primary common γ chain-binding cytokine required for human B-cell differentiation in vivo

Blood ◽  
2011 ◽  
Vol 118 (26) ◽  
pp. 6824-6835 ◽  
Author(s):  
Mike Recher ◽  
Lucinda J. Berglund ◽  
Danielle T. Avery ◽  
Morton J. Cowan ◽  
Andrew R. Gennery ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
Humoral Immunity ◽  
Antibody Responses ◽  
Cytokine Signaling ◽  
Cell Engraftment ◽  
Cell Immunity

Abstract SCID resulting from mutations in IL2RG or JAK3 is characterized by lack of T and natural killer cells; B cells are present in normal number, but antibody responses are defective. Hematopoietic cell transplantation (HCT) is curative for SCID. However, B-cell dysfunction persists in a substantial proportion of patients. We hypothesized that impaired B-cell responses after HCT in IL2RG/JAK3 deficiency results from poor donor B-cell engraftment and defective γc-dependent cytokine signaling in host B cells. To test this, and to identify which γc cytokine(s) is critical for humoral immunity, we studied 28 transplanted patients with IL2RG/JAK3 deficiency. Lack of donor B-cell engraftment associated with persistent humoral dysfunction and significantly reduced memory B cells. B-cell proliferation induced by CD40L alone or together with CpG, anti-Ig, IL-4, IL-10, or IL-13 was comparable in healthy controls and in post-HCT SCID patients, irrespective of their chimerism status. However, in vitro stimulation with CD40L/IL-21 induced B-cell proliferation, plasmablast differentiation, and antibody secretion in patients with donor B cells, but not in patients with autologous B cells. These data imply that IL-21–mediated signaling is critical for long-lived humoral immunity and to restore antibody responses in IL2RG/JAK3-deficient patients after HCT. Furthermore, in vitro stimulation with CD40L/IL-21 can predict in vivo B-cell immunity in IL2RG/JAK3 SCID after transplantation.

scholarly journals Investigating the Effect of Biomaterials Such as Poly-(l-Lactic Acid) Particles on Collagen Synthesis In Vitro: Method Is Matter

2020 ◽  
Vol 11 (3) ◽  
pp. 51
Author(s):  
Subarna Ray ◽  
Hang T. Ta
Keyword(s):  
Cell Proliferation ◽  
Lactic Acid ◽  
Collagen Synthesis ◽  
Fibrous Tissue ◽  
Clinical Applications ◽  
In Vitro Method ◽  
Stimulation Of ◽  
Collagen Stimulation

Poly-l-lactic acid (PLLA), a synthetic, biocompatible, biodegradable polymer, has been safely used in several clinical applications in recent decades. Typically, SculptraTM, the commercially injectable PLLA in the form of microparticles, has been used as facial volumizer in the treatment of lipoatrophy in HIV patients. It also has various applications in tissue engineering by improving cell proliferation and adhesion. Sculptra™ can be categorised as a stimulatory filler as it stimulates the synthesis and deposition of fibrous tissue and collagen. Collagen is one of the most significant components of the extracellular matrix and beneficial for the normal physiology. It is also the structural component of a human body. In most of the studies, the effect of Sculptra on collagen synthesis was investigated in vivo and the majority of the data were from clinical and histological reports. There is only one study reporting this effect in vitro using fibroblasts. Here, we investigated whether PLLA in the form of nanoparticles can provide the same effect on collagen synthesis in fibroblasts as Sculptra. We surprisingly found that there was no stimulation of collagen in fibroblasts alone, whereas the co-cultures of fibroblast and macrophage had shown collagen stimulation by PLLA nanoparticles. It is also confirmed that collagen synthesis was caused by fibroblasts but not macrophages. Although further study needs to be conducted to evaluate its mechanism, our findings showed that choosing an appropriate method is essential for investigating the effect of PLLA or other biomaterials on collagen synthesis by fibroblasts in vitro.

scholarly journals Obesity Potentiates Esophageal Squamous Cell Carcinoma Growth and Invasion by AMPK-YAP Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jia-Huang Liu ◽  
Qi-Fei Wu ◽  
Jun-Ke Fu ◽  
Xiang-Ming Che ◽  
Hai-Jun Li
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Nude Mice ◽  
Serum Glucose ◽  
Migration And Invasion ◽  
Endocrine Effect

Obesity could increase the risk of esophageal squamous cell carcinoma (ESCC) and affect its growth and progression, but the mechanical links are unclear. The objective of the study was to explore the impact of obesity on ESCC growth and progression utilizing in vivo trials and cell experiments in vitro. Diet-induced obese and lean nude mice were inoculated with TE-1 cells, then studied for 4 weeks. Serum glucose, insulin, leptin, and visfatin levels were assayed. Sera of nude mice were obtained and then utilized to culture TE-1. MTT, migration and invasion assays, RT-PCR, and Western blotting were used to analyze endocrine effect of obesity on cell proliferation, migration, invasion, and related genes expression of TE-1. Obese nude mice bore larger tumor xenografts than lean animals, and were hyperglycemic and hyperinsulinemic with an elevated level of leptin and visfatin in sera, and also were accompanied by a fatty liver. As for the subcutaneous tumor xenograft model, tumors were more aggressive in obese nude mice than lean animals. Tumor weight correlated positively with mouse body weight, liver weight of mice, serum glucose, HOMA-IR, leptin, and visfatin. Obesity prompted significant TE-1 cell proliferation, migration, and invasion by endocrine mechanisms and impacted target genes. The expression of AMPK and p-AMPK protein decreased significantly ( P < 0.05 ); MMP9, total YAP, p-YAP, and nonphosphorylated YAP protein increased significantly ( P < 0.05 ) in the cells cultured with conditioned media and xenograft tumor from the obese group; the mRNA expression of AMPK decreased significantly ( P < 0.05 ); YAP and MMP9 mRNA expression increased significantly ( P < 0.05 ) in the cells exposed to conditioned media from the obese group. In conclusion, the altered adipokine milieu and metabolites in the context of obesity may promote ESCC growth in vivo; affect proliferation, migration, and invasion of ESCC cells in vitro; and regulate MMP9 and AMPK-YAP signaling pathway through complex effects including the endocrine effect.

scholarly journals Aberrantly high activation of a FoxM1–STMN1 axis contributes to progression and tumorigenesis in FoxM1-driven cancers

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Jun Liu ◽  
Jipeng Li ◽  
Ke Wang ◽  
Haiming Liu ◽  
Jianyong Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Soft Agar ◽  
Transcriptional Level ◽  
Regulation Mechanism ◽  
Strong Positive Correlation ◽  
Cell Viability Assay ◽  
High Level

AbstractFork-head box protein M1 (FoxM1) is a transcriptional factor which plays critical roles in cancer development and progression. However, the general regulatory mechanism of FoxM1 is still limited. STMN1 is a microtubule-binding protein which can inhibit the assembly of microtubule dimer or promote depolymerization of microtubules. It was reported as a major responsive factor of paclitaxel resistance for clinical chemotherapy of tumor patients. But the function of abnormally high level of STMN1 and its regulation mechanism in cancer cells remain unclear. In this study, we used public database and tissue microarrays to analyze the expression pattern of FoxM1 and STMN1 and found a strong positive correlation between FoxM1 and STMN1 in multiple types of cancer. Lentivirus-mediated FoxM1/STMN1-knockdown cell lines were established to study the function of FoxM1/STMN1 by performing cell viability assay, plate clone formation assay, soft agar assay in vitro and xenograft mouse model in vivo. Our results showed that FoxM1 promotes cell proliferation by upregulating STMN1. Further ChIP assay showed that FoxM1 upregulates STMN1 in a transcriptional level. Prognostic analysis showed that a high level of FoxM1 and STMN1 is related to poor prognosis in solid tumors. Moreover, a high co-expression of FoxM1 and STMN1 has a more significant correlation with poor prognosis. Our findings suggest that a general FoxM1-STMN1 axis contributes to cell proliferation and tumorigenesis in hepatocellular carcinoma, gastric cancer and colorectal cancer. The combination of FoxM1 and STMN1 can be a more precise biomarker for prognostic prediction.

scholarly journals BRD4 PROTAC degrader ARV-825 inhibits T-cell acute lymphoblastic leukemia by targeting 'Undruggable' Myc-pathway genes

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shuiyan Wu ◽  
You Jiang ◽  
Yi Hong ◽  
Xinran Chu ◽  
Zimu Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Acute Lymphoblastic Leukemia ◽  
Caspase 3 ◽  
Lymphoblastic Leukemia ◽  
Rna Seq ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Bet Protein

Abstract Background T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease with a high risk of induction failure and poor outcomes, with relapse due to drug resistance. Recent studies show that bromodomains and extra-terminal (BET) protein inhibitors are promising anti-cancer agents. ARV-825, comprising a BET inhibitor conjugated with cereblon ligand, was recently developed to attenuate the growth of multiple tumors in vitro and in vivo. However, the functional and molecular mechanisms of ARV-825 in T-ALL remain unclear. This study aimed to investigate the therapeutic efficacy and potential mechanism of ARV-825 in T-ALL. Methods Expression of the BRD4 were determined in pediatric T-ALL samples and differential gene expression after ARV-825 treatment was explored by RNA-seq and quantitative reverse transcription-polymerase chain reaction. T-ALL cell viability was measured by CCK8 assay after ARV-825 administration. Cell cycle was analyzed by propidium iodide (PI) staining and apoptosis was assessed by Annexin V/PI staining. BRD4, BRD3 and BRD2 proteins were detected by western blot in cells treated with ARV-825. The effect of ARV-825 on T-ALL cells was analyzed in vivo. The functional and molecular pathways involved in ARV-825 treatment of T-ALL were verified by western blot and chromatin immunoprecipitation (ChIP). Results BRD4 expression was higher in pediatric T-ALL samples compared with T-cells from healthy donors. High BRD4 expression indicated a poor outcome. ARV-825 suppressed cell proliferation in vitro by arresting the cell cycle and inducing apoptosis, with elevated poly-ADP ribose polymerase and cleaved caspase 3. BRD4, BRD3, and BRD2 were degraded in line with reduced cereblon expression in T-ALL cells. ARV-825 had a lower IC50 in T-ALL cells compared with JQ1, dBET1 and OTX015. ARV-825 perturbed the H3K27Ac-Myc pathway and reduced c-Myc protein levels in T-ALL cells according to RNA-seq and ChIP. In the T-ALL xenograft model, ARV-825 significantly reduced tumor growth and led to the dysregulation of Ki67 and cleaved caspase 3. Moreover, ARV-825 inhibited cell proliferation by depleting BET and c-Myc proteins in vitro and in vivo. Conclusions BRD4 indicates a poor prognosis in T-ALL. The BRD4 degrader ARV-825 can effectively suppress the proliferation and promote apoptosis of T-ALL cells via BET protein depletion and c-Myc inhibition, thus providing a new strategy for the treatment of T-ALL.

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