Stage-dependent detection of CD14+ and CD16+ cells in the human heart after myocardial infarction
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Published on: August 1, 2014
Frauke S Czepluch1, Magdalena Schlegel, Felix Bremmer
1Department of Cardiology and Pulmonary Medicine, University Medical Center Göttingen, Germany.
Insights
Human monocytes (CD14+ and CD16+) play a role in heart repair after myocardial infarction (MI). Their distribution in heart tissue changes with MI stage, influencing cardiac healing and fibrosis.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pathology
Background:
- Monocytes are crucial for cardiovascular wound healing.
- Human monocytes are classified into CD14+ and CD16+ subsets.
- Understanding monocyte roles post-myocardial infarction (MI) is key for cardiac repair.
Purpose of the Study:
- To investigate the distribution of CD14+ and CD16+ monocytes in human heart and spleen after MI.
- To correlate monocyte presence with cardiac repair markers, including fibrosis and vascularization.
- To examine monocyte dynamics in different stages of MI: acute (AMI), subacute (SAMI), and old (OMI).
Main Methods:
- Autopsy heart samples from MI patients (AMI, SAMI, OMI) and controls were histologically analyzed.
- Immunohistochemistry was used to assess CD14, CD16, CD56, carbonic anhydrase IX, and osteopontin expression.
- Capillary density and fibrosis were quantified in heart tissues.
Main Results:
- Significant fibrosis and CD56 expression were observed in OMI, correlating with fibrosis.
- Reduced capillary numbers were found in OMI compared to controls and AMI.
- Hypoxia marker carbonic anhydrase IX was elevated in AMI and SAMI; osteopontin was higher in SAMI.
- CD14+ monocyte numbers correlated with CD16+ cells and inversely with fibrosis.
Conclusions:
- Stage-specific alterations in CD14+ and CD16+ monocytes occur in the human heart post-MI.
- These monocyte changes likely contribute to cardiac repair processes and fibrosis development.
- Monocyte distribution and expression patterns offer insights into MI healing mechanisms.
Abstract:
Monocytes are critically involved in cardiovascular wound healing processes. Human monocytes can be classified into two subsets based on the expression of CD14 and CD16. Here, we examined the temporal and spatial distribution of CD14⁺ and CD16⁺ cells after myocardial infarction (MI) in human heart and spleen tissue and correlated it with markers of cardiac repair. Heart samples obtained at autopsy were histologically classified into acute (AMI; n = 11), subacute (SAMI; n = 10) and old (OMI; n = 16) MI, or control myocardium (CONTR; n = 8). Histochemical analyses revealed marked fibrosis in OMI (p < 0.001 vs. CONTR). The adhesion molecule CD56 was also strongly expressed in OMI (p < 0.01 vs. CONTR) and found to correlate with fibrosis (p < 0.001). The number of capillaries was reduced in OMI (p < 0.01 vs. CONTR; p < 0.05 vs. AMI), whereas the hypoxia indicator carbonic anhydrase IX was predominantly expressed in AMI (p < 0.01 vs. OMI and CONTR) and SAMI (p < 0.05 vs. OMI and CONTR). The monocyte chemoattractrant osteopontin was also more highly expressed in hearts of SAMI patients (p < 0.01 vs. CONTR). Numbers of CD14⁺ monocytes were found to correlate with CD16⁺ cells (p < 0.05) and inversely with fibrosis (p < 0.05). Regarding a MI-associated release of monocytes from spleen reservoirs, a non-significant reduction of splenic CD14⁺ and CD16⁺ cells was detected in subjects with AMI. In conclusion, disease stage-specific alterations in CD14⁺ and CD16 cells in human heart may contribute to cardiac repair processes following MI.
