Tags

Type your tag names separated by a space and hit enter

The cardioprotective effects of parathyroid hormone are independent of endogenous granulocyte-colony stimulating factor release.
Cardiovasc Res. 2012 Feb 01; 93(2):330-9.CR

Abstract

AIMS

Parathyroid hormone (PTH) administration after myocardial infarction (MI) is known to attenuate ischaemic cardiomyopathy. This effect mainly resulted from an increase in mobilization and homing of CD34+/CD45+ cells into the ischaemic myocardium. PTH-related stem cell mobilization was shown to be related to endogenous granulocyte-colony stimulating factor (G-CSF) release. The aim of our study is to determine the role of G-CSF on the cardioprotective effects of PTH.

METHODS AND RESULTS

G-CSF +/+ (C57BL/6) and G-CSF -/- mice were treated with PTH for 6 days after inducing a MI. The myocardial homing factor stromal cell-derived factor-1 (SDF-1) was analysed on day 2 with enzyme-linked immunosorbent assay. Stem cell populations in peripheral blood and hearts were examined by FACS on days 6 and 2, respectively. Cardiac function and immunohistochemistry were investigated on day 6 and day 30. PTH treatment resulted in a significant increase in CD45+/CD34+ cells in peripheral blood in G-CSF +/+ but not in G-CSF -/- mice. However, a significant increase in SDF-1 and enhanced migration of CD45+/CD34+ cells into the ischaemic myocardium was revealed after PTH administration in both G-CSF +/+ and G-CSF -/- mice. Enhanced stem cell homing was associated with improved cardiac function and post-MI survival after PTH treatment. Furthermore, infarct size, wall thickness, and neovascularization showed a significant improvement in both groups 30 days after MI.

CONCLUSION

The cardioprotective effects of PTH were shown to be independent of endogenous G-CSF release and therefore from stem cell mobilization. This puts more emphasis on the role of stem cell homing into ischaemic myocardium.

Authors+Show Affiliations

Department of Internal Medicine I, Ludwig-Maximilians-University, Campus Grosshadern, Munich, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22080594

Citation

Brunner, Stefan, et al. "The Cardioprotective Effects of Parathyroid Hormone Are Independent of Endogenous Granulocyte-colony Stimulating Factor Release." Cardiovascular Research, vol. 93, no. 2, 2012, pp. 330-9.
Brunner S, Weinberger T, Huber BC, et al. The cardioprotective effects of parathyroid hormone are independent of endogenous granulocyte-colony stimulating factor release. Cardiovasc Res. 2012;93(2):330-9.
Brunner, S., Weinberger, T., Huber, B. C., Segeth, A., Zaruba, M. M., Theiss, H. D., Assmann, G., Herbach, N., Wanke, R., Mueller-Hoecker, J., & Franz, W. M. (2012). The cardioprotective effects of parathyroid hormone are independent of endogenous granulocyte-colony stimulating factor release. Cardiovascular Research, 93(2), 330-9. https://doi.org/10.1093/cvr/cvr303
Brunner S, et al. The Cardioprotective Effects of Parathyroid Hormone Are Independent of Endogenous Granulocyte-colony Stimulating Factor Release. Cardiovasc Res. 2012 Feb 1;93(2):330-9. PubMed PMID: 22080594.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The cardioprotective effects of parathyroid hormone are independent of endogenous granulocyte-colony stimulating factor release. AU - Brunner,Stefan, AU - Weinberger,Tobias, AU - Huber,Bruno C, AU - Segeth,Alexander, AU - Zaruba,Marc-Michael, AU - Theiss,Hans D, AU - Assmann,Gerald, AU - Herbach,Nadja, AU - Wanke,Ruediger, AU - Mueller-Hoecker,Josef, AU - Franz,Wolfgang-Michael, Y1 - 2011/11/10/ PY - 2011/11/15/entrez PY - 2011/11/15/pubmed PY - 2012/5/23/medline SP - 330 EP - 9 JF - Cardiovascular research JO - Cardiovasc Res VL - 93 IS - 2 N2 - AIMS: Parathyroid hormone (PTH) administration after myocardial infarction (MI) is known to attenuate ischaemic cardiomyopathy. This effect mainly resulted from an increase in mobilization and homing of CD34+/CD45+ cells into the ischaemic myocardium. PTH-related stem cell mobilization was shown to be related to endogenous granulocyte-colony stimulating factor (G-CSF) release. The aim of our study is to determine the role of G-CSF on the cardioprotective effects of PTH. METHODS AND RESULTS: G-CSF +/+ (C57BL/6) and G-CSF -/- mice were treated with PTH for 6 days after inducing a MI. The myocardial homing factor stromal cell-derived factor-1 (SDF-1) was analysed on day 2 with enzyme-linked immunosorbent assay. Stem cell populations in peripheral blood and hearts were examined by FACS on days 6 and 2, respectively. Cardiac function and immunohistochemistry were investigated on day 6 and day 30. PTH treatment resulted in a significant increase in CD45+/CD34+ cells in peripheral blood in G-CSF +/+ but not in G-CSF -/- mice. However, a significant increase in SDF-1 and enhanced migration of CD45+/CD34+ cells into the ischaemic myocardium was revealed after PTH administration in both G-CSF +/+ and G-CSF -/- mice. Enhanced stem cell homing was associated with improved cardiac function and post-MI survival after PTH treatment. Furthermore, infarct size, wall thickness, and neovascularization showed a significant improvement in both groups 30 days after MI. CONCLUSION: The cardioprotective effects of PTH were shown to be independent of endogenous G-CSF release and therefore from stem cell mobilization. This puts more emphasis on the role of stem cell homing into ischaemic myocardium. SN - 1755-3245 UR - https://www.unboundmedicine.com/medline/citation/22080594/The_cardioprotective_effects_of_parathyroid_hormone_are_independent_of_endogenous_granulocyte_colony_stimulating_factor_release_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/cvr303 DB - PRIME DP - Unbound Medicine ER -