Fibroblast growth factor 16 (FGF16) is preferentially expressed in the heart after birth, suggesting its regulation is associated with tissue-specific chromatin remodeling and DNA-protein interactions. Here we have mapped the transcription initiation site of murine FGF16 to approximately 1.1 kilobases (kb) upstream of the translation start codon (ATG). Hybrid reporter genes directed by about 4.7 kb of upstream FGF16 DNA were expressed specifically in transfected neonatal rat cardiac myocytes, as well as in the heart of transgenic mice. A DNaseI hypersensitive site was mapped to a region about 1.2 kb upstream of the transcription initiation site in heart but not kidney tissue, and a nuclease protection assay gave evidence of a cardiac-specific protein-DNA interaction in this region. Deletion analysis indicated that a hybrid gene with 1205 bp but not 1054 bp of upstream DNA directed FGF16 promoter activity in transfected neonatal rat cardiac myocytes. We identified a putative myocyte enhancer factor 2 (MEF2)-binding site at nucleotides -1159/-1148, confirmed by electrophoretic mobility shift assay and MEF2 antibody binding. Mutation of the MEF2 site resulted in a blunting of FGF16 promoter activity in transfected neonatal rat cardiac myocytes. These data suggest that chromatin remodeling and MEF2 binding in the FGF16 promoter contribute to expression in the postnatal heart.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1089/dna.2007.0689 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Mechanism of Modulation of Cardiac Force by Temperature.
Int J Mol Sci
January 2025
PhysioLab, University of Florence, 50019 Sesto Fiorentino, Italy.
In maximally Ca-activated demembranated fibres from the mammalian skeletal muscle, the depression of the force by lowering the temperature below the physiological level (~35 °C) is explained by the reduction of force in the myosin motor. Instead, cooling is reported to not affect the force per motor in Ca-activated cardiac trabeculae from the rat ventricle. Here, the mechanism of the cardiac performance depression by cooling is reinvestigated with fast sarcomere-level mechanics.
View Article and Find Full Text PDFSerpina3k lactylation protects from cardiac ischemia reperfusion injury.
Nat Commun
January 2025
State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Lactate produced during ischemia-reperfusion injury is known to promote lactylation of proteins, which play controversial roles. By analyzing the lactylomes and proteomes of mouse myocardium during ischemia-reperfusion injury using mass spectrometry, we show that both Serpina3k protein expression and its lactylation at lysine 351 are increased upon reperfusion. Both Serpina3k and its human homolog, SERPINA3, are abundantly expressed in cardiac fibroblasts, but not in cardiomyocytes.
View Article and Find Full Text PDFAstragali Radix-Notoginseng Radix et Rhizoma medicine pair prevents cardiac remodeling by improving mitochondrial dynamic balance.
Chin J Nat Med
January 2025
Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Research Center for Traceability and Standardization of TCMs, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address:
Astragali Radix (AR) and Notoginseng Radix et Rhizoma (NR) are frequently employed in cardiovascular disease treatment. However, the efficacy of the AR-NR medicine pair (AN) in improving cardiac remodeling and its underlying mechanism remains unclear. This study aimed to evaluate AN's cardioprotective effect and potential mechanism on cardiac remodeling using transverse aortic constriction (TAC) in mice and angiotensin II (Ang II)-induced neonatal rat cardiomyocytes (NRCMs) and fibroblasts in vitro.
View Article and Find Full Text PDFTianxiangdan (TXD) alleviates myocardial ischemia reperfusion-induced ferroptosis through the activation of estrogen receptor alpha (ERα).
Chin J Nat Med
January 2025
Department of Pharmacy, The Fourth College of Clinical Medicine, Xinjiang Medical University, Urumqi 830000, China; Department of Pharmacy, Xinjiang Uygur Autonomous Region Hospital of Traditional Chinese Medicine, Urumqi 830000, China. Electronic address:
Tianxiangdan (TXD), a traditional Chinese herbal remedy, demonstrates efficacy in mitigating myocardial ischemia-reperfusion (I/R)-induced damage. This study employed network pharmacology to evaluate the therapeutic targets and mechanisms of TXD in treating I/R. High-performance liquid chromatography-mass spectrometry (HPLC-MS) identified 86 compounds in TXD.
View Article and Find Full Text PDFACSL4 Regulates LPS-Induced Ferroptosis in Cardiomyocytes through FASN.
Ann Clin Lab Sci
November 2024
Emergency Department, Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, Zhejiang, China
Objective: Myocardial injury is a prevalent complication of sepsis. This study aims to shed light on the role of Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) in regulating Fatty Acid Synthase (FASN) to identify the intrinsic molecular mechanisms of sepsis-induced myocardial injury.
Method: H9c2 cells were treated with Lipopolysaccharide (LPS) to model sepsis-induced cardiomyocyte injury and were subsequently divided into seven groups: Control, LPS, LPS+sh-NC, LPS+sh-ACSL4, LPS+sh-ACSL4+Erastin, LPS+sh-ACSL4+oe-NC, and LPS+sh-ACSL4+oe-FASN.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!