Prominin-1+/CD133+ bone marrow-derived heart-resident cells suppress experimental autoimmune myocarditis

Kania, Gabriela; Błyszczuk, Przemysław; Valaperti, Alan; Dieterle, Thomas; Leimenstoll, Bernd; Dirnhofer, Stephan; Zulewski, Henryk; Eriksson, Urs

doi:10.1093/cvr/cvn190

Cited by 36 publications

(46 citation statements)

References 38 publications

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“…However, heart-infiltrating prominin-1 ϩ cells showed impaired regenerative capacity (new cardiomyocytes formation). This is in strong contrast to prominin-1 ϩ cells derived from healthy heart, 16 despite the high similarity regarding the expression of stem/progenitor cell markers and immunomodulatory properties. Thus, our findings point to careful evaluation of stem/progenitor cells isolated from injured organs for use in regenerative medicine.…”

Section: Discussionmentioning

confidence: 59%

“…Prominin-1 is a well-established marker of hematopoietic, embryonic and adult progenitors. 16,23,24 We illustrated that heart-infiltrating prominin-1 ϩ cells represent a common progenitor for fibroblasts and macrophages in EAM. However, heart-infiltrating prominin-1 ϩ cells showed impaired regenerative capacity (new cardiomyocytes formation).…”

Section: Discussionmentioning

confidence: 77%

“…16 Prominin-1 ϩ cells were isolated by magnetic cell sorting and further expanded in vitro in culture expansion medium (Online Data Supplement, available at http://circres.ahajournals.org). To generate single-cell-derived clones, a single prominin-1 ϩ /EGFP ϩ cell was coplated with prominin-1 ϩ / EGFP Ϫ feeder cells derived from the healthy heart and cultured for 2 to 3 weeks.…”

Section: Micementioning

confidence: 99%

“…16 For real-time RT-PCR analysis, cDNA was amplified using the Power SYBR Green PCR Master Mix (Applied Biosystems) and oligonucleotides complementary to transcripts of the analyzed genes (Online Table I). …”

Section: Rt-pcr and Real-time Rt-pcrmentioning

confidence: 99%

“…Fixation and immunostaining procedures were performed as described previously (Online Data Supplement). 16 …”

Section: Immunocytochemistrymentioning

confidence: 99%

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Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Kania¹,

Błyszczuk²,

Stein³

et al. 2009

Circulation Research

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 77%

Section: Micementioning

confidence: 99%

Section: Rt-pcr and Real-time Rt-pcrmentioning

confidence: 99%

“…Fixation and immunostaining procedures were performed as described previously (Online Data Supplement). 16 …”

Section: Immunocytochemistrymentioning

confidence: 99%

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Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Kania¹,

Błyszczuk²,

Stein³

et al. 2009

Circulation Research

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Characterization of dendritic cells in human and experimental myocarditis

et al. 2020

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Aims Dendritic cells (DCs) are central mediators of adaptive immunity, and there is growing evidence of their role in myocardial inflammatory disease. We hypothesized that plasmacytoid and myeloid DCs are involved in the mechanisms of myocarditis and analysed these two main subtypes in human myocarditis subjects, as well as in a murine model of experimental autoimmune myocarditis (EAM). Methods and results Circulating DCs were analysed by flow cytometry in patients with acute myocarditis, dilated cardiomyopathy, and controls. Myocardial biopsies were immunostained for the presence of DCs and compared with non-diseased controls. In a mouse model of acute myocarditis induced through synthetic cardiac myosine peptide injection, effects of immunomodulation including DC inhibition through MCS-18 versus placebo treatment were tested at the peak of inflammation (Day 21), as well as 1 week later (partial recovery). Circulatory pDCs and mDCs were significantly reduced in myocarditis patients compared with controls (P < 0.01 for both) and remained so even after 6 months of follow-up. Human myocarditis biopsies showed accumulation of pDCs (two-fold CD304+/three-fold CD123+, all P < 0.05) compared with controls. Myocardial pDCs and mDCs accumulated in EAM (P for both <0.0001). MCS-18 treatment reduced pDC levels (P = 0.009), reduced myocardial inflammation (myocarditis score reduction from 2.6 to 1.8, P = 0.026), and improved ejection fraction (P = 0.03) in EAM at Day 21 (peak of inflammation). This effect was not observed during the partial recovery of inflammation on Day 28. Conclusions Circulating DCs are reduced in human myocarditis and accumulate in the inflamed myocardium. MCS-18 treatment reduces DCs in EAM, leading to amelioration of inflammation and left ventricular remodelling during the acute phase of myocarditis. Our data further elucidate the role of DCs and their specific subsets in acute inflammatory cardiomyopathies.

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Cooperation of Th1 and Th17 cells determines transition from autoimmune myocarditis to dilated cardiomyopathy

et al. 2012

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Myocarditis is a potentially lethal inflammatory heart disease of children and young adults that frequently leads to dilated cardiomyopathy (DCM). Since diagnostic procedures and efficient therapies are lacking, it is important to characterize the critical immune effector pathways underlying the initial cardiac inflammation and the transition from myocarditis to DCM. We describe here a T-cell receptor (TCR) transgenic mouse model with spontaneously developing autoimmune myocarditis that progresses to lethal DCM. Cardiac magnetic resonance imaging revealed early inflammation-associated changes in the ventricle wall including transient thickening of the left ventricle wall. Furthermore, we found that IFN-γ was a major effector cytokine driving the initial inflammatory process and that the cooperation of IFN-γ and IL-17A was essential for the development of the progressive disease. This novel TCR transgenic mouse model permits the identification of the central pathophysiological and immunological processes involved in the transition from autoimmune myocarditis to DCM.

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Prominin-1+/CD133+ bone marrow-derived heart-resident cells suppress experimental autoimmune myocarditis

Abstract: Prominin-1-expressing, heart-resident, bone marrow-derived cells combine high plasticity, T cell-suppressing capacity, and anti-inflammatory in vivo effects.

Cited by 36 publications

References 38 publications

Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Characterization of dendritic cells in human and experimental myocarditis

Cooperation of Th1 and Th17 cells determines transition from autoimmune myocarditis to dilated cardiomyopathy

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Prominin-1+/CD133+ bone marrow-derived heart-resident cells suppress experimental autoimmune myocarditis

Abstract: Prominin-1-expressing, heart-resident, bone marrow-derived cells combine high plasticity, T cell-suppressing capacity, and anti-inflammatory in vivo effects.

Cited by 36 publications

References 38 publications

Heart-Infiltrating Prominin-1 + /CD133 + Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Heart-Infiltrating Prominin-1 + /CD133 + Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Characterization of dendritic cells in human and experimental myocarditis

Cooperation of Th1 and Th17 cells determines transition from autoimmune myocarditis to dilated cardiomyopathy

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Product

Resources

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Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis

Heart-Infiltrating Prominin-1 ⁺ /CD133 ⁺ Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis