Skip to main content

Advertisement

SpringerLink
Log in

Effect of HSP65 on the Expression of Adhesion Molecules in Mice Heart Endothelial Cells

  • Published:
Inflammation Aims and scope Submit manuscript

Abstract

This study aims to research the effect of HSP65 on the expression of adhesion molecules in activated mice heart endothelial cells (MHECs), which were from myocardial tissue of newborn animals. We used different concentrations of LPS as potent inducers to stimulate MHECs, adhesion molecule expression in vitro, including intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-, and P-selectins, then compared the mRNA and protein levels of adhesion molecules expression with or without HSP65 treatment at different levels. The optimal concentration of LPS to induce MHECs adhesion molecule expression is 100 ng/ml; HSP65 treatment significantly reduced the mRNA and protein levels of MHECs’ ICAM-1, VCAM-1, E-, and P-selectins expression (p < 0.05), and the optimal concentration of HSP65 in inhibiting MHECs activation is 0.8 ng. HSP65 has the inhibitory effect on adhesion molecules expression in activated MHECs.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2
Fig. 3
Fig. 4
Fig. 5
Fig. 6
Fig. 7
Fig. 8
Fig. 9

Similar content being viewed by others

References

  1. Lu, H.H., Z.Q. Sheng, Y. Wang, and L. Zhang. 2010. Levels of soluble adhesion molecules in patients with various clinical presentations of coronary atherosclerosis. Chinese Medical Journal 123(21): 3123–3126.

    PubMed  Google Scholar 

  2. Sitia, S., L. Tomasoni, F. Atzeni, et al. 2010. From endothelial dysfunction to atherosclerosis. Autoimmunity Reviews 9(12): 830–834.

    Article  PubMed  CAS  Google Scholar 

  3. Ribeiro, F., A.J. Alves, M. Teixeira, et al. 2009. Endothelial function and atherosclerosis: Circulatory markers with clinical usefulness. Revista Portuguesa de Cardiologia 28(10): 1121–1151.

    PubMed  Google Scholar 

  4. Xu, Q. 2002. Role of heat shock proteins in atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology 22(10): 1547–1559.

    Article  PubMed  CAS  Google Scholar 

  5. Mayr, M., S. Kiechl, J. Willeit, et al. 2000. Infections, immunity, and atherosclerosis: associations of antibodies to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus with immune reactions to heat-shock protein 60 and carotid or femoral atherosclerosis. Circulation 102: 833–839.

    PubMed  CAS  Google Scholar 

  6. Maron, R., G. Sukhova, A.M. Faria, et al. 2002. Mucosal administration of heat shock protein-65 decreases atherosclerosis and inflammation in aortic arch of low-density lipoprotein receptor-deficient mice. Circulation 106(13): 1708–1715.

    Article  PubMed  CAS  Google Scholar 

  7. Xiong, Q., J. Li, L. Jin, et al. 2009. Nasal immunization with heat shock protein 65 attenuates atherosclerosis and reduces serum lipids in cholesterol-fed wild-type rabbits probably through different mechanisms. Immunology Letters 125(1): 40–45.

    Article  PubMed  CAS  Google Scholar 

  8. Lim, Y.C., G. Garcia-Cardena, J.R. Allport, et al. 2003. Heterogeneity of endothelial cells from different organ sites in T-cell subset recruitment. American Journal of Pathology 162: 1591.

    Article  PubMed  CAS  Google Scholar 

  9. Tokgözoğlu, L. 2009. Atherosclerosis and the role of inflammation. Türk Kardiyoloji Derneği Arşivi 37(Suppl 4): 1–6.

    PubMed  Google Scholar 

  10. Shimada, K. 2009. Immune system and atherosclerotic disease: heterogeneity of leukocyte subsets participating in the pathogenesis of atherosclerosis. Circulation Journal 73(6): 994–1001.

    Article  PubMed  CAS  Google Scholar 

  11. Patti, G., R. Melfi, and G. Di Sciascio. 2005. The role of endothelial dysfunction in the pathogenesis and in clinical practice of atherosclerosis. Current evidences. Recenti Progressi in Medicina 96(10): 499–507.

    PubMed  Google Scholar 

  12. Tousoulis, D., M. Charakida, and C. Stefanadis. 2008. Endothelial function and inflammation in coronary artery disease. Postgraduate Medical Journal 84(993): 368–371.

