Immunohistochemical Analysis of Expression, Phosphorylation, and Nuclear Translocation of NF-κB Proteins in Human Tissues

2021 ◽  
pp. 27-42
Author(s):  
Davide Vecchiotti ◽  
Daniela Verzella ◽  
Daria Capece ◽  
Jessica Cornice ◽  
Mauro Di Vito Nolfi ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Immunohistochemical Analysis ◽  
Human Tissues

scholarly journals Immunohistochemical analysis of NY-ESO-1 antigen expression in normal and malignant human tissues

2001 ◽  
Vol 92 (6) ◽  
pp. 856-860 ◽  
Author(s):  
Achim A. Jungbluth ◽  
Yao-Tseng Chen ◽  
Elisabeth Stockert ◽  
Klaus J. Busam ◽  
Denise Kolb ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Antigen Expression ◽  
Human Tissues

scholarly journals Anti-Inflammatory Effect of Feiyangchangweiyan Capsule on Rat Pelvic Inflammatory Disease through JNK/NF-κB Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Yao Li ◽  
Yang Liu ◽  
Qian Yang ◽  
Zhihui Shi ◽  
Yanhua Xie ◽  
...  
Keyword(s):  
Pelvic Inflammatory Disease ◽  
Inflammatory Disease ◽  
Genital Tract ◽  
Nuclear Translocation ◽  
Immunohistochemical Analysis ◽  
Dependent Manner ◽  
Preventive Effect ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Inflammatory Effect

Objectives. In this study, we aimed to illustrate the preventive effect and possible mechanisms of Feiyangchangweiyan capsule (FYCWYC) on rat pelvic inflammatory disease (PID) model. Methods. To construct the rat PID model, upper genital tract was infected by multipathogen, and then drugs were orally administered for 8 days. The histological examination, immunohistochemical analysis, and ELISA were carried out. Furthermore, Western blotting was used to analyze the expression of Akt, MAPKs, NF-κB p65, and IκB-α in uterus. Results. As the results showed, infiltrations of neutrophils and lymphocytes in uterus were significantly suppressed, and IL-1β, IL-6, CXCL-1, and TNF-α were also reduced in a dose-dependent manner. We also found that FYCWYC inhibited apoptosis induced by infection. Furthermore, FYCWYC could block the infection-induced nuclear translocation of NF-κB. We found that FYCWYC treatment only decreased the phosphorylation of JNK induced by infection and had no effects on Akt and P38. Additional, the effects of SP600125, an inhibitor of phospho-JNK, were similar to the results of FYCWYC. Conclusions. Taken together, our results demonstrated that FYCWYC had anti-inflammatory effect in pathogen-induced PID model, and the mechanism might be through inhibiting NF-κB nuclear translocation which is mediated by JNK.

scholarly journals COMPARATIVE IMMUNOHISTOCHEMICAL EVALUATION OF E-CADHERIN AND Β-KATENIN EXPRESSION IN METASTATIC AND NON-METASTATIC BREAST CANCER OF NON-SPECIFIC TYPE

2018 ◽  
Vol 14 (2) ◽  
pp. 14-20
Author(s):  
M. V. Mnikhovich ◽  
L. V. Kakturskiy ◽  
T. V. Bezuglova ◽  
K. Yu. Midiber ◽  
K. V. Bun’kov ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nuclear Translocation ◽  
Metastatic Breast ◽  
Immunohistochemical Analysis ◽  
Immunohistochemical Method ◽  
Immune Reactivity ◽  
Study Group ◽  
Aberrant Expression ◽  
Total Absence ◽  
Favorable Prognosis

