Change in Nox4 expression is accompanied by changes in myogenic marker expression in differentiating C2C12 myoblasts

2013 ◽  
Vol 465 (8) ◽  
pp. 1181-1196 ◽  
Author(s):  
S. Acharya ◽  
A. M. Peters ◽  
A. S. Norton ◽  
G. K. Murdoch ◽  
R. A. Hill
Keyword(s):  
C2c12 Myoblasts ◽  
Marker Expression ◽  
Myogenic Marker

scholarly journals Myogenic marker expression as a function of age and exercise-based therapy in the tongue

2020 ◽  
Vol 142 ◽  
pp. 111104
Author(s):  
Heidi Kletzien ◽  
Cynthia A. Kelm-Nelson ◽  
Sabrina Wang ◽  
Masatoshi Suzuki ◽  
Nadine P. Connor
Keyword(s):  
Marker Expression ◽  
Myogenic Marker

scholarly journals Aging increases CCN1 expression leading to muscle senescence

2014 ◽  
Vol 306 (1) ◽  
pp. C28-C36 ◽  
Author(s):  
Jie Du ◽  
Janet D. Klein ◽  
Faten Hassounah ◽  
Jin Zhang ◽  
Cong Zhang ◽  
...  
Keyword(s):  
Sharp Increase ◽  
Matricellular Protein ◽  
Dependent Manner ◽  
C2c12 Myoblasts ◽  
Protein Levels ◽  
Cell Arrest ◽  
Aging Muscle ◽  
Dose Dependent ◽  
Myogenic Marker ◽  
Elderly Humans

Using microarray analysis, we found that aging sarcopenia is associated with a sharp increase in the mRNA of the matricellular protein CCN1 (Cyr61/CTGF/Nov). CCN1 mRNA was upregulated 113-fold in muscle of aged vs. young rats. CCN1 protein was increased in aging muscle in both rats (2.8-fold) and mice (3.8-fold). When muscle progenitor cells (MPCs) were treated with recombinant CCN1, cell proliferation was decreased but there was no change in the myogenic marker myoD. However, the CCN1-treated MPCs did express a senescence marker (SA-βgal). Interestingly, we found CCN1 increased p53, p16Ink4A, and pRP (hypophosphorylated retinoblastoma protein) protein levels, all of which can arrest cell growth in MPCs. When MPCs were treated with aged rodent serum CCN1 mRNA increased by sevenfold and protein increased by threefold suggesting the presence of a circulating regulator. Therefore, we looked for a circulating regulator. Wnt-3a, a stimulator of CCN1 expression, was increased in serum from elderly humans (2.6-fold) and aged rodents (2.0-fold) compared with young controls. We transduced C2C12 myoblasts with wnt-3a and found that CCN1 protein was increased in a time- and dose-dependent manner. We conclude that in aging muscle, the circulating factor wnt-3a acts to increase CCN1 expression, prompting muscle senescence by activating cell arrest proteins.

Ectodermal and ectomesenchymal marker expression in primary cell lines of complex and compound odontomas: a pilot study

2019 ◽  
Vol 68 (3) ◽  
Author(s):  
David A. Trejo-Remigio ◽  
Luis F. Jacinto-Alemán ◽  
Elba R. Leyva-Huerta ◽  
Bogdan R. Navarro-Bustos ◽  
Javier Portilla-Robertson
Keyword(s):  
Pilot Study ◽  
Cell Lines ◽  
Primary Cell ◽  
Primary Cell Lines ◽  
Marker Expression

scholarly journals Ghrelin peptide improves glial conditioned medium effects on neuronal differentiation of human adipose mesenchymal stem cells

2021 ◽  
Author(s):  
Cristina Russo ◽  
Giuliana Mannino ◽  
Martina Patanè ◽  
Nunziatina Laura Parrinello ◽  
Rosalia Pellitteri ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Conditioned Medium ◽  
Neural Differentiation ◽  
Conditioned Media ◽  
Glial Fibrillary Acid Protein ◽  
Ghrelin Receptor ◽  
Neuronal Markers ◽  
Adipose Mesenchymal Stem Cells ◽  
Marker Expression

