Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease

Stephen J Horgan; Chris J Watson; Nadia Glezeva; Pat Collier; Roisin Neary; Isaac J Tea; Niamh Corrigan; Mark Ledwidge; Ken McDonald; John A Baugh

doi:10.1007/s12265-015-9661-1

Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease

Stephen J Horgan, Chris J Watson, Nadia Glezeva, Pat Collier, Roisin Neary, Isaac J Tea, Niamh Corrigan, Mark Ledwidge, Ken McDonald, John A Baugh

School of Medicine, Dentistry and Biomedical Sciences

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

4 Citations (Scopus)

Abstract

The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR - SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (p < 0.01), perivascular collagen (p < 0.01), and cardiomyocyte size (p < 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (p < 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.

Original language	English
Pages (from-to)	554-66
Number of pages	13
Journal	Journal of Cardiovascular Translational Research
Volume	8
Issue number	9
Early online date	17 Nov 2015
DOIs	https://doi.org/10.1007/s12265-015-9661-1
Publication status	Published - Dec 2015

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@article{9c8730ac0d8f4eeeaa7728770e451c84,

title = "Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease",

abstract = "The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR - SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (p < 0.01), perivascular collagen (p < 0.01), and cardiomyocyte size (p < 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (p < 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.",

author = "Horgan, {Stephen J} and Watson, {Chris J} and Nadia Glezeva and Pat Collier and Roisin Neary and Tea, {Isaac J} and Niamh Corrigan and Mark Ledwidge and Ken McDonald and Baugh, {John A}",

year = "2015",

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language = "English",

volume = "8",

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journal = "Journal of Cardiovascular Translational Research",

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Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease. / Horgan, Stephen J; Watson, Chris J; Glezeva, Nadia; Collier, Pat; Neary, Roisin; Tea, Isaac J; Corrigan, Niamh; Ledwidge, Mark; McDonald, Ken; Baugh, John A.

In: Journal of Cardiovascular Translational Research, Vol. 8, No. 9, 12.2015, p. 554-66.

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

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T1 - Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease

AU - Horgan, Stephen J

AU - Watson, Chris J

AU - Glezeva, Nadia

AU - Collier, Pat

AU - Neary, Roisin

AU - Tea, Isaac J

AU - Corrigan, Niamh

AU - Ledwidge, Mark

AU - McDonald, Ken

AU - Baugh, John A

PY - 2015/12

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N2 - The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR - SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (p < 0.01), perivascular collagen (p < 0.01), and cardiomyocyte size (p < 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (p < 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.

AB - The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR - SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (p < 0.01), perivascular collagen (p < 0.01), and cardiomyocyte size (p < 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (p < 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.

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SN - 1937-5387

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Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease

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