Objective:an immunohistochemical analysis of the features of expression, distribution and interaction of E-сadherin and β-сatenin proteins in primary mammary tumors.Materials and methods.The study group consisted of 148 relevant patients with breast cancer (BC), including patients with metastases in lymph nodes (n = 12) and liver (n = 45). E-сadherin and β-сatenin expression on BC cells was determined using immunohistochemical method with specific antibodies.Results.It was shown that the reduction and the total absence of E-сadherin expression was observed much more often in patients with BC with metastases in liver, than in patients without metastases (70 % of cases versus 30 % of cases respectively). An increase of cytoplasmic immune reactivity and a nuclear translocation of β-сatenin are found in more than 80 % cases of BC with metastases.Conclusion.The changes in the expression of E-сadherin and β-сatenin in tumor cell can be considered as factors of a non-favorable prognosis of BC. The emergence of β-сatenin expression indicates the activation of a signaling pathway which is triggered by the aberrant expression of epithelial cadherins leading to an increased mobility and invasion of tumor cells.

scholarly journals The protein expression profile of ACE2 in human tissues

2020 ◽  
Author(s):  
Feria Hikmet ◽  
Loren Méar ◽  
Åsa Edvinsson ◽  
Patrick Micke ◽  
Mathias Uhlén ◽  
...  
Keyword(s):  
Host Cell ◽  
Immunohistochemical Analysis ◽  
Cell Types ◽  
Cell Entry ◽  
Cell Surface Receptor ◽  
Renal Tubules ◽  
Human Tissues ◽  
Specific Expression ◽  
Ductal Cells ◽  
Host Cell Entry

ABSTRACTThe novel SARS-coronavirus 2 (SARS-CoV-2) poses a global challenge on healthcare and society. For understanding the susceptibility for SARS-CoV-2 infection, the cell type-specific expression of the host cell surface receptor is necessary. The key protein suggested to be involved in host cell entry is Angiotensin I converting enzyme 2 (ACE2). Here, we report the expression pattern of ACE2 across >150 different cell types corresponding to all major human tissues and organs based on stringent immunohistochemical analysis. The results were compared with several datasets both on the mRNA and protein level. ACE2 expression was mainly observed in enterocytes, renal tubules, gallbladder, cardiomyocytes, male reproductive cells, placental trophoblasts, ductal cells, eye and vasculature. In the respiratory system, the expression was limited, with no or only low expression in a subset of cells in a few individuals, observed by one antibody only. Our data constitutes an important resource for further studies on SARS-CoV-2 host cell entry, in order to understand the biology of the disease and to aid in the development of effective treatments to the viral infection.

Electroacupuncture Exerts An Anti-Inflammatory Effect in a Rat Tissue Chamber Model of Inflammation via Suppression of Nf-κB Activation

2014 ◽  
Vol 32 (4) ◽  
pp. 340-345 ◽  
Author(s):  
Fang Liu ◽  
Jianqiao Fang ◽  
Xiaomei Shao ◽  
Yi Liang ◽  
Yuanyuan Wu ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Diseases ◽  
Physiological Saline ◽  
Immunohistochemical Analysis ◽  
Underlying Mechanism ◽  
Nuclear Staining ◽  
Time Points ◽  
Beneficial Effects ◽  
Chamber Model ◽  
Rat Tissue

Objective Electroacupuncture (EA) has beneficial effects in patients with various inflammatory diseases. However, the underlying mechanism remains unclear. As the kappa B inhibitor/nuclear factor-kappa B (IκB/NF-κB) pathway exerts a pivotal role in the mammalian immune response, we examined the involvement of the IκB/NF-κB pathway in EA-induced anti-inflammation. Methods Ninety tissue chamber implanted rats were randomly divided into control (C), model (M) and EA (E) groups. Physiological saline and human recombinant interleukin-1β (hr IL-1β) were injected into the rats in groups C and M, respectively, and EA treatment was applied to the rats in group E after IL-1β injection. Nuclear staining of p65 (a subunit of NF-κB) was quantified in the exudate cells by immunohistochemical analysis and IκBα expression in the cytoplasm was quantified by western blot analysis. Results Our results showed that, compared with group C, the percentage of cells with nuclear-localised p65 was increased in group M by 71.3%, 50.7% and 33.1% at 1, 5 and 24 h time points (p<0.01), respectively. This increase was fully inhibited in group E at 5 and 24 h time points (p<0.01). The expression of IκBα was stably enhanced in group M (p<0.05) during the test period. Compared with group M, greater expression of IκBα in group E was only observed at the 1 h time point (p<0.01). Conclusions Collectively, our data suggest that EA inhibits the nuclear translocation of p65 and increases the expression of IκBα, which leads to the suppression of NF-κB activation in a rat tissue chamber model of inflammation.

