Isomyosin expression patterns in tubular stages of chicken heart development: a 3-D immunohistochemical analysis

1987 ◽  
Vol 177 (1) ◽  
pp. 81-90 ◽  
Author(s):  
F. Jong ◽  
W. J. C. Geerts ◽  
W. H. Lamers ◽  
J. A. Los ◽  
A. F. M. Moorman
Keyword(s):  
Heart Development ◽  
Expression Patterns ◽  
Immunohistochemical Analysis ◽  
Chicken Heart

scholarly journals Survivin drives tumor-associated macrophage reprogramming: a novel mechanism with potential impact for obesity

2021 ◽  
Author(s):  
E. Benaiges ◽  
V. Ceperuelo-Mallafré ◽  
A. Madeira ◽  
R. Bosch ◽  
C. Núñez-Roa ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Expression Patterns ◽  
Intracellular Localization ◽  
Immunohistochemical Analysis ◽  
Subcellular Fractionation ◽  
Migration And Invasion ◽  
Macrophage Phenotype ◽  
Tumor Associated Macrophages ◽  
Obesity And Cancer ◽  
The Impact

Abstract Purpose Recent studies point to adipose-derived stem cells (ASCs) as a link between obesity and cancer. We aimed to determine whether survivin, which is highly secreted by ASCs from subjects with obesity, might drive a pro-tumoral phenotype in macrophages. Methods The effect of ASC conditioned medium on the macrophage phenotype was assessed by expression studies. Survivin intracellular localization and internalization were examined by subcellular fractionation and immunofluorescence, respectively. Loss- and gain-of-function studies were performed using adenoviral vectors, and gene expression patterns, migration and invasion capacities of cancer cells were examined. Heterotypic cultures of ASCs, macrophages and cancer cells were established to mimic the tumor microenvironment. Survivin-blocking experiments were used to determine the impact of survivin on both macrophages and cancer cells. Immunohistochemical analysis of survivin was performed in macrophages from ascitic fluids of cancer patients and healthy controls. Results We found that obese-derived ASCs induced a phenotypic switch in macrophages characterized by the expression of both pro- and anti-inflammatory markers. Macrophages were found to internalize extracellular survivin, generating hybrid macrophages with a tumor-associated phenotype that included secretion of survivin. Exogenous expression of survivin in macrophages generated a similar phenotype and enhanced the malignant characteristics of cancer cells by a mechanism dependent on survivin phosphorylation at threonine 34. Survivin secreted by both ASCs from subjects with obesity and tumor-associated macrophages synergistically boosted the malignancy of cancer cells. Importantly, survivin was mainly detected in ascites-associated macrophages from patients with a malignant diagnosis. Conclusion Our data indicate that survivin may serve as a molecular link between obesity and cancer and as a novel marker for tumor-associated macrophages.

Abstract 255: A Fibroblast Population Shares A Developmental Origin With Cardiovascular Lineages

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Sara Ranjbarvaziri ◽  
Shah Ali ◽  
Mahmood Talkhabi ◽  
Peng Zhao ◽  
Young-Jae Nam ◽  
...  
Keyword(s):  
Heart Development ◽  
Cardiac Fibroblasts ◽  
Immunohistochemical Analysis ◽  
Cell Types ◽  
Mouse Heart ◽  
Developmental Potential ◽  
Reporter Mice ◽  
Significant Difference ◽  
Definition Of

Rationale: The traditional definition of “cardiovascular” lineages describes the eponymous cell types - cardiomyoctes, endothelial cells, and smooth muscle cells - that arise from a common mesodermal progenitor cell during heart development. Fibroblasts are an abundant mesenchymal population in the mammalian heart which may have multiple, discrete developmental origins. Mesp1 represents the earliest marker of cardiovascular progenitors, contributing to the majority of cardiac lineages. To date no link between Mesp1 and fibroblast generation has been reported. Objective: We hypothesized progenitor cells expressing Mesp1 can also give rise to cardiac fibroblasts during heart development. Methods and Results: We generated Mesp1cre/+;R26RmTmG reporter mice where Cre-mediated recombination results in GFP activation in all Mesp1 expressing cells and their progeny. To explore their developmental potential, we isolated GFP+ cells from E7.5 Mesp1cre/+;R26RmTmG mouse. In vitro culture and transplantation studies into SCID mouse kidney capsule as wells as chick embryos showed fibroblastic adoption. Results showed that at E9.5 Mesp1+ and Mesp1- progenitors contributed to the proepicardium organ and later at E11.5 they formed epicardium. Analysis of adult hearts demonstrated that the majority of cardiac fibroblasts are derived from Mesp1 expressing cells. Immunohistochemical analysis of heart sections demonstrated expression of fibroblast markers (including DDR2, PDGFRα and Col1) in cells derived from both Mesp1+ and Mesp1- progenitors. Additionally, we investigated whether the two distinct fibroblast populations have different potency towards reprogramming to cardiomyocytes. Results showed no significant difference between Mesp1 and non-Mesp1 isolated fibroblasts to convert to cardiomyocyte fate. Conclusions: Our data demonstrates that cardiovascular progenitors expressing Mesp1 contribute to the proepicardium. These cells, as cardiovascular progenitors, also give rise to the highest portion of cardiac fibroblasts in the mouse heart.

