Characteristics of pericardial interstitial cells and their implications in pericardial fibrocalcification

Liu, Xiaohong; Tan, Mengwei; Gong, Daozhi; Han, Lin; Lu, Fanglin; Huang, Shengdong; Zhao, Xu

doi:10.1016/j.yjmcc.2012.09.008

Cited by 10 publications

(12 citation statements)

References 40 publications

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“…First, although the rat's parietal pericardium is thin and different from that of human's, the autopsy showed similar pathological features as thickening and rigidity and the histological findings further confirmed pericardial fibrosis. This present study complies with the findings of the studies conducted by Liu et al and Afanasyeva et al 15,19,20 …”

Section: Discussionsupporting

confidence: 94%

A novel model of constrictive pericarditis associated with myocardial fibrosis in rats

Qiao

Wang

et al. 2020

Clin Exp Pharma Physio

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An efficient animal model is fundamental for studies on the underlying mechanisms of constrictive pericarditis (CP). A novel CP rat model was established by pericardial injection composing of lipopolysaccharides (LPS) and talcum powder without thoracotomy. Pathological changes were confirmed by histological staining. E‐flow Doppler of mitral valve, tissue Doppler E′ in the medial mitral annular (E′sep) and the lateral mitral annular (E′lat) were measured to assess ventricular filling function. Circumferential, longitudinal, and radial strains (SC, SL and SR) and the respective strain rates (SrC, SrL and SrR) were analyzed in interventricular septum (IVS) and left ventricular free wall (LVFW). Rat cardiac fibroblasts (CFs) were treated with LPS. The activation of transforming growth factor β1 (TGF‐β1) was confirmed by Q‐PCR and western blot assays. Thickening of pericardium and fibrosis in pericardium and subepicardial myocardium were showed in the model group. Diastolic dysfunction in the CP group was indicated by decreased E′lat and E′lat/E′sep, increased E/E′lat, decreased EFW of SrC and SrL, increased AIVS and decreased E/A of SrC, SrL and SrR. Systolic dysfunction was indicated by decreased SCFW and SLFW in CP rats. The levels of TGF‐β1, p‐Smad2/3, α‐smooth muscle actin (α‐SMA), and collagen‐I/III (COL‐I/III) were increased in the CP group. The increased TGF‐β1 that induced by LPS activated and phosphorylated Smad2/3 resulting in the secretion of α‐SMA and COL‐I/III. This model is of vital importance in studying the pathogenesis of CP.

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Section: Discussionsupporting

confidence: 94%

A novel model of constrictive pericarditis associated with myocardial fibrosis in rats

Qiao

Wang

et al. 2020

Clin Exp Pharma Physio

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“…The active regulation of both pro- and anti-inflammatory mediators by mesothelial cells suggests a key role for the cells in maintaining pericardial homeostasis and also in the pathogenesis of pericardial fibrosis. Pericardial interstitial cells (PICs) have also been implicated in the production of ECM and calcification in the pericardium[ 77 ].…”

Section: The Fibrotic Process and Constrictive Pericarditismentioning

confidence: 99%

“…TGF-β and bone morphogenetic protein 2 (BMP-2) were associated with the trans-differentiation process. TGF-β increased PIC mRNA expression of collagens I and III whilst decreasing the matrix metalloprotease-2 and -9 mRNA levels which are important for elastin degradation, thus regulating the fibrotic process by modulating fibrosis related gene expression[ 77 ].…”

Section: The Fibrotic Process and Constrictive Pericarditismentioning

confidence: 99%

Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis

Ramasamy¹,

Mayosi²,

Sturrock³

et al. 2018

WJC

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This review article aims to: (1) discern from the literature the immune and inflammatory processes occurring in the pericardium following injury; and (2) to delve into the molecular mechanisms which may play a role in the progression to constrictive pericarditis. Pericarditis arises as a result of a wide spectrum of pathologies of both infectious and non-infectious aetiology, which lead to various degrees of fibrogenesis. Current understanding of the sequence of molecular events leading to pathological manifestations of constrictive pericarditis is poor. The identification of key mechanisms and pathways common to most fibrotic events in the pericardium can aid in the design and development of novel interventions for the prevention and management of constriction. We have identified through this review various cellular events and signalling cascades which are likely to contribute to the pathological fibrotic phenotype. An initial classical pattern of inflammation arises as a result of insult to the pericardium and can exacerbate into an exaggerated or prolonged inflammatory state. Whilst the implication of major drivers of inflammation and fibrosis such as tumour necrosis factor and transforming growth factor β were foreseeable, the identification of pericardial deregulation of other mediators (basic fibroblast growth factor, galectin-3 and the tetrapeptide Ac-SDKP) provides important avenues for further research.

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“…The cCFU-F lineage doubtless also contributes to pathological fibrosis in hypertension and other cardiac pathologies and the fibro-fatty infiltration that accompanies certain myopathies [77]. Fibro-calcification of the pericardium and cardiac valves may also involve CFU-F/MSC-like cells [78]. This view of the cCFU-F lineage hierarchy requires rigorous testing.…”

Section: Lineage Potency Of Cardiac Msc-like Cellsmentioning

confidence: 99%

Epicardial Origin of Resident Mesenchymal Stem Cells in the Adult Mammalian Heart

Asli

Xaymardan

Harvey

2014

JDB

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The discovery of stem and progenitor cells in the adult mammalian heart has added a vital dimension to the field of cardiac regeneration. Cardiac-resident stem cells are likely sequestered as reserve cells within myocardial niches during the course of embryonic cardiogenesis, although they may also be recruited from external sources, such as bone marrow. As we begin to understand the nature of cardiac-resident stem and progenitor cells using a variety of approaches, it is evident that they possess an identity embedded within their gene regulatory networks that favours cardiovascular lineage potential. In addition to contributing lineage descendants, cardiac stem cells may also be stress sensors, offering trophic cues to other cell types, including cardiomyocytes and vasculature cells, and likely other stem cells and immune cells, during adaptation and repair. This presents numerous possibilities for endogenous cardiac stem and progenitor cells to be used in cell therapies

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Characteristics of pericardial interstitial cells and their implications in pericardial fibrocalcification

Cited by 10 publications

References 40 publications

A novel model of constrictive pericarditis associated with myocardial fibrosis in rats

A novel model of constrictive pericarditis associated with myocardial fibrosis in rats

Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis

Epicardial Origin of Resident Mesenchymal Stem Cells in the Adult Mammalian Heart

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