Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction

Joseph J. Sepe; Ryan T. Gardner; Matthew R. Blake; Deja M. Brooks; Melanie A. Staffenson; Courtney B. Betts; Sam Sivagnanam; William Larson; Sushil Kumar; Richard G. Bayles; Haihong Jin; Michael S. Cohen; Lisa M. Coussens; Beth A. Habecker

doi:10.1016/j.jacbts.2022.04.009

Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction

Joseph J. Sepe, Ryan T. Gardner, Matthew R. Blake, Deja M. Brooks, Melanie A. Staffenson, Courtney B. Betts, Sam Sivagnanam, William Larson, Sushil Kumar, Richard G. Bayles, Haihong Jin, Michael S. Cohen, Lisa M. Coussens, Beth A. Habecker

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

7 Scopus citations

Abstract

Myocardial infarction (MI) triggers an inflammatory response that transitions from pro-inflammatory to reparative over time. Restoring sympathetic nerves in the heart after MI prevents arrhythmias. This study investigated if reinnervation altered the immune response after MI. This study used quantitative multiplex immunohistochemistry to identify the immune cells present in the heart 2 weeks after ischemia-reperfusion. Two therapeutics stimulated reinnervation, preventing arrhythmias and shifting the immune response from inflammatory to reparative, with fewer pro-inflammatory macrophages and more regulatory T cells and reparative macrophages. Treatments did not alter macrophage phenotype in vitro, which suggested reinnervation contributed to the altered immune response.

Original language	English (US)
Pages (from-to)	915-930
Number of pages	16
Journal	JACC: Basic to Translational Science
Volume	7
Issue number	9
DOIs	https://doi.org/10.1016/j.jacbts.2022.04.009
State	Published - Sep 2022
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2022 The Authors

Keywords

inflammation
macrophages
multiplex IHC
myocardial infarction
sympathetic nervous system

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.jacbts.2022.04.009

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Sepe, J. J., Gardner, R. T., Blake, M. R., Brooks, D. M., Staffenson, M. A., Betts, C. B., Sivagnanam, S., Larson, W., Kumar, S., Bayles, R. G., Jin, H., Cohen, M. S., Coussens, L. M., & Habecker, B. A. (2022). Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction. JACC: Basic to Translational Science, 7(9), 915-930. https://doi.org/10.1016/j.jacbts.2022.04.009

Sepe, JJ, Gardner, RT, Blake, MR, Brooks, DM, Staffenson, MA, Betts, CB, Sivagnanam, S, Larson, W, Kumar, S, Bayles, RG, Jin, H, Cohen, MS, Coussens, LM & Habecker, BA 2022, 'Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction', JACC: Basic to Translational Science, vol. 7, no. 9, pp. 915-930. https://doi.org/10.1016/j.jacbts.2022.04.009

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title = "Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction",

abstract = "Myocardial infarction (MI) triggers an inflammatory response that transitions from pro-inflammatory to reparative over time. Restoring sympathetic nerves in the heart after MI prevents arrhythmias. This study investigated if reinnervation altered the immune response after MI. This study used quantitative multiplex immunohistochemistry to identify the immune cells present in the heart 2 weeks after ischemia-reperfusion. Two therapeutics stimulated reinnervation, preventing arrhythmias and shifting the immune response from inflammatory to reparative, with fewer pro-inflammatory macrophages and more regulatory T cells and reparative macrophages. Treatments did not alter macrophage phenotype in vitro, which suggested reinnervation contributed to the altered immune response.",

keywords = "inflammation, macrophages, multiplex IHC, myocardial infarction, sympathetic nervous system",

author = "Sepe, {Joseph J.} and Gardner, {Ryan T.} and Blake, {Matthew R.} and Brooks, {Deja M.} and Staffenson, {Melanie A.} and Betts, {Courtney B.} and Sam Sivagnanam and William Larson and Sushil Kumar and Bayles, {Richard G.} and Haihong Jin and Cohen, {Michael S.} and Coussens, {Lisa M.} and Habecker, {Beth A.}",

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year = "2022",

month = sep,

doi = "10.1016/j.jacbts.2022.04.009",

language = "English (US)",

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AU - Sepe, Joseph J.

AU - Gardner, Ryan T.

AU - Blake, Matthew R.

AU - Brooks, Deja M.

AU - Staffenson, Melanie A.

AU - Betts, Courtney B.

AU - Sivagnanam, Sam

AU - Larson, William

AU - Kumar, Sushil

AU - Bayles, Richard G.

AU - Jin, Haihong

AU - Cohen, Michael S.

AU - Coussens, Lisa M.

AU - Habecker, Beth A.

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AB - Myocardial infarction (MI) triggers an inflammatory response that transitions from pro-inflammatory to reparative over time. Restoring sympathetic nerves in the heart after MI prevents arrhythmias. This study investigated if reinnervation altered the immune response after MI. This study used quantitative multiplex immunohistochemistry to identify the immune cells present in the heart 2 weeks after ischemia-reperfusion. Two therapeutics stimulated reinnervation, preventing arrhythmias and shifting the immune response from inflammatory to reparative, with fewer pro-inflammatory macrophages and more regulatory T cells and reparative macrophages. Treatments did not alter macrophage phenotype in vitro, which suggested reinnervation contributed to the altered immune response.

KW - inflammation

KW - macrophages

KW - multiplex IHC

KW - myocardial infarction

KW - sympathetic nervous system

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Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction

Abstract

Bibliographical note

Keywords

UN SDGs

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