Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy

Harmen R. Zandbergen; Umesh C. Sharma; Sudhir Gupta; Johan W.H. Verjans; Susanne Van Den Borne; Saraswati Pokharel; Thomas Van Brakel; Adriaan Duijvestijn; Nico Van Rooijen; Jos G. Maessen; Chris Reutelingsperger; Yigal M. Pinto; Jagat Narula; Leo Hofstra

doi:10.1177/1074248408329860

Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy

Harmen R. Zandbergen, Umesh C. Sharma, Sudhir Gupta, Johan W.H. Verjans, Susanne Van Den Borne, Saraswati Pokharel, Thomas Van Brakel, Adriaan Duijvestijn, Nico Van Rooijen, Jos G. Maessen, Chris Reutelingsperger, Yigal M. Pinto, Jagat Narula, Leo Hofstra

Research output: Contribution to journal › Article › peer-review

53 Scopus citations

Abstract

Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure-prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate- treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.

Original language	English
Pages (from-to)	68-75
Number of pages	8
Journal	Journal of Cardiovascular Pharmacology and Therapeutics
Volume	14
Issue number	1
DOIs	https://doi.org/10.1177/1074248408329860
State	Published - Mar 2009
Externally published	Yes

Keywords

Heart failure
Hypertension
Inflammation
Ventricular remodeling

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Zandbergen, H. R., Sharma, U. C., Gupta, S., Verjans, J. W. H., Van Den Borne, S., Pokharel, S., Van Brakel, T., Duijvestijn, A., Van Rooijen, N., Maessen, J. G., Reutelingsperger, C., Pinto, Y. M., Narula, J., & Hofstra, L. (2009). Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy. Journal of Cardiovascular Pharmacology and Therapeutics, 14(1), 68-75. https://doi.org/10.1177/1074248408329860

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title = "Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy",

abstract = "Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure-prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate- treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.",

keywords = "Heart failure, Hypertension, Inflammation, Ventricular remodeling",

author = "Zandbergen, {Harmen R.} and Sharma, {Umesh C.} and Sudhir Gupta and Verjans, {Johan W.H.} and {Van Den Borne}, Susanne and Saraswati Pokharel and {Van Brakel}, Thomas and Adriaan Duijvestijn and {Van Rooijen}, Nico and Maessen, {Jos G.} and Chris Reutelingsperger and Pinto, {Yigal M.} and Jagat Narula and Leo Hofstra",

year = "2009",

month = mar,

doi = "10.1177/1074248408329860",

language = "English",

volume = "14",

pages = "68--75",

journal = "Journal of Cardiovascular Pharmacology and Therapeutics",

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Zandbergen, HR, Sharma, UC, Gupta, S, Verjans, JWH, Van Den Borne, S, Pokharel, S, Van Brakel, T, Duijvestijn, A, Van Rooijen, N, Maessen, JG, Reutelingsperger, C, Pinto, YM, Narula, J & Hofstra, L 2009, 'Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy', Journal of Cardiovascular Pharmacology and Therapeutics, vol. 14, no. 1, pp. 68-75. https://doi.org/10.1177/1074248408329860

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AU - Zandbergen, Harmen R.

AU - Sharma, Umesh C.

AU - Gupta, Sudhir

AU - Verjans, Johan W.H.

AU - Van Den Borne, Susanne

AU - Pokharel, Saraswati

AU - Van Brakel, Thomas

AU - Duijvestijn, Adriaan

AU - Van Rooijen, Nico

AU - Maessen, Jos G.

AU - Reutelingsperger, Chris

AU - Pinto, Yigal M.

AU - Narula, Jagat

AU - Hofstra, Leo

PY - 2009/3

Y1 - 2009/3

N2 - Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure-prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate- treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.

AB - Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure-prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate- treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.

KW - Heart failure

KW - Hypertension

KW - Inflammation

KW - Ventricular remodeling

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Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy

Abstract

Keywords

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