scholarly journals Dynamic patterns of expression of BMP isoforms 2, 4, 5, 6, and 7 during chicken heart development

2004 ◽  
Vol 279A (1) ◽  
pp. 636-651 ◽  
Author(s):  
Semir Somi ◽  
Anita A.M. Buffing ◽  
Antoon F.M. Moorman ◽  
Maurice J.B. Van Den Hoff
Keyword(s):  
Heart Development ◽  
Chicken Heart ◽  
Dynamic Patterns

scholarly journals Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation

2020 ◽  
Vol 178 (2) ◽  
pp. 325-337
Author(s):  
Matthew de Gannes ◽  
Chia-I Ko ◽  
Xiang Zhang ◽  
Jacek Biesiada ◽  
Liang Niu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Heart Development ◽  
Expression Patterns ◽  
Embryonic Stem Cell Line ◽  
Molecular Networks ◽  
Unknown Etiology ◽  
Postnatal Maturation ◽  
Complex Interactions ◽  
And Function

Abstract Congenital heart disease (CHD), the leading birth defect worldwide, has a largely unknown etiology, likely to result from complex interactions between genetic and environmental factors during heart development, at a time when the heart adapts to diverse physiological and pathophysiological conditions. Crucial among these is the regulation of cardiomyocyte development and postnatal maturation, governed by dynamic changes in DNA methylation. Previous work from our laboratory has shown that exposure to the environmental toxicant tetrachlorodibenzo-p-dioxin (TCDD) disrupts several molecular networks responsible for heart development and function. To test the hypothesis that the disruption caused by TCDD in the heart results from changes in DNA methylation and gene expression patterns of cardiomyocytes, we established a stable mouse embryonic stem cell line expressing a puromycin resistance selectable marker under control of the cardiomyocyte-specific Nkx2-5 promoter. Differentiation of these cells in the presence of puromycin induces the expression of a large suite of cardiomyocyte-specific markers. To assess the consequences of TCDD treatment on gene expression and DNA methylation in these cardiomyocytes, we subjected them to transcriptome and methylome analyses in the presence of TCDD. Unlike control cardiomyocytes maintained in vehicle, the TCDD-treated cardiomyocytes showed extensive gene expression changes, with a significant correlation between differential RNA expression and DNA methylation in 111 genes, many of which are key elements of pathways that regulate cardiovascular development and function. Our findings provide an important clue toward the elucidation of the complex interactions between genetic and epigenetic mechanisms after developmental TCDD exposure that may contribute to CHD.

scholarly journals Detection of a ventricular-specific myosin heavy chain in adult and developing chicken heart.

1986 ◽  
Vol 102 (4) ◽  
pp. 1480-1484 ◽  
Author(s):  
Y Zhang ◽  
S A Shafiq ◽  
D Bader
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Heart Development ◽  
In Ovo ◽  
Specific Expression ◽  
Adult Chicken ◽  
Chicken Heart ◽  
Developing Heart ◽  
Caudal Portion ◽  
Atrial Myosin

In the present study, a monoclonal antibody (McAb), ALD19, generated against myosin of slow tonic muscle, was shown to react with the heavy chain of ventricular myosin in the adult chicken heart. With this antibody, it was possible to detect a ventricular-specific myosin during myocardial differentiation and to show that the epitope recognized by ALD19 was present from the earliest stages of ventricular differentiation and maintained throughout development only in the ventricle. A second McAb, specific for atrial myosin heavy chain (MHC) (Gonzalez-Sanchez, A., and D. Bader, 1984, Dev. Biol., 103:151-158), was used as a control to detect an atrial-specific myosin in the caudal portion of the developing heart at Hamburger-Hamilton stage 15. It was found that the appearance of ventricular MHC predated the expression of atrial MHC by approximately 1 d in ovo and that specific MHCs were always differentially distributed. While a common primordial MHC may be present in the early heart, this study showed the tissue-specific expression of a ventricular MHC during the initial stages of heart development and its differential accumulation throughout development.

Expression patterns and immunohistochemical analysis of ERK, HRAS and MEK1 proteins during ovarian prehierarchical follicular development in Zi geese (Anser cygnoides)

2019 ◽  
Author(s):  
H. Lu ◽  
C. T. Sello ◽  
C. Liu ◽  
Y. Sui ◽  
C. Xu ◽  
...  
Keyword(s):  
Protein Localization ◽  
Quantitative Polymerase Chain Reaction ◽  
Expression Patterns ◽  
Follicular Development ◽  
Immunohistochemical Analysis ◽  
Mitogen Activated Protein Kinase ◽  
Expression Levels ◽  
Protein Levels ◽  
Spatiotemporal Expression ◽  
Mitogen Activated Protein

