Effects of epinephrine on angiogenesis-related gene expressions in cultured rat cardiomyocytes

Henry Liu, Lisa Sangkum, Geoffrey Liu, Michael Green, Marilyn Li, Alan D. Kaye

PDF(239 KB)
PDF(239 KB)
Journal of Biomedical Research ›› 2016, Vol. 30 ›› Issue (5) : 380-385. DOI: 10.7555/JBR.30.20160024
Original Article
Original Article

Effects of epinephrine on angiogenesis-related gene expressions in cultured rat cardiomyocytes

Author information +
History +

Abstract

Epinephrine is often used for the treatment of patients with heart failure, low cardiac output and cardiac arrest. It can acutely improve hemodynamic parameters; however, it does not seem to improve longer term clinical outcomes. Therefore, we hypothesized that epinephrine may induce unfavorable changes in gene expression of cardiomyocyte. Thus, we investigated effects of epinephrine exposure on the mediation or modulation of gene expression of cultured cardiomyocytes at a genome-wide scale. Our investigation revealed that exposure of cardiomyocytes to epinephrine in an in vitro environment can up-regulate the expression of angiopoietin-2 gene (+2.1 times), and down-regulate the gene expression of neuregulin 1 (−3.7 times), plasminogen activator inhibitor-1 (−2.4 times) and SPARC-related modular calcium-binding protein-2 (−4.5 times). These changes suggest that epinephrine exposure may induce inhibition of angiogenesis-related gene expressions in cultured rat cardiomyocytes. The precise clinical significance of these changes in gene expression, which was induced by epinephrine exposure, warrants further experimental and clinical investigations.

Keywords

epinephrine / angiogenesis / gene expression / cardiomyocytes / angiopoietin-2 / neuregulin 1 / plasminogen activator inhibitor-1 / SPARC-related modular calcium-binding protein

Cite this article

Download citation ▾
Henry Liu, Lisa Sangkum, Geoffrey Liu, Michael Green, Marilyn Li, Alan D. Kaye. Effects of epinephrine on angiogenesis-related gene expressions in cultured rat cardiomyocytes. Journal of Biomedical Research, 2016, 30(5): 380‒385 https://doi.org/10.7555/JBR.30.20160024

