Molecular interaction between tissue repair via SDF-1/CXCR4 signaling and the inflammatory response in acute myocardial infarction with ST-segment elevation

Melissa Kristochek da Silva; Marco Antônio de Bastiani; Lucinara Dadda Dias; Raphael Boesche Guimarães; Marcela Corso Arend; Melissa Medeiros Markoski

doi:10.29327/multiscience.2022002

Keywords:

tissue damage

SDF-1/CXCR4 axis

inflammation

inflammatory response

myocardial infarction

heart repair

Abstract

The inflammatory response/ischemic damage relationship is a prerequisite for the initiation of the process of adaptation of the post-infarction cardiac tissue, in which the SDF-1/CXCR4 signaling plays a central role in tissue repair. This study aimed to investigate the modulation exerted by the SDF-1/CXCR4 axis on the inflammatory response after ST-segment elevation acute myocardial infarction (STEMI). Therefore, we developed Bayesian Networks from microarray (GEO) data and evaluated the expression of transcripts of interest in patients with STEMI by qPCR. In the chronic and anti-inflammatory scenario, we verified a relationship between proteins involved in tissue remodeling and the blockade of apoptotic pathways. The expression levels of the transcripts evaluated were increased in the initial moments after the infarction. In conclusion, the effects promoted by the SDF-1/CXCR4 interaction can be modulated according to the immunological profile, directly influencing its adaptive and cardioprotective effects. Therefore, we believe that students can contribute to the awareness of family and friends about COVID-19 and fake news.
References
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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

How to cite

Silva, M. K. da, de Bastiani, M. A., Dias, L. D., Guimarães, R. B., Corso Arend, M., & Medeiros Markoski, M. (2021). Molecular interaction between tissue repair via SDF-1/CXCR4 signaling and the inflammatory response in acute myocardial infarction with ST-segment elevation. Multidisciplinary Science Journal, 4(1), 2022002. https://doi.org/10.29327/multiscience.2022002

[1] Anderson LR, Owens TW, Naylor MJ (2014) Structural and mechanical functions of integrins. Biophys Ver. DOI: 10.1007/s12551-013-0124-0

[2] Ashburner M, Ball C, Blake J, et al. (2000) Gene ontology: tool for the unification of biology. Nat Genet. DOI: 10.1038/75556

[3] Barandon L, Casassus F, Leroux L, Moreau C, Allières C, Lamazière JM, Dufourcq P, Couffinhal T, Duplàa C (2011) Secreted frizzled-related protein improves postinfarction scar formation through a modulation of inflammatory response. Arterioscler Thromb Vasc Biol. DOI: 10.1161/ATVBAHA.111.232280

[4] Becker M, De Bastiani MA, Parisi MM, Guma FTCR, Markoski MM, Castro MAA, Kaplan MH, Barbé-Tuana FM & Klamt F (2015) Integrated Transcriptomics Establish Macrophage Polarization Signatures and have Potential Applications for Clinical Health and Disease. Scientific Reports. DOI: 10.1038/srep13351

[5] Dobaczewski M, Gonzalez-Quesada C, Frangogiannis NG (2010) The extracellular matrix as a modulator of the inflammatory and reparative response following myocardial infarction. J Mol Cell Cardiol. DOI: 10.1016/j.yjmcc.2009.07.015

[6] Flower DR (1999) Modelling G-protein-coupled receptors for drug design. Biochim Biophys Acta. DOI: 10.1016/s0304-4157(99)00006-4

[7] Frangogiannis NG and Rosenzweig A (2012) Regulation of the inflammatory response in cardiac repair. Circ Res. DOI: 10.1161/CIRCRESAHA.111.243162

[8] Frangogiannis NG (2015) Inflammation in cardiac injury, repair and regeneration. Curr Opin Cardiol. DOI: 10.1097/HCO.0000000000000158

[9] Frantz S, Nahrendorf M (2014) Cardiac macrophages and their role in ischaemic heart disease. Cardiovasc Res. DOI:10.1093/cvr/cvu025

[10] Gordon S, Martinez FO (2010) Alternative activation of macrophages: mechanism and functions. Immunity. DOI: 10.1016/j.immuni.2010.05.007

[11] Hermans KC, Daskalopoulos EP and Blankesteijn WM (2012) Interventions in Wnt signaling as a novel therapeutic approach to improve myocardial infarct healing. Fibrogenesis Tissue Repair. DOI: 10.1186/1755-1536-5-16

[12] Hu X, Dai S, Wu WJ, Tan W, Zhu X, Mu J, Guo Y, Bolli R, and Rokosh G (2007) Stromal cell derived factor-1 alpha confers protection against myocardial ischemia/reperfusion injury: role of the cardiac stromal cell derived factor-1 alpha CXCR4 axis. Circulation. DOI: 10.1161/CIRCULATIONAHA.106.672451

[13] Kiliszek M, Burzynska B, Michalak M, Gora M, Winkler A, Maciejak A, Leszczynska A, Gajda E, Kochanowski J, Opolskit G (2012) Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction. PLoS One. DOI: org/10.1371/journal.pone.0050054

