[1] McCaffrey TA, Fu C, Du B, et al. High level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis [J]. J Clin Invest, 2000, 105(5): 653-662. [2] Yan SF, Lu J, Zou YS, et al. Hypoxia-associated induction of early growth response-1 gene expression [J]. J Biol Chem, 1999, 274(21):15030-15040. [3] Moukarbel GV, Ayoub CM, Abchee AB. Pharmacological therapy for myocardial reperfusion injury [J]. Curr Opin Pharmacol, 2004, 4(2): 147-153. [4] Bruneau BG, Piazza LA , de Bold AJ . Alpha 1-adrenergic stimulation of isolated rat atria results in discoordinate increases in natriuretic peptide secretion and gene expression and enhances Egr-1 and c-Myc expression [J]. Endocrinology, 1996, 137(1): 137-143. [5] Kacimi R, Chentoufi J, Honbo N, et al. Hypoxia differentially regulates stress proteins in cultured cardiomyocytes: role of the p38 stress-activated kinase signaling cascade, and relation to cytoprotection [J]. Cardiovasc Res, 2000, 46(1): 139-150. [6] Kacimi R, Karliner JS, Koudssi F, et al. Expression and regulation of adhesion molecules in cardiac cells by cytokines: response to acute hypoxia [J]. Circ Res, 1998, 82(5): 576-586. [7] Zhang YM, Shi GG, Tang Z, et al. Effects of N-n-butyl haloperidol iodide on myocardial ischemia/reperfusion injury and Egr-1 expression in rat [J]. Acta Biochim Biophys Sin (Shanghai), 2006, 38(6): 435-441. [8] Yan SF, Fujita T, Lu J, et al. Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress [J]. Nat Med, 2000, 6(12): 1355-1361. [9] Hoffman JW, Gilbert TB, Poston RS, et al. Myocardial reperfusion injury: etiology, mechanisms, and therapies [J]. J Extra Corpor Technol, 2004, 36(4): 391-411. [10] Susini S, Roche E, Prentki M, et al. Glucose and glucoincretin peptides synergize to induce c-fos, c-jun, junB, zif-268, and nur-77 gene expression in pancreatic beta(INS-1) cells [J]. FASEB J, 1998, 12(2): 1173-1182. [11] Bernal-Mizrachi E, Wice B, Inoue H, et al. Activation of serum response factor in the depolarization induction of Egr-1 transcription in pancreatic islet beta-cells [J]. J Biol Chem, 2000, 275(33): 25681-25689. [12] Lo LW, Cheng JJ, Chiu JJ, et al. Endothelial exposure to hypoxia induces Egr-1 expression involving PKCalpha-mediated Ras/Raf-1/ERK1/2 pathway [J]. J Cell Physiol, 2001, 188(3): 304-312. [13] Summers BA, Overholt JL, Prabhakar NR. Augmentation of L-type calcium current by hypoxia in rabbit carotid body glomus cells: evidence for a PKC-sensitive pathway BETH A [J]. J Neurophysiol,2000 ,84(3):1636-1644. [14] Sakamoto KM, Bardeleben C, Yates KE, et al. 5' upstream sequence and genomic structure of the human primary response gene, EGR-1/TIS8 [J]. Oncogene, 1991, 6(5): 867-871. [15] Susini S, Van Haasteren G, Li S, et al. Essentiality of intron control in the induction of c-fos by glucose and glucoincretin peptides in INS-1 beta-cells [J]. FASEB J, 2000, 14(1):128-136. [16] Grohe C, Nouskas J, Vetter H, et al. Effects of nisoldipine on endothelin-1- and angiotensin II-induced immediate/early gene expression and protein synthesis in adult rat ventricular cardiomyocytes [J]. J Cardiovasc Pharmacol, 1994, 24(1): 13-16. |