Coronary artery mechanics induces human saphenous vein remodelling <i>via</i> recruitment of adventitial myofibroblast-like cells mediated by Thrombospondin-1

Garoffolo, Gloria; Ruiter, Matthijs S.; Piola, Marco; Brioschi, Marcos Leal; Thomas, Anita C.; Agrifoglio, Marco; Polvani, Gianluca; Coppadoro, Pietro Lorenzo; Zoli, Stefano; Saccu, Claudio; Spinetti, Gaia; Banfi, Cristina; Fiore, Gianfranco Beniamino; Madeddu, Paolo; Soncini, Monica; Pesce, Maurizio

doi:10.7150/thno.40595

Cited by 24 publications

(29 citation statements)

References 50 publications

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“…In this study, cyclic strain induced a switching of VSMCs from contractile to synthetic phenotype, associated with a consistent release of Thrombospondin-1, a pro-fibrotic matricellular protein, with chemoattractant effects on saphenous vein progenitor cells (SVPs) (Fig. 2) (43). In addition, this protein, in conjunction with TGF-β1, increased SVP proliferation rate and collagen production, resulting into myofibroblast-like differentiation of vein progenitor cells (Fig.…”

Section: Cell Mechanosensing Participates To Pro-pathological Vessel Wall Remodelingmentioning

confidence: 76%

“…Although this pathology has been considered for many years as an endothelial-inflammatory disease, nowadays, recent evidences highlight a strong implication of cell- and tissue-based mechanosensitivity in the initiation of this disease. Indeed, it has been demonstrated that the direct exposure of human saphenous vein to coronary pulsatile pressure causes a complete remodeling of the vessel wall, both at the cell and tissue level ( 43 ). In this study, cyclic strain induced a switching of VSMCs from contractile to synthetic phenotype, associated with a consistent release of thrombospondin-1, a pro-fibrotic matricellular protein, with chemoattractant effects on saphenous vein progenitor cells (SVPs) ( Fig.…”

Section: Cell Mechanosensing Participates To Pro-pathological Vessel Wall Remodelingmentioning

confidence: 99%

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Vascular dysfunction and pathology: focus on mechanical forces

Garoffolo

Pesce

2021

Vascular Biology

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The role of mechanical forces is emerging as a new player in pathophysiologic programming of the cardiovascular system. The ability of the cells to ‘sense’ mechanical forces does not relate only to perception of movement or flow, as intended traditionally, but also to the biophysical properties of the extracellular matrix, the geometry of the tissues and the force distribution inside them. This is also supported by the finding that cells can actively translate mechanical cues into discrete gene expression and epigenetic programming. In the present review we will contextualize these new concepts in the vascular pathologic programming.

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Section: Cell Mechanosensing Participates To Pro-pathological Vessel Wall Remodelingmentioning

confidence: 76%

Section: Cell Mechanosensing Participates To Pro-pathological Vessel Wall Remodelingmentioning

confidence: 99%

Vascular dysfunction and pathology: focus on mechanical forces

Garoffolo

Pesce

2021

Vascular Biology

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“…In particular, the position and the arrangement of vascular smooth muscle cells (VSMCs) inside the vessel wall affect their ability to sense and respond to this oscillatory pulsatile pressure [ 122 ]. An interesting example in which altered wall strain forces due to coronary flow pattern contribute to the setting of vascular pathology is the coronary venous bypass grafting [ 123 ]. This surgical procedure involves the use of venous conduits, preferentially saphenous veins, which are implanted in peripheral/coronary position in patients with chronic ischemic heart disease.…”

Section: Blood Vesselsmentioning

confidence: 99%

“…Vein conduits are subjected to a shift from a low and constant flow to a high and pulsatile coronary pattern, which affects both the endothelium, which experiences high and perturbed shear stress, and the VSMCs, due to the high cyclic strain. Direct exposure of human saphenous veins to pulsatile flow determines remodeling in the vessel wall resulting in a conversion of VSMCs from a contractile to a synthetic/proliferative phenotype with a consistent release of Thrombospondin-1 (TSP-1), a matricellular protein involved in the TGF-β pro-fibrotic pathway [ 123 ]. This protein has a direct chemotactic effect on saphenous vein adventitial progenitor cells, which migrate from adventitia to the media layer and differentiate in myofibroblast-like cells, thus contributing to the pro-pathologic programming of the graft.…”

Section: Blood Vesselsmentioning

confidence: 99%

“…Evidence suggests that TGF-β is able to transcriptionally modulate miR-22 expression level through a p53-dependant mechanism [ 147 ]. Since the TGF-β pathway was found to be upregulated in coronary artery-like mechanical stimulated human veins [ 123 ], vascular grafts functionalized with this miRNA could represent an innovative strategy to prevent cell pathological activation leading to altered ECM remodeling and thus vascular fibrosis.…”

Section: Blood Vesselsmentioning

confidence: 99%

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Harnessing Mechanosensation in Next Generation Cardiovascular Tissue Engineering

et al. 2020

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The ability of the cells to sense mechanical cues is an integral component of ”social” cell behavior inside tissues with a complex architecture. Through ”mechanosensation” cells are in fact able to decrypt motion, geometries and physical information of surrounding cells and extracellular matrices by activating intracellular pathways converging onto gene expression circuitries controlling cell and tissue homeostasis. Additionally, only recently cell mechanosensation has been integrated systematically as a crucial element in tissue pathophysiology. In the present review, we highlight some of the current efforts to assess the relevance of mechanical sensing into pathology modeling and manufacturing criteria for a next generation of cardiovascular tissue implants.

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CD (Cluster of Differentiation)

Encyclopedic Reference of Immunotoxicology

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CD47, also known as integrin-associated protein, is a constitutively and ubiquitously expressed transmembrane receptor. CD47 is conserved across amniotes including mammals, reptiles, and birds. Expression is increased in many cancers and, in non-malignant cells, by stress and with aging. The up-regulation of CD47 expression is generally epigenetic, whereas gene amplification occurs with low frequency in some cancers. CD47 is a high affinity signaling receptor for the secreted protein thrombospondin-1 (THBS1) and the counter-receptor for signal regulatory protein-α (SIRPA, SIRPα) and SIRPγ (SIRPG). CD47 interaction with SIRPα serves as a marker of self to innate immune cells and thereby protects cancer cells from phagocytic clearance. Consequently, higher CD47 correlates with a poor prognosis in some cancers, and therapeutic blockade can suppress tumor growth by enhancing innate antitumor immunity. CD47 expressed on cytotoxic T cells, dendritic cells, and NK cells mediates inhibitory THBS1 signaling that further limits antitumor immunity. CD47 laterally associates with several integrins and thereby regulates cell adhesion and migration. CD47 has additional lateral binding partners in specific cell types, and ligation of CD47 in some cases modulates their function. THBS1-CD47 signaling in non-malignant cells inhibits nitric oxide/cGMP, calcium, and VEGF signaling, mitochondrial homeostasis, stem cell maintenance, protective autophagy, and DNA damage response, and promotes NADPH oxidase activity. CD47 signaling is a physiological regulator of platelet activation, angiogenesis and blood flow. THBS1/CD47 signaling is frequently dysregulated in chronic diseases.

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Coronary artery mechanics induces human saphenous vein remodelling via recruitment of adventitial myofibroblast-like cells mediated by Thrombospondin-1

Cited by 24 publications

References 50 publications

Vascular dysfunction and pathology: focus on mechanical forces

Vascular dysfunction and pathology: focus on mechanical forces

Harnessing Mechanosensation in Next Generation Cardiovascular Tissue Engineering

CD (Cluster of Differentiation)

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