The objective of this study was to investigate the spatiotemporal expression levels and protein localization of extracellular regulated MAP kinase (ERK), HRas proto-oncogene, GTPase (HRAS), and mitogen-activated protein kinase kinase 1 (MEK1) genes in ovarian prehierarchical follicles of geese. The prehierarchical follicles from healthy laying geese (n=6) at the age of 35 to 37 weeks were harvested. The relative expression levels of ERK, HRAS, and MEK1 in various sized prehierarchical follicles were detected by real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, and follicular wall localization was investigated by using immunohistochemistry. The results revealed that the candidate genes were expressed differently at mRNA and protein levels at five stages of prehierarchical follicle development. These results suggest that ERK, HRAS, and MEK1 might be associated to the key biological mechanisms regulating Zi geese folliculogenesis.

scholarly journals Broad Up-Regulation of Innate Defense Factors during Acute Cholera

2007 ◽  
Vol 75 (5) ◽  
pp. 2343-2350 ◽  
Author(s):  
Carl-Fredrik Flach ◽  
Firdausi Qadri ◽  
Taufiqur R. Bhuiyan ◽  
Nur H. Alam ◽  
Eva Jennische ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Lamina Propria ◽  
Intestinal Epithelium ◽  
Defense Mechanisms ◽  
Expression Patterns ◽  
Immunohistochemical Analysis ◽  
Duodenal Mucosa ◽  
Innate Defense ◽  
Microarray Screening

ABSTRACT We used a whole-genome microarray screening system (Affymetrix human GeneChips covering 47,000 different transcripts) to examine the gene expression in duodenal mucosa during acute cholera. Biopsies were taken from the duodenal mucosa of seven cholera patients 2 and 30 days after the onset of diarrhea, and the gene expression patterns in the acute- and convalescent-phase samples were compared pairwise. Of about 21,000 transcripts expressed in the intestinal epithelium, 29 were defined as transcripts that were up-regulated and 33 were defined as transcripts that were down-regulated during acute cholera. The majority of the up-regulated genes characterized were found to have an established or possible role in the innate defense against infections; these genes included the LPLUNC1, LF, VCC1, TCN1, CD55, SERPINA3, MMP1, MMP3, IL1B, LCN2, SOCS3, GDF15, SLPI, CXCL13, and MUC1 genes. The results of confirmative PCR correlated well with the microarray data. An immunohistochemical analysis revealed increased expression of lactoferrin in lamina propria cells and increased expression of CD55 in epithelial cells, whereas increased expression of the SERPINA3 protein (α1-antichymotrypsin) was detected in both lamina propria and epithelial cells during acute cholera. The expression pattern of CD55 and SERPINA3 in cholera toxin (CT)-stimulated Caco-2 cells was the same as the pattern found in the intestinal mucosa during acute cholera, indicating that the activation of the CD55 and SERPINA3 genes in intestinal epithelium was induced by CT. In conclusion, during acute cholera infection, innate defense mechanisms are switched on to an extent not described previously. Both direct effects of CT on the epithelial cells and changes in the lamina propria cells contribute to this up-regulation.

Molecular similarities between primary peritoneal and primary ovarian carcinomas

2003 ◽  
Vol 13 (6) ◽  
pp. 749-755 ◽  
Author(s):  
L.-M. Chen ◽  
S. D. Yamada ◽  
Y.-S. Fu ◽  
R. L. Baldwin ◽  
B. Y. Karlan
Keyword(s):  
Expression Patterns ◽  
Immunohistochemical Analysis ◽  
Antigen Expression ◽  
Metastatic Tumor ◽  
Peritoneal Carcinoma ◽  
Ovarian Carcinomas ◽  
Serous Ovarian Carcinoma ◽  
Biologic Markers ◽  
Her 2 ◽  
Tissue Site

The objective of this paper was to characterize expression patterns of biologic markers to distinguish papillary serous peritoneal carcinoma (PPC) from papillary serous ovarian carcinoma (POC). Immunohistochemical analysis of HER-2/neu, p53, bcl-2, and nm23-H1 expression was performed on archival paraffin-embedded tissues. Antigen expression was compared at ovarian and extra-ovarian sites. Thirty-two PPC cases were compared to 18 POC cases. Mean age, stage, grade, and survival outcome were comparable between the two groups. Antigen expression patterns were not significantly different between PPC and POC for the four markers studied. In all cases, nm23-H1 was expressed. Conversely, bcl-2 was expressed at only a single tissue site in three of 32 (9.4%) PPC cases and in one of 18 (5.6%) POC cases. Eleven of 32 (34.4%) PPC cases overexpressed HER-2/neu, vs. four of 18 (22.2%) POC cases. P53 staining results were positive in 23 of 32 (71.9%) PPC and 13 of 18 (72.2%) POC cases. Intrapatient antigen expression was identical at primary and metastatic tumor sites in 50% of the POC and 48.4% of the PPC cases. We conclude that PPC and POC have a comparable immunohistochemical phenotype for these four molecular markers, which is reflected by their similar clinical courses.

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