S100A8/A9 in Myocardial Infarction

  • Gopalkrishna Sreejit
  • Sunil Kiran Nooti
  • Baskaran Athmanathan
  • Prabhakara Reddy NagareddyEmail author
Part of the Methods in Molecular Biology book series (MIMB, volume 1929)


S100A8/A9 represents a novel biomarker and therapeutic target in sterile inflammatory diseases. Among the various S100 proteins, S100A8 and S100A9 have been shown to be the most important of all the damage-associated molecular pattern (DAMP) proteins in sterile inflammatory conditions such as diabetes, cardiovascular disease, autoimmune disorders, etc. We present here methods to quantify S100A8/A9 expression in various tissues in mouse models of myocardial infarction (MI) using flow cytometry (FC), immunofluorescence, quantitative real-time polymerase chain reaction (q-RT-PCR), and enzyme-linked immunosorbent assays (ELISA).

Key words

S100A8/A9 Myocardial infarction Neutrophils Mononuclear cells 


  1. 1.
    Altwegg LA, Neidhart M, Hersberger M et al (2007) Myeloid-related protein 8/14 complex is released by monocytes and granulocytes at the site of coronary occlusion: a novel, early, and sensitive marker of acute coronary syndromes. Eur Heart J 28:941–948CrossRefGoogle Scholar
  2. 2.
    Morrow DA, Wang Y, Croce K et al (2008) Myeloid-related protein 8/14 and the risk of cardiovascular death or myocardial infarction after an acute coronary syndrome in the Pravastatin or Atorvastatin Evaluation and Infection Theraphy: Thrombolysis in Myocardial Infarction (PROVE IT-TIMI 22) trial. Am Heart J 155:49–55CrossRefGoogle Scholar
  3. 3.
    Schaub N, Reichlin T, Meune C et al (2012) Markers of plaque instability in the early diagnosis and risk stratification of acute myocardial infarction. Clin Chem 58:246–256CrossRefGoogle Scholar
  4. 4.
    Averill MM, Kerkhoff C, Bornfeldt KE (2012) S100A8 and S100A9 in cardiovascular biology and disease. Arterioscler Thromb Vasc Biol 32:223–229CrossRefGoogle Scholar
  5. 5.
    Hsu K, Champaiboon C, Guenther BD et al (2009) Anti-infective protective properties of S100 calgranulins. Antiinflamm Antiallergy Agents Med Chem 8:290–305CrossRefGoogle Scholar
  6. 6.
    Foell D, Wittkowski H, Vogl T et al S100 proteins expressed in phagocytes: a novel group of damage-associated molecular pattern molecules. J Leukoc Biol 81:28–37CrossRefGoogle Scholar
  7. 7.
    Geczy CL, Chung YM, Hiroshima Y (2014) Calgranulins may contribute vascular protection in atherogenesis. Circ J 78:271–280CrossRefGoogle Scholar
  8. 8.
    van LPLEM, Blom AB, Schelbergen RFP et al (2012) Active involvement of alarmins S100A8 and S100A9 in the regulation of synovial activation and joint destruction during mouse and human osteoarthritis. Arthritis Rheum 64:1466–1476CrossRefGoogle Scholar
  9. 9.
    Vogl T, Tenbrock K, Ludwig S et al (2007) Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock. Nat Med 13:1042CrossRefGoogle Scholar
  10. 10.
    Passey RJ, Williams E, Lichanska AM et al (1999) A null mutation in the inflammation-associated S100 protein S100A8 causes early resorption of the mouse embryo. J Immunol 163:2209–2216PubMedGoogle Scholar
  11. 11.
    Hobbs JAR, May R, Tanousis K et al (2003) Myeloid cell function in MRP-14 (S100A9) null mice. Mol Cell Biol 23:2564–2576CrossRefGoogle Scholar
  12. 12.
    Manitz M-P, Horst B, Seeliger S et al (2003) Loss of S100A9 (MRP14) results in reduced interleukin-8-induced CD11b surface expression, a polarized microfilament system, and diminished responsiveness to chemoattractants In vitro. Mol Cell Biol 23:1034–1043CrossRefGoogle Scholar
  13. 13.
    Katashima T, Naruko T, Terasaki F et al (2010) Enhanced expression of the S100A8/A9 complex in acute myocardial infarction patients. Circ J 74:741–748CrossRefGoogle Scholar
  14. 14.
    Volz HC, Laohachewin D, Seidel C et al (2012) S100A8/A9 aggravates post-ischemic heart failure through activation of RAGE-dependent NF-κB signaling. Basic Res Cardiol 107:250CrossRefGoogle Scholar
  15. 15.
    Knorr M, Münzel T, Wenzel P (2014) Interplay of NK cells and monocytes in vascular inflammation and myocardial infarction. Front Physiol 5:295CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Gopalkrishna Sreejit
    • 1
  • Sunil Kiran Nooti
    • 1
  • Baskaran Athmanathan
    • 1
  • Prabhakara Reddy Nagareddy
    • 1
    Email author
  1. 1.Department of PathologyUniversity of AlabamaBirminghamUSA

Personalised recommendations