    Article  PubMed  CAS  Google Scholar 

  13. Snoeckx, L.H., R.N. Cornelussen, F.A. Van Nieuwenhoven, R.S. Reneman, and G.J. Van Der Vusse. 2001. Heat shock proteins and cardiovascular pathophysiology. Physiological Reviews 81: 1461–1497.

    PubMed  CAS  Google Scholar 

  14. Wu, C. 1995. Heat shock transcription factors: Structure and regulation. Annual Review of Cell and Developmental Biology 11: 441–469.

    Article  PubMed  CAS  Google Scholar 

  15. Pirkkala, L., P. Nykanen, and L. Sistonen. 2001. Roles of the heat shock transcription factors in regulation of the heat shock response and beyond. The FASEB Journal 15: 1118–1131.

    Article  CAS  Google Scholar 

  16. Hoj, A., and B.K. Jakobsen. 1994. A short element required for turning off heat shock transcription factor: Evidence that phosphorylation enhances deactivation. EMBO Journal 13: 2617–2624.

    PubMed  CAS  Google Scholar 

  17. Hu, Y., L. Cheng, B.W. Hochleitner, and Q. Xu. 1997. Activation of mitogen-activated protein kinases (ERK/JNK) and AP-1 transcription factor in rat carotid arteries after balloon injury. Arteriosclerosis, Thrombosis, and Vascular Biology 17: 2808–2816.

    Article  PubMed  CAS  Google Scholar 

  18. Guyton, K.Z., Y. Liu, M. Gorospe, Q. Xu, and N.J. Holbrook. 1996. Activation of mitogen-activated protein kinase by H2O2: role in cell survival following oxidant injury. Journal of Biological Chemistry 271: 4138–4142.

    Article  PubMed  CAS  Google Scholar 

  19. Metzler, B., C. Li, Y. Hu, G. Sturm, N. Ghaffari-Tabrizi, and Q. Xu. 1999. LDL stimulates mitogen-activated protein kinase phosphatase-1 expression, independent of LDL receptors, in vascular smooth muscle cells. Arteriosclerosis, Thrombosis, and Vascular Biology 19: 1862–1871.

    Article  PubMed  CAS  Google Scholar 

  20. Metzler, B., Y. Hu, G. Sturm, G. Wick, and Q. Xu. 1998. Induction of mitogen-activated protein kinase phosphatase-1 by arachidonic acid in vascular smooth muscle cells. Journal of Biological Chemistry 273: 33320–33326.

    Article  PubMed  CAS  Google Scholar 

  21. Hu, Y., H. Dietrich, B. Metzler, G. Wick, and Q. Xu. 2000. Hyperexpression and activation of extracellular signal-regulated kinases (ERK1/2) in atherosclerotic lesions of cholesterol-fed rabbits. Arteriosclerosis, Thrombosis, and Vascular Biology 20: 18–26.

    Article  PubMed  CAS  Google Scholar 

  22. Metzler, B., Y. Hu, H. Dietrich, and Q. Xu. 2000. Increased expression and activation of stress-activated protein kinases/c-Jun NH(2)-terminal protein kinases in atherosclerotic lesions coincide with p53. American Journal of Pathology 156: 1875–1886.

    Article  PubMed  CAS  Google Scholar 

  23. Li, C., and Q. Xu. 2000. Mechanical stress-initiated signal transductions in vascular smooth muscle cells. Cellular Signalling 12: 435–445.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Laboratory Center, Affiliated Hospital of Nantong University, Nantong, China, 226001

    Changjiang Sun, Huoyan Ji, Juan Yu & Jianxin Wang

Authors
  1. Changjiang Sun
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Huoyan Ji
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Juan Yu
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Jianxin Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Changjiang Sun.

Electronic Supplementary Material

Below is the link to the electronic supplementary material.

Fig. s1

The inhibitory effect of HSP65 on endogenous VCAM-1, ICAM-1, P- and E-selectins expression determined by ELISA. Collected supernatants of MHECs cultures incubating with or without HSP65, then protein levels of VCAM-1, ICAM-1, P-, and E-selectins were detected after 12 h of incubation. The experiment has been performed for four times. (JPEG 18 kb)

High-resolution image file (TIFF 1175 kb)

Rights and permissions

Reprints and permissions

About this article

Cite this article

Sun, C., Ji, H., Yu, J. et al. Effect of HSP65 on the Expression of Adhesion Molecules in Mice Heart Endothelial Cells. Inflammation 35, 1049–1057 (2012). https://doi.org/10.1007/s10753-011-9410-9

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10753-011-9410-9

KEY WORDS

Search

Navigation