Electrical Stimulation of Neonatal Cardiac Myocytes Activates the NFAT3 and GATA4 Pathways and Up-regulates the Adenylosuccinate Synthetase 1 Gene

Xia, Yang; McMillin, Jeanie B.; Lewis, Amy L.; Moore, Meredith; Zhu, Wenjun; Williams, R. Sanders; Kellems, Rodney E.

doi:10.1074/jbc.275.3.1855

Cited by 109 publications

(102 citation statements)

References 47 publications

(70 reference statements)

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“…Total cellular RNA (10 g/lane) was electrophoresed in 1.0% agarose under denaturing conditions as described previously (35), and transferred to nylon membranes. RNA was cross-linked to the membrane by ultraviolet irradiation and incubated with an Adss1 probes as described before (13). Following multiple stringent washings the membranes were subjected to autoradiography for 24 -48 h at Ϫ70°C.…”

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

“…The putative cAMP response element-binding protein binding site within 1.9Adss1/ CAT was disrupted using a PCR site-directed mutagenesis kit from Stratagene (13). The consensus CRE, TGACGTCA, was mutated to TGtgGTCA as published previously (35).…”

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

“…Preparation of Plasmids and Transient Transfection-The reporter construct, 1.9Adss1/CAT, has been described before (13). The putative cAMP response element-binding protein binding site within 1.9Adss1/ CAT was disrupted using a PCR site-directed mutagenesis kit from Stratagene (13).…”

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

“…Neonatal rat cardiac myocytes (1-2 days old) were isolated as described previously (13) and grown in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% calf serum (Hyclone). Cells were plated in six-well dishes (21 cm 2 per well) at a density of 5 ϫ 10 5 cells per well for RNA isolation, total cellular protein isolation, and transient transfection experiments (34).…”

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

“…In this regard the calcineurin-NFAT signaling pathway has received the most attention (12,13). However, in eukaryotic cells one of the most important intracellular transducers of growth-related signaling is the rapamycin-sensitive pathway associated with mammalian target of rapamycin (mTOR), a phosphatidylinositol kinase-related protein kinase that is regulated in response to growth factors and nutritional status (14).…”

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confidence: 99%

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Mammalian Target of Rapamycin and Protein Kinase A Signaling Mediate the Cardiac Transcriptional Response to Glutamine

Xia¹,

Wen²,

Young³

et al. 2003

Journal of Biological Chemistry

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The addition of glutamine as a major nutrient to cultured neonatal rat cardiomyocytes produced an increase in myocyte size and the organization of actin into myofibrillar arrays. The cellular response was associated with increased abundance of the mRNAs encoding the contractile proteins, ␣-myosin heavy chain and cardiac ␣-actin, and the metabolic enzymes, muscle carnitine palmitoyl transferase I and muscle adenylosuccinate synthetase (ADSS1). Adss1 gene expression was induced ϳ5-fold in glutamine-treated rat neonatal cardiac myocytes. The induction was mediated through the protein kinase A and mammalian target of rapamycin signaling pathways and required a cyclic AMP response element associated with the promoter region of the Adss1 gene. These results highlight glutamine as a major nutrient regulator of cardiac gene expression and identify protein kinase A and mammalian target of rapamycin signaling pathways as mediators of the cardiomyocyte transcriptional response.

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Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

Section: Rat Neonatal Cardiac Myocyte Culture and Glutamine Treatment-mentioning

confidence: 99%

mentioning

confidence: 99%

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Mammalian Target of Rapamycin and Protein Kinase A Signaling Mediate the Cardiac Transcriptional Response to Glutamine

Xia¹,

Wen²,

Young³

et al. 2003

Journal of Biological Chemistry

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DYRK1A activates NFATC1 to increase glioblastoma migration

et al. 2021

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Glioma is the most common brain cancer, and high-grade gliomas, including glioblastoma multiforme (GBM), are the most aggressive types of glioma. 1 The current standard treatment for GBM involves surgical resection followed by the administration of an alkylating agent, temozolomide, both concurrent with and after radiotherapy. Bevacizumab is administered as a second-line treatment after relapse. 2,3 However, GBM is resistant to chemotherapy and radiotherapy, with a median patient survival time of approximately one year. 1,4 The highly invasive nature of GBM cells is thought to contribute to the poor prognosis of this tumor, necessitating the exploration of alternative therapies. Many factors are involved in the migration and invasion of malignant tumors, including the nuclear factor of activated T cells (NFAT). [5][6][7] NFAT, originally found in activated T cells, is a transcription factor that induces gene transcription during the immune response. 8 The NFAT transcription factor family consists of five members: NFAT1 (NFATC2, NFATp),

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Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

Chao

Badrealam

et al. 2019

J of Cellular Biochemistry

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Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)‐induced cardiomyocyte hypertrophy and apoptosis remains elusive. In the current research endeavor, we have elucidated the role of Tid1‐S on LPS‐induced cardiac hypertrophy and apoptosis. Interestingly, we found that overexpression of Tid1‐S suppressed TLR‐4, NFATc3, and BNP protein expression which eventually led to inhibition of LPS‐induced cardiac hypertrophy. Moreover, Tid1‐S overexpression attenuated cellular apoptosis and activated survival proteins p‐PI3K and pser473Akt. Besides this, Tid1‐S overexpression enhanced ER‐a protein expression. Collectively, our data suggest that Tid1‐S plausibly enhance ER‐a protein and further activate p‐PI3K and p ser473Akt survival protein expression; which thereby led to attenuation of LPS‐induced apoptosis in cardiomyoblast cells. Interestingly, our data suggest that Tid1‐S is involved in attenuation of cardiomyoblast cells damages induced by LPS.

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Electrical Stimulation of Neonatal Cardiac Myocytes Activates the NFAT3 and GATA4 Pathways and Up-regulates the Adenylosuccinate Synthetase 1 Gene

Cited by 109 publications

References 47 publications

Mammalian Target of Rapamycin and Protein Kinase A Signaling Mediate the Cardiac Transcriptional Response to Glutamine

Mammalian Target of Rapamycin and Protein Kinase A Signaling Mediate the Cardiac Transcriptional Response to Glutamine

DYRK1A activates NFATC1 to increase glioblastoma migration

Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

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