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Research ArticleIntegrative Cardiovascular Physiology and Pathophysiology


ROLE OF MACROPHAGES IN REGRESSION OF MYOCARDIAL FIBROSIS FOLLOWING ALLEVIATION
OF LEFT VENTRICULAR PRESSURE OVERLOAD

 * Lily S. Neff,
 * Rachel M. Biggs,
 * Yuhua Zhang,
 * An O. Van Laer,
 * Catalin F. Baicu,
 * Suganya Subramanian,
 * Stefano Berto,
 * Kristine DeLeon-Pennell,
 * Michael R. Zile, and
 * Amy D. Bradshaw

Lily S. Neff

Division of Cardiology, Department of Medicine, Medical University of South
Carolina, Charleston, United States

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,
Rachel M. Biggs

Medicine, Medical University of South Carolina, United States

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,
Yuhua Zhang

Medicine, Medical University of South Carolina, Charleston, South Carolina,
United States

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,
An O. Van Laer

Division of Cardiology, Department of Medicine, Medical University of South
Carolina, Charleston, SC, United States

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,
Catalin F. Baicu

Division of Cardiology, Department of Medicine, Medical University of South
Carolina, Charleston, South Carolina, United States

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,
… See all authors
Published Online:16 Feb 2024https://doi.org/10.1152/ajpheart.00240.2023
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ABSTRACT

Sustained hemodynamic pressure-overload(PO) produced by murine transverse aortic
constriction(TAC) causes myocardial fibrosis; removal of TAC(unTAC) returns LV
hemodynamic load to normal and results in significant, but incomplete regression
of myocardial fibrosis. However, the cellular mechanisms that result in these
outcomes have not been defined. The objective was to determine temporal changes
in myocardial macrophage phenotype in TAC and unTAC and determine whether
macrophage depletion alters collagen degradation after unTAC. Myocardial
macrophage abundance and phenotype were assessed by immunohistochemistry, flow
cytometry, and gene expression by rt-PCR in control(non-TAC),2wkTAC,4wkTAC, and
2wk,4wk, and 6wkunTAC. Myocardial cytokine profiles and collagen degrading
enzymes were determined by immunoassay and immunoblots. Initial collagen
degradation were detected with collagen hybridizing peptide(CHP). At unTAC,
macrophages were depleted with clodronate liposomes and endpoints measured at
2wkunTAC. Macrophage number had a defined temporal pattern: increased in 2wk and
4wkTAC, followed by increases at 2wkunTAC (over 4wkTAC), that then decreased at
4wk and 6wkunTAC. At 2wkunTAC, macrophage area was significantly increased and
was regionally associated with CHP reactivity. Cytokine profiles in unTAC
reflected a pro-inflammatory milieu versus the TAC-induced pro-fibrotic milieu.
Single cell sequencing analysis of 2wkTAC versus 2 and 6wkunTAC revealed
distinct macrophage gene expression profiles at each time point demonstrating
unique macrophage populations in unTAC versus TAC myocardium. Clodronate
liposome depletion at unTAC reduced CHP reactivity and decreased Cathepsin K and
proMMP2. We conclude that temporal changes in number and phenotype of
macrophages play a critical role in both TAC-induced development and
unTAC-mediated partial, but incomplete, regression of myocardial fibrosis.




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    Kiyokazu Koga et al., American Journal of Physiology - Heart and Circulatory
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 3. Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in
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    Jieyun You et al., American Journal of Physiology - Heart and Circulatory
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    Ming QIAN et al., Chinese Journal of Natural Medicines, 2022
 5. Luteoloside protects the vascular endothelium against iron overload injury
    via the ROS/ADMA/DDAH II/eNOS/NO pathway
    Shu-Ping CHEN et al., Chinese Journal of Natural Medicines, 2022

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Published 2/16/24 7:10 AM


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Copyright © 2024, American Journal of Physiology-Heart and Circulatory
Physiology

 * https://doi.org/10.1152/ajpheart.00240.2023
 * PubMed38363214

History
Received 25 April 2023
Accepted 12 February 2024
Published online 16 February 2024
Keywords
 * Macrophages
 * Fibrosis
 * Heart Failure
 * LVPO
 * Collagen Degradation

--------------------------------------------------------------------------------


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