scholarly journals IL-13 Augments Histone Demethylase JMJD2B/KDM4B Expression Levels, Activity, and Nuclear Translocation in Airway Fibroblasts in Asthma

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Khuloud Bajbouj ◽  
Mahmood Y. Hachim ◽  
Rakhee K. Ramakrishnan ◽  
Huwaida Fazel ◽  
Jumana Mustafa ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Immunohistochemical Analysis ◽  
Bioinformatic Analysis ◽  
Gene Expression Omnibus ◽  
Histone Demethylase ◽  
Lung Fibroblasts ◽  
Expression Levels ◽  
Downstream Target ◽  
Gene And Protein Expression ◽  
Bronchial Biopsies

Purpose. Asthma is one of the most common obstructive pulmonary diseases worldwide. Epigenetic alterations, including DNA methylation and histone modifications, have been reported to contribute to asthma pathogenesis. Since the inflammation mediator and remodeling trigger, IL-13, is known to play a central role in the pathophysiology of asthma, this study was aimed to identify novel IL-13-regulated epigenetic modifiers in asthma that may contribute to subepithelial fibrosis. Methods. Publicly available transcriptomic datasets from Gene Expression Omnibus (GEO) were used to identify differentially expressed genes on an epigenetic level upon IL-13 exposure in lung fibroblasts. Bronchial fibroblasts isolated from healthy and asthmatic individuals were assessed for the gene and protein expression levels of the identified gene at baseline and upon IL-13 treatment using qRT-PCR and western blotting, respectively. Its subcellular localization and tissue distribution were examined in bronchial fibroblasts as well as bronchial biopsies by immunofluorescence and immunohistochemical analysis, respectively. Results. Bioinformatic analysis revealed the differential expression of the histone demethylase JMJD2B/KDM4B, a well-known epigenetic modulator that leads to the demethylation of different lysine residues on histones, in IL-13-treated lung fibroblasts. The baseline expression levels of JMJD2B were higher in asthmatic fibroblasts and in bronchial biopsies in comparison to healthy ones. There was also an increase in JMJD2B activity as evidenced by the demethylation of its downstream target, H3K36me3. Furthermore, IL-13 stimulation induced JMJD2B expression and further demethylation of H3K36me3 in asthmatic fibroblasts. This was accompanied by increased translocation of JMJD2B into the nucleus. Conclusion. This study highlights the novel pathological involvement of the histone demethylase JMJD2B/KDM4B in asthmatic airway fibroblasts that are regulated by IL-13. Clinical implications. Given that there is no single therapeutic medicine to effectively treat the various subtypes of asthma, this study provides promising insights into JMJD2B as a new therapeutic target that could potentially improve the treatment and management of asthma.

Immunohistochemical analysis of Bin1/Amphiphysin II in human tissues: Diverse sites of nuclear expression and losses in prostate cancer

2003 ◽  
Vol 88 (3) ◽  
pp. 635-642 ◽  
Author(s):  
James B. DuHadaway ◽  
Frank J. Lynch ◽  
Shawn Brisbay ◽  
Carlos Bueso-Ramos ◽  
Patricia Troncoso ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Immunohistochemical Analysis ◽  
Human Tissues ◽  
Nuclear Expression

Immunohistochemical analysis of P185 and ASL activity in transformed human tissues

1997 ◽  
Vol 30 (3) ◽  
pp. 285
Author(s):  
L. Terzuoli ◽  
B. Frosi ◽  
B. Porcelli ◽  
F. Carlucci ◽  
C. Minacci ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Human Tissues

Estrogen-induced upregulation of AR expression and enhancement of AR nuclear translocation in mouse fallopian tubes in vivo