[14] Lachtermacher S, Esporcatte BL, Montalvão F, Costa PC, Rodrigues DC, Belem L, Rabischoffisky A, Faria Neto HC, Vasconcellos R, Iacobas S, Iacobas DA, Dohmann HF, Spray DC, Goldenberg RC, Campos-de-Carvalho AC (2010) Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure. Braz J Med Biol Res. DOI: 10.1590/s0100-879x2010007500014

[15] Liehn EA, Tuchscheerer N, Kanzler I, Drechsler M, Fraemohs L, Schuh A, Koenen RR, Zander S, Soehnlein O, Hristov M, Grigorescu G, Urs AO, Leabu M, Bucur I, Merx MW, Zernecke A, Ehling J, Gremse F, Lammers T, Kiessling F, Bernhagen J, Schober A, Weber C (2011) Double-edged role of the CXCL12/CXCR4 axis in experimental myocardial infarction. J Am Coll Cardiol. DOI: 10.1016/j.jacc.2011.08.033

[16] Livak KJ and Schmittgen TD (2001) Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. DOI: 10.1006/meth.2001.1262

[17] Maciejak A, Kiliszek M, Michalak M, Tulacz D, Opolski G, Matlak K, Dobrzycki S, Segiet A, Gora M, Burzynska B (2015) Gene expression profiling reveals potential prognostic biomarkers associated with the progression of heart failure. Genome Med. DOI: 10.1186/s13073-015-0149-z

[18] Marchant DJ, Boyd JH, Lin DC, Granville DJ, Garmaroudi FS, McManus B (2012) Inflammation in myocardial diseases. Circ Res. DOI: 10.1161/CIRCRESAHA.111.243170

[19] Neves SR, Ramand PT and Iyengar RR (2002) G protein pathways. Science. DOI: 10.1126/science.107155

[20] Ni Y, Müller P, Wei L, Ji Y (2018) Bayesian graphical models for computational network biology. BMC Bioinformatics. DOI: 10.1186/s12859-018-2063-z

[21] Okkenhaug K (2013) Signaling by the phosphoinositide 3-kinase family in immune cells. Annu Rev Immunol. DOI: 10.1146/annurev-immunol-032712-095946

[22] Peterson MR, Haller SE, Ren J, Nair S, He G (2016) CARD9 as a potential target in cardiovascular disease. Drug Des Devel Ther. DOI: 10.2147/DDDT.S122508.

[23] Pfeffer MA, Braunwald E (1990) Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. DOI: 10.1161/01.cir.81.4.1161

[24] Raychaudhuri S, Prinz WA (2010) The diverse functions of oxysterol-binding proteins. Annu Rev Cell Dev Biol. Doi: 10.1146/annurev.cellbio.042308.113334

[25] Ren J, Yang M, Qi G, Zheng J, Jia L, Cheng J, Tian C, Li H, Lin X, Du J (2011) Proinflammatory protein CARD9 is essential for infiltration of monocytic fibroblast precursors and cardiac fibrosis caused by Angiotensin II infusion. Am J Hypertens. DOI: 10.1038/ajh.2011.42

[26] Saxena A, Fish JE, White MD, Yu S, Smyth JW, Shaw RM, DiMaio JM, Srivastava D (2008) Stromal cell-derived factor-1alpha is cardioprotective after myocardial infarction. Circulatio. DOI: 10.1161/CIRCULATIONAHA.107.694992

[27] Schulte G, Bryja V (2007) The Frizzled family of unconventional G-protein-coupled receptors. Trends Pharmacol Sci. DOI: 10.1016/j.tips.2007.09.001

[28] Subramanian A, Tamayo P, Mootha VK, Mukherjee S, Ebert BL, Gillette MA, Paulovich A, Pomeroy SL, Golub TR, Lander ES, Mesirov JP (2005) Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc Natl Acad Sci U S A. DOI: 10.1073/pnas.0506580102

[29] Suresh R, Li X, Chiriac A, Goel K, Terzic A, Perez-Terzic C, Nelson TJ (2014) Transcriptome from circulating cells suggests dysregulated pathways associated with long-term recurrent events following first-time myocardial infarction. J Mol Cell Cardiol. DOI: 10.1016/j.yjmcc.2014.04.017

[30] Wang K, Zhao X, Kuang C, Qian D, Wang H, Jiang H, Deng M, Huang L (2012) Overexpression of SDF-1α enhanced migration and engraftment of cardiac stem cells and reduced infarcted size via CXCR4/PI3K pathway. PLoS One. DOI: 10.1371/journal.pone.0043922

[31] Yu J, Li M, Qu Z, Yan D, Li D, Ruan Q (2010) SDF-1/CXCR4-mediated migration of transplanted bone marrow stromal cells toward areas of heart myocardial infarction through activation of PI3K/Akt. J Cardiovasc Pharmacol. DOI: 10.1097/FJC.0b013e3181d7a384

[32] Zheng H, Fu G, Dai T, Huang H (2007) Migration of endothelial progenitor cells mediated by stromal cell-derived factor-1alpha/CXCR4 via PI3K/Akt/eNOS signal transduction pathway. J Cardiovasc Pharmacol. DOI: 10.1097/FJC.0b013e318093ec8f

Abstract

References

How to cite