AbstractThe influences of ghrelin on neural differentiation of adipose-derived mesenchymal stem cells (ASCs) were investigated in this study. The expression of typical neuronal markers, such as protein gene product 9.5 (PGP9.5) and Microtubule Associated Protein 2 (MAP2), as well as glial Fibrillary Acid Protein (GFAP) as a glial marker was evaluated in ASCs in different conditions. In particular, 2 µM ghrelin was added to control ASCs and to ASCs undergoing neural differentiation. For this purpose, ASCs were cultured in Conditioned Media obtained from Olfactory Ensheathing cells (OEC-CM) or from Schwann cells (SC-CM). Data on marker expression were gathered after 1 and 7 days of culture by fluorescence immunocytochemistry and flow cytometry. Results show that only weak effects were induced by the addition of only ghrelin. Instead, dynamic ghrelin-induced modifications were detected on the increased marker expression elicited by glial conditioned media. In fact, the combination of ghrelin and conditioned media consistently induced a further increase of PGP9.5 and MAP2 expression, especially after 7 days of treatment. The combination of ghrelin with SC-CM produced the most evident effects. Weak or no modifications were found on conditioned medium-induced GFAP increases. Observations on the ghrelin receptor indicate that its expression in control ASCs, virtually unchanged by the addition of only ghrelin, was considerably increased by CM treatment. These increases were enhanced by combining ghrelin and CM treatment, especially at 7 days. Overall, it can be assumed that ghrelin favors a neuronal rather than a glial ASC differentiation.

Uterine PEComas: correlation between melanocytic marker expression and TSC alterations/TFE3 fusions

2021 ◽  
Author(s):  
Jennifer A. Bennett ◽  
Zehra Ordulu ◽  
Andre Pinto ◽  
Pankhuri Wanjari ◽  
Cristina R. Antonescu ◽  
...  
Keyword(s):  
Marker Expression

scholarly journals Epigenetic Modulation of Radiation-Induced Diacylglycerol Kinase Alpha Expression Prevents Pro-Fibrotic Fibroblast Response

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2455
Author(s):  
Chun-Shan Liu ◽  
Reka Toth ◽  
Ali Bakr ◽  
Ashish Goyal ◽  
Md Saiful Islam ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Drug Effects ◽  
Diacylglycerol Kinase ◽  
Dna Demethylation ◽  
Dermal Fibroblasts ◽  
Common Component ◽  
Radiation Induced ◽  
Marker Expression ◽  
Epigenetic Modulation ◽  
Genomic Editing

Radiotherapy, a common component in cancer treatment, can induce adverse effects including fibrosis in co-irradiated tissues. We previously showed that differential DNA methylation at an enhancer of diacylglycerol kinase alpha (DGKA) in normal dermal fibroblasts is associated with radiation-induced fibrosis. After irradiation, the transcription factor EGR1 is induced and binds to the hypomethylated enhancer, leading to increased DGKA and pro-fibrotic marker expression. We now modulated this DGKA induction by targeted epigenomic and genomic editing of the DGKA enhancer and administering epigenetic drugs. Targeted DNA demethylation of the DGKA enhancer in HEK293T cells resulted in enrichment of enhancer-related histone activation marks and radiation-induced DGKA expression. Mutations of the EGR1-binding motifs decreased radiation-induced DGKA expression in BJ fibroblasts and caused dysregulation of multiple fibrosis-related pathways. EZH2 inhibitors (GSK126, EPZ6438) did not change radiation-induced DGKA increase. Bromodomain inhibitors (CBP30, JQ1) suppressed radiation-induced DGKA and pro-fibrotic marker expression. Similar drug effects were observed in donor-derived fibroblasts with low DNA methylation. Overall, epigenomic manipulation of DGKA expression may offer novel options for a personalized treatment to prevent or attenuate radiotherapy-induced fibrosis.

Sign in / Sign up

Export Citation Format

Share Document