2007 ◽  
Vol 292 (2) ◽  
pp. E604-E614 ◽  
Author(s):  
Ruijin Shao ◽  
Karin Ljungström ◽  
Birgitta Weijdegård ◽  
Emil Egecioglu ◽  
Julia Fernandez-Rodriguez ◽  
...  
Keyword(s):  
Fallopian Tube ◽  
Time Course ◽  
Nuclear Translocation ◽  
Immunohistochemical Analysis ◽  
Subsequent Treatment ◽  
Dependent Manner ◽  
Fallopian Tubes ◽  
Testosterone Levels ◽  
17Β Estradiol

Female mice lacking AR display alterations in ovarian and uterine function. However, the biology of AR in the fallopian tube is not fully understood. To gain an insight into potential roles of AR in this tissue, we demonstrated that eCG treatment increased AR expression in a time-dependent manner and subsequent treatment with hCG decreased AR expression in mouse fallopian tubes. This expression pattern was positively associated with 17β-estradiol and testosterone levels in vivo. Immunohistochemical analysis of fallopian tube epithelial cells revealed that nuclear localization of AR increased in parallel with decreased AR in the cytoplasm following eCG treatment. Moreover, we found that treatment with flutamide upregulated AR expression in immature mice in association with a decrease in serum testosterone levels, whereas the same treatment resulted in downregulation of AR expression in gonadotropin-stimulated mice with concomitant decreases in serum 17β-estradiol concentrations, suggesting that androgen differs from estrogen in the regulation of AR expression. Furthermore, we demonstrated that DES increased both AR protein expression and nuclear location over a 48-h time course. DHT had rapid effects, with induction of AR expression and translocation at 6 h after injection, but unlike DES it had prolonged efficacy. In addition, we provided direct in vivo evidence that nuclear protein interaction between AR and p21Cip1, a previously reported AR-regulated gene, was enhanced by gonadotropin stimulation. To our knowledge, this study provides the first demonstration to illustrate that estrogen as a principal regulator may contribute to regulate and activate AR in the fallopian tubes in vivo.

scholarly journals Pdx-1 Is Not Sufficient for Repression of Proglucagon Gene Transcription in Islet or Enteroendocrine Cells

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 441-449 ◽  
Author(s):  
Grace Flock ◽  
Xiemin Cao ◽  
Daniel J. Drucker
Keyword(s):  
Gene Expression ◽  
Gene Transcription ◽  
Nuclear Translocation ◽  
Immunohistochemical Analysis ◽  
Enteroendocrine Cells ◽  
Cell Phenotype ◽  
Protein Overexpression ◽  
Adenoviral Transduction ◽  
Glucagon Like Peptide 1 ◽  
The Relationship

Pdx-1 plays a key role in the development of the pancreas and the control of islet gene transcription and has also been proposed as a dominant regulator of the α- vs. β-cell phenotype via extinction of proglucagon expression. To ascertain the relationship between Pdx-1 and proglucagon gene expression, we examined the effect of enhanced pdx-1 expression on proglucagon gene expression in murine islet αTC-1 and GLUTag enteroendocrine cells. Although adenoviral transduction increased the levels of pdx-1 mRNA transcripts and nuclear Pdx-1 protein, overexpression of pdx-1 did not repress endogenous proglucagon gene expression in αTC-1 or GLUTag cells or murine islets. Immunohistochemical analysis of cells transduced with Ad-pdx-1 demonstrated multiple individual islet or enteroendocrine cells exhibiting both nuclear Pdx-1 and cytoplasmic glucagon-like peptide-1 immunopositivity. The failure of pdx-1 to inhibit endogenous proglucagon gene expression was not attributable to defects in Pdx-1 nuclear translocation or DNA binding as demonstrated using Western blotting and EMSA analyses. Furthermore, Ad-pdx-1 transduction did not repress proglucagon promoter activity in αTC-1 or GLUTag cells. Taken together, these findings demonstrate that pdx-1 alone is not sufficient for specification of the hormonal phenotype or extinction of proglucagon gene expression in islet or enteroendocrine cells.

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