Platelet-Rich Plasma Prevents In Vitro Transforming Growth Factor-β1-Induced Fibroblast to Myofibroblast Transition: Involvement of Vascular Endothelial Growth Factor (VEGF)-A/VEGF Receptor-1-Mediated Signaling †

Chellini, Flaminia; Tani, Akio; Vallone, Larissa; Nosi, Daniele; Pavan, Paola; Bambi, Franco; Orlandini, Sandra Zecchi; Sassoli, Chiara

doi:10.3390/cells7090142

Cited by 40 publications

(63 citation statements)

References 105 publications

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“…In this regard, Platelet-Rich Plasma (PRP)-defined as a plasma fraction with a concentration of platelets above baseline levels and representing a source of numerous biologically active molecules-may offer promising perspectives [30]. Indeed, many in vitro and in vivo studies have demonstrated the anti-fibrotic potential of this blood product in different tissues [31][32][33][34][35][36][37][38], including skeletal muscle [30,[39][40][41][42][43][44][45][46], and have indicated the fibroblast-myofibroblast transition as the cell process target of its action [31][32][33]36,38,44,47,48]. Furthermore, the positive contribution of PRP to skeletal muscle regeneration has been demonstrated either in vivo or in vitro, thanks to its capability to promote the myogenic program [30].…”

Section: Prp As An Anti-fibrotic Agentmentioning

confidence: 99%

“…In particular, we focused the attention on the GJIC. The experimental model to evaluate fibroblast to myofibroblast transition has been previously validated [23,24,48,[55][56][57] and consists in the culture of the cells in low serum conditions in the presence of TGF-β1. The treatment with PRP was also conducted as previously reported [48,57,58].…”

Section: Gap Junction Intercellular Communication (Gjic)mentioning

confidence: 99%

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Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-β1–Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis

Squecco

Chellini

Idrizaj

et al. 2020

Cells

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Skeletal muscle repair/regeneration may benefit by Platelet-Rich Plasma (PRP) treatment owing to PRP pro-myogenic and anti-fibrotic effects. However, PRP anti-fibrotic action remains controversial. Here, we extended our previous researches on the inhibitory effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the effector cells of fibrosis, focusing on gap junction (GJ) intercellular communication. The myofibroblastic phenotype was evaluated by cell shape analysis, confocal fluorescence microscopy and Western blotting analyses of α-smooth muscle actin and type-1 collagen expression, and electrophysiological recordings of resting membrane potential, resistance, and capacitance. PRP negatively regulated myofibroblast differentiation by modifying all the assessed parameters. Notably, myofibroblast pairs showed an increase of voltage-dependent GJ functionality paralleled by connexin (Cx) 43 expression increase. TGF-β1-treated cells, when exposed to a GJ blocker, or silenced for Cx43 expression, failed to differentiate towards myofibroblasts. Although a minority, myofibroblast pairs also showed not-voltage-dependent GJ currents and coherently Cx26 expression. PRP abolished the TGF-β1-induced voltage-dependent GJ current appearance while preventing Cx43 increase and promoting Cx26 expression. This study adds insights into molecular and functional mechanisms regulating fibroblast-myofibroblast transition and supports the anti-fibrotic potential of PRP, demonstrating the ability of this product to hamper myofibroblast generation targeting GJs.

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Section: Prp As An Anti-fibrotic Agentmentioning

confidence: 99%

Section: Gap Junction Intercellular Communication (Gjic)mentioning

confidence: 99%

Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-β1–Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis

Squecco

Chellini

Idrizaj

et al. 2020

Cells

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“…10 Among these materials, platelet-rich plasma (PRP) can be defined as a plasma fraction with platelet concentration higher than the baseline concentration in whole blood and that has antifibrotic action. 11 Autologous fat grafts have been commonly used to prevent the epidural adhesion after lumbar laminectomy. 3,12 Collagen dural matrix (DuraGen) is a chemical cross-linked type 1collagen foam made from bovine tendon and has been suggested to reduce fibrosis.…”

Section: Resultsmentioning

confidence: 99%

Effect of Platelet-Rich Plasma, Fat Pad and Dural Matrix in Preventing Epidural Fibrosis

et al. 2020

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Objective: Epidural fibrosis is one of the main reasons for requiring repeated surgical intervention. Our objective was to compare the effect of Platelet Rich Plasma (PRP) on the development of epidural fibrosis with collagen dural matrix and free autogenous fat graft. Methods: Male rats were separated into 3 groups. Laminectomy was implemented on the rats and epidural fat pad was placed in the first group (n = 7); equal size of collagen dural matrix was applied in the second group (n = 7); a single dose of PRP was applied in the third group (n = 7). Results: Epidural fibrosis was more common in the group that collagen dural matrix was applied when compared the ones that PRP was applied. PRP group presented better values in preventing epidural fibrosis when compared to the fat pad group, however this difference was not statistically significant. Conclusion: PRP is a material that can be easily obtained from the very blood of patients and at an extremely low cost; the main clinical relevance of our study is that the PRP might be an efficient material for better clinical results after laminectomy surgery due to its tissue healing and epidural fibroris preventing potentials. Level of Evidence V, Animal research.

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“…Thus, it is likely that in the context of L‐PRF, the effect of released TGF‐β on NHGFs is counteracted by other molecules released from the membrane. Notably, a recent study demonstrates that L‐PRF‐derived VEGF‐A can attenuate TGF‐β signalling and myofibroblastic differentiation (Chellini et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Leucocyte‐ and platelet‐rich fibrin regulates expression of genes related to early wound healing in human gingival fibroblasts

Intriago

Koivisto

et al. 2020

J Clinic Periodontology

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Background Leucocyte‐ and platelet‐rich fibrin (L‐PRF) is a blood‐derived biomaterial rich in leucocytes and platelets embedded in a high‐density fibrin network that can be compressed into a membrane and used in surgical applications to stimulate tissue regeneration and wound healing, especially in oral cavity. This study aimed to determine the combined effects of the growth factors and cells present in L‐PRF on fibroblasts that directly face the L‐PRF membranes placed during surgical procedures. Methods The effect of L‐PRF from six donors on the expression of 84 key wound healing genes in normal human gingival fibroblasts was tested by RT‐qPCR. Results L‐PRF significantly regulated the expression of 33 fibroblast genes (39%), including interleukins, myofibroblast‐, extracellular matrix‐ and angiogenesis‐associated genes, and matrix metalloproteinase‐1 and −3. L‐PRF regulated fibroblast gene expression both time‐ and dose‐dependently, and the effects were mediated by mitogen‐activated protein kinases ERK1/2, JNK and p38. L‐PRF also stimulated fibroblast wound closure and promoted the ability of fibroblasts to induce endothelial tube formation. L‐PRF‐induced gene expression changes in fibroblast were similar to those observed in early human and pig wounds. Conclusions This study provides new insights into the biological mechanism by which L‐PRF regulates key gingival fibroblast functions important in wound healing.

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Platelet-Rich Plasma Prevents In Vitro Transforming Growth Factor-β1-Induced Fibroblast to Myofibroblast Transition: Involvement of Vascular Endothelial Growth Factor (VEGF)-A/VEGF Receptor-1-Mediated Signaling †

Cited by 40 publications

References 105 publications

Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-β1–Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis

Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-β1–Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis

Effect of Platelet-Rich Plasma, Fat Pad and Dural Matrix in Preventing Epidural Fibrosis

Leucocyte‐ and platelet‐rich fibrin regulates expression of genes related to early wound healing in human gingival fibroblasts

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