Activation of p38/MEF2C pathway by all-trans retinoic acid in cardiac myoblasts

Ren, Xiangxia; Li, Yong; Ma, Xi; Zheng, Liping; Xu, Yuping; Wang, Junbo

doi:10.1016/j.lfs.2007.04.037

Cited by 14 publications

(6 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in keeping with previous reports pointing to p38 MAPK activation as a critical event in the adrenergic-, rosiglitazone-and RA-induced signaling cascades leading to UCP1 expression in brown adipocytes (29)(30)(31)(32). Although steps from ATRA to p38 MAPK remain unclear, our results are also in keeping with reports showing that exposure to RA isomers triggers a rapid and transient increase in p38 MAPK phosphorylation in adipocytes and other cell systems (21,30,40). The effect of ATRA on p38 MAPK phosphorylation was evidenced under serumfree conditions typically used in cell culture experiments dealing with the regulation of p38 MAPK.…”

Section: Discussionsupporting

confidence: 93%

Induction of Uncoupling Protein‐1 in Mouse Embryonic Fibroblast‐derived Adipocytes by Retinoic Acid

Mercader

Palou

Bonet

2010

Obesity

View full text Add to dashboard Cite

The uncoupling protein‐1 (UCP1) is the molecular effector of thermogenesis in brown adipocytes, a process in which there is a renewed interest after the recent recognition of its relevance in adult humans. Typical white adipocytes do not express UCP1. We investigated the capacity of retinoic acid (RA), the carboxylic acid form of vitamin A and a known positive regulator of UCP1 gene transcription in brown adipocytes, to stimulate UCP1 expression in adipocytes differentiated in culture from primary mouse embryonic fibroblasts (MEFs), which are commonly used as white adipocyte model cells. Exposure to all‐trans RA (ATRA), but not to rosiglitazone or isoproterenol, potently induced UCP1 expression at both the mRNA and protein level in MEF‐derived adipocytes, in a dose‐dependent manner. The effect on UCP1 mRNA was reproduced by retinoid receptor agonists and by retinaldehyde, required p38 mitogen‐activated protein kinase activity (p38 MAPK), and appeared to be dissociated from increases in mitochondria biogenesis and oxidative capacity. MEF‐derived adipocytes exhibited a high mRNA expression level of the brown fat determination factor PRDM16. The results highlight a specific potential of retinoids to induce UCP1 gene expression in adipose cells, and may have implications for the elucidation of the signaling pathways to the UCP1 gene, as well as for research using MEF‐derived adipocytes.

show abstract

Section: Discussionsupporting

confidence: 93%

Induction of Uncoupling Protein‐1 in Mouse Embryonic Fibroblast‐derived Adipocytes by Retinoic Acid

Mercader

Palou

Bonet

2010

Obesity

View full text Add to dashboard Cite

show abstract

“…It is well‐established that p38 MAPK is a key mediator for many drugs to upregulate ALP activity in pre‐osteoblasts . On the other hand, ATRA is also found to transiently activate p38 signaling . Although a short‐term treatment of either Hst1 or ATRA seemed not sufficient to induce ALP activity, in combination Hst1 and ATRA significantly upregulated ALP (Fig.…”

Section: Resultsmentioning

confidence: 89%

All‐trans retinoic acid and human salivary histatin‐1 promote the spreading and osteogenic activities of pre‐osteoblasts in vitro

Sun

Shi

et al. 2020

FEBS Open Bio

View full text Add to dashboard Cite

Cell‐based bone tissue engineering techniques utilize both osteogenic cells and biomedical materials, and have emerged as a promising approach for large‐volume bone repair. The success of such techniques is highly dependent on cell adhesion, spreading, and osteogenic activities. In this study, we investigated the effect of co‐administration of all‐trans retinoic acid (ATRA) and human salivary peptide histatin‐1 (Hst1) on the spreading and osteogenic activities of pre‐osteoblasts on bio‐inert glass surfaces. Pre‐osteoblasts (MC3T3‐E1 cell line) were seeded onto bio‐inert glass slides in the presence and absence of ATRA and Hst1. Cell spreading was scored by measuring surface areas of cellular filopodia and lamellipodia using a point‐counting method. The distribution of fluorogenic Hst1 within osteogenic cells was also analyzed. Furthermore, specific inhibitors of retinoic acid receptors α, β, and γ, such as ER‐50891, LE‐135, and MM‐11253, were added to identify the involvement of these receptors. Cell metabolic activity, DNA content, and alkaline phosphatase (ALP) activity were assessed to monitor their effects on osteogenic activities. Short‐term (2 h) co‐administration of 10 μm ATRA and Hst1 to pre‐osteoblasts resulted in significantly higher spreading of pre‐osteoblasts compared to ATRA or Hst1 alone. ER‐50891 and LE‐135 both nullified these effects of ATRA. Co‐administration of ATRA and Hst1 was associated with significantly higher metabolic activity, DNA content, and ALP activity than either ATRA or Hst1 alone. In conclusion, co‐administration of Hst1 with ATRA additively stimulated the spreading and osteogenicity of pre‐osteoblasts on bio‐inert glass surfaces in vitro.

show abstract

“…We identified interferon regulatory factor 1 (IRF1) and the myocyte enhancer factor 2 (MEF2) family of transcription factors as significantly associated with the gene lists from both MDA-MB-231 and MDA-MB-468 cells. atRA is known to activate MEF2C 65 and to induce expression of IRF1 66 . To prioritize further experiments, we then examined the expression of all indicated transcription factors in the microarray data (Supplementary Figure S6 ).…”

Section: Resultsmentioning

confidence: 99%

Profiling of the transcriptional response to all-trans retinoic acid in breast cancer cells reveals RARE-independent mechanisms of gene expression

Coyle

Maxwell

Thomas

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Retinoids, derivatives of vitamin A, are key physiological molecules with regulatory effects on cell differentiation, proliferation and apoptosis. As a result, they are of interest for cancer therapy. Specifically, models of breast cancer have varied responses to manipulations of retinoid signaling. This study characterizes the transcriptional response of MDA-MB-231 and MDA-MB-468 breast cancer cells to retinaldehyde dehydrogenase 1A3 (ALDH1A3) and all-trans retinoic acid (atRA). We demonstrate limited overlap between ALDH1A3-induced gene expression and atRA-induced gene expression in both cell lines, suggesting that the function of ALDH1A3 in breast cancer progression extends beyond its role as a retinaldehyde dehydrogenase. Our data reveals divergent transcriptional responses to atRA, which are largely independent of genomic retinoic acid response elements (RAREs) and consistent with the opposing responses of MDA-MB-231 and MDA-MB-468 to in vivo atRA treatment. We identify transcription factors associated with each gene set. Manipulation of the IRF1 transcription factor demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). This study provides a paradigm for complex responses of breast cancer models to atRA treatment, and illustrates the need to characterize RARE-independent responses to atRA in a variety of models.

show abstract

Activation of p38/MEF2C pathway by all-trans retinoic acid in cardiac myoblasts

Cited by 14 publications

References 35 publications

Induction of Uncoupling Protein‐1 in Mouse Embryonic Fibroblast‐derived Adipocytes by Retinoic Acid

Induction of Uncoupling Protein‐1 in Mouse Embryonic Fibroblast‐derived Adipocytes by Retinoic Acid

All‐trans retinoic acid and human salivary histatin‐1 promote the spreading and osteogenic activities of pre‐osteoblasts in vitro

Profiling of the transcriptional response to all-trans retinoic acid in breast cancer cells reveals RARE-independent mechanisms of gene expression

Contact Info

Product

Resources

About