References

[1]
Morici N, Sacco A, Oliva F, Epinephrine for acute decompensated heart failure and low output state: friend or foe? [J]. Int J Cardiol, 2011, 149(3): 384–385.
CrossRef Pubmed Google scholar
[2]
Mebazaa A, Parissis J, Porcher R, Short-term survival by treatment among patients hospitalized with acute heart failure: the global ALARM-HF registry using propensity scoring methods [J]. Intensive Care Med, 2011, 37(2): 290–301.
CrossRef Pubmed Google scholar
[3]
Hayashi Y, Iwami T, Kitamura T, Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest [J]. Circ J, 2012, 76(7): 1639–1645.
CrossRef Pubmed Google scholar
[4]
Donnino MW, Salciccioli JD, Howell MD, , and the American Heart Association’s Get With The Guidelines-Resuscitation Investigators. Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry [J]. BMJ, 2014, 348(may20 2): g3028. Page 1–9.
CrossRef Pubmed Google scholar
[5]
Koscik C, Pinawin A, McGovern H, Rapid epinephrine administration improves early outcomes in out-of-hospital cardiac arrest [J]. Resuscitation, 2013, 84(7): 915–920.
CrossRef Pubmed Google scholar
[6]
Nakahara S, Tomio J, Takahashi H, Evaluation of pre-hospital administration of adrenaline (epinephrine) by emergency medical services for patients with out of hospital cardiac arrest in Japan: controlled propensity matched retrospective cohort study [J]. BMJ, 2013, 347(dec10 1): f6829. 1–12.
CrossRef Pubmed Google scholar
[7]
Kastrup M, Braun J, Kaffarnik M, Catecholamine dosing and survival in adult intensive care unit patients [J]. World J Surg, 2013, 37(4): 766–773.
CrossRef Pubmed Google scholar
[8]
Callaway CW. Questioning the use of epinephrine to treat cardiac arrest [J]. JAMA, 2012, 307(11): 1198–1200.
CrossRef Pubmed Google scholar
[9]
Rossinen J, Harjola VP, Siirila-Waris K, and the For The FINN-AKVA Study Group. The use of more than one inotrope in acute heart failure is associated with increased mortality: a multi-centre observational study [J]. Acute Card Care, 2008, 10(4): 209–213.
CrossRef Pubmed Google scholar
[10]
Merten KE, Jiang Y, Feng W, Calcineurin activation is not necessary for Doxorubicin-induced hypertrophy in H9c2 embryonic rat cardiac cells: involvement of the phosphoinositide 3-kinase-Akt pathway [J]. J Pharmacol Exp Ther, 2006, 319(2): 934–940.
CrossRef Pubmed Google scholar
[11]
Risau W, Flamme I. Vasculogenesis. Annu Rev Cell Dev Biol, 1995, 11(1): 73–91.
CrossRef Pubmed Google scholar
[12]
Flamme I, Frölich T, Risau W. Molecular mechanisms of vasculogenesis and embryonic angiogenesis [J]. J Cell Physiol, 1997, 173(2): 206–210.
CrossRef Pubmed Google scholar
[13]
Novakova V, Sandhu GS, Dragomir-Daescu D, Apelinergic system in endothelial cells and its role in angiogenesis in myocardial ischemia [J]. Vascul Pharmacol, <Date>2015 Aug 5</Date>. pii: S1537-1891(15)00181-0.
CrossRef Google scholar
[14]
Margulis K, Neofytou EA, Beygui RE, et al. Celecoxib Nanoparticles for Therapeutic Angiogenesis [J]. ACS Nano,<Date> 2015 Aug 10</Date>.
Pubmed
[15]
Cheung AH, Stewart RJ, Marsden PA. Endothelial Tie2/Tek ligands angiopoietin-1 (ANGPT1) and angiopoietin-2 (ANGPT2): regional localization of the human genes to 8q22.3-q23 and 8p23 [J]. Genomics, 1998, 48(3): 389–391.
CrossRef Pubmed Google scholar
[16]
Fiedler U, Krissl T, Koidl S, Angiopoietin-1 and angiopoietin-2 share the same binding domains in the Tie-2 receptor involving the first Ig-like loop and the epidermal growth factor-like repeats [J]. J Biol Chem (United States),2003, 278 (3): 1721–7.ISSN 0021-9258.
CrossRef Pubmed Google scholar
[17]
Britsch S. The neuregulin-I/ErbB signaling system in development and disease [J]. Adv Anat Embryol Cell Biol, 2007, 190: 1–65.ISBN 978-3-540-37105-2.
CrossRef Pubmed Google scholar
[18]
Xu Y, Li X, Liu X, Neuregulin-1/ErbB signaling and chronic heart failure [J]. Adv Pharmacol, 2010, 59: 31–51.
CrossRef Pubmed Google scholar
[19]
Steinthorsdottir V, Stefansson H, Ghosh S, Multiple novel transcription initiation sites for NRG1 [J]. Gene, 2004, 342(1): 97–105.
CrossRef Pubmed Google scholar
[20]
Yutzey KE. Regenerative biology: Neuregulin 1 makes heart muscle[J]. Nature, 2015, 520(7548): 445–446.
CrossRef Pubmed Google scholar
[21]
Vaughan DE. PAI-1 and atherothrombosis [J]. J Thromb Haemost, 2005, 3(8): 1879–1883.
CrossRef Pubmed Google scholar
[22]
Minowa H, Takahashi Y, Tanaka T, Four cases of bleeding diathesis in children due to congenital plasminogen activator inhibitor-1 deficiency [J]. Haemostasis, 1999, 29(5): 286–291
Pubmed
[23]
Tezuka T, Ogawa H, Azuma M, IMD-4690, a novel specific inhibitor for plasminogen activator inhibitor-1, reduces allergic airway remodeling in a mouse model of chronic asthma via regulating angiogenesis and remodeling-related mediators[J]. PLoS One, 2015, 10(3): e0121615.
CrossRef Pubmed Google scholar
[24]
Rocnik EF, Liu P, Sato K, The novel SPARC family member SMOC-2 potentiates angiogenic growth factor activity[J]. J Biol Chem, 2006, 281(32): 22855–22864.
CrossRef Pubmed Google scholar
[25]
Vannahme C, Gösling S, Paulsson M, Characterization of SMOC-2, a modular extracellular calcium-binding protein [J]. Biochem J, 2003, 373(Pt 3): 805–814.
CrossRef Pubmed Google scholar

Acknowledgement

This study was supported by internal funding from the Department of Anesthesiology and Perioperative Medicine. A portion of our study results was presented as an abstract in the American Society of Anesthesiologists annual meeting on October 13th, 2014 in New Orleans, Louisiana.

RIGHTS & PERMISSIONS

2016 2016 by the Journal of Biomedical Research. All rights reserved.
PDF(239 KB)

Accesses

Citations

Detail

Sections
Recommended

/