Analysis of cytokine profile and growth factors in platelet-rich plasma obtained by open systems and commercial columns

Pochini, Alberto de Castro; Antonioli, Eliane; Bucci, Daniella Zanetti; Sardinha, Luiz Roberto; Andreoli, Carlos Vicente; Ferretti, Mário; Ejnisman, Benno; Goldberg, Anna Carla; Cohen, Moisés

doi:10.1590/s1679-45082016ao3548

Cited by 37 publications

(27 citation statements)

References 36 publications

(51 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Leukocytes values found in the E-PRP were particularly low, showing a reduction of 82% in respect to the baseline. This concentration was comparable to that found by some authors in PRP 25 , 37 or slightly higher than that described by others for PRGF. 38 , 39 This small number of leukocytes found in the E-PRP do not classify the E-PRP as a blood derivative “with” leukocytes.…”

Section: Discussionsupporting

confidence: 91%

Quantification of Growth Factors and Fibronectin in Diverse Preparations of Platelet-Rich Plasma for the Treatment of Ocular Surface Disorders (E-PRP)

Rodrı́guez

Gisbert

Palazón

et al. 2020

Trans. Vis. Sci. Tech.

View full text Add to dashboard Cite

Purpose The purpose of this study was to quantify the presence of growth factors (GFs) and fibronectin in autologous platelet-rich plasma for topical ocular use (E-PRP) comparing their concentration when different preparation and preservation procedures were applied. Methods E-PRP was prepared with blood from healthy volunteers. The count of platelets, leukocytes, and red blood cells in the whole blood and E-PRP were performed. The concentration of the GFs platelet-derived growth factor BB (PDGF-BB), transforming growth factor β1 (TGF-β1), epidermal growth factor (EGF), vascular endothelial growth factor A (VEGF-A), and fibronectin was determined in each of the four procedures applied including fresh, frozen at −20°C for 3 months, fresh-spin, and frozen-spin at −20°C E-PRP samples. Posterior statistical analysis was performed to establish significant differences between groups and between GFs in relation to the amounts of platelets. Results Platelets in the E-PRP doubled in the number of basal values of whole blood ( P ≤ 0.01). The blood cells in the E-PRP decreased drastically in red cells (99%) and also in leukocytes (82%). The concentration of PDGF-BB and EGF was significantly higher ( P < 0.01) when the E-PRP samples were frozen at −20°C. However, no significant differences were observed for TGF-β1, VEGF-A, and fibronectin ( P > 0.05). The concentration of GFs in the E-PRP did not necessarily correlate with the number of platelets. Conclusions Freezing the E-PRP for 3 months at −20°C increased the concentration of important proteins, such as PDGF-BB and EGF, and maintained the levels of others. These findings are essential because treatments, such as E-PRP, used by patients with ocular surface dysfunctions tend to prolong it in time. In addition, subsequent centrifugation of the E-PRP decreased the values of TFG-β1, but not the other GFs, which would allow adjusting the concentration of TFG-β1, as necessary. This procedure guarantees their correct conservation and viability. Translational Relevance This work demonstrates how clinical application can be improved by starting from basic research. The quantification of GFs and fibronectin in platelet-rich plasma (PRP) helps to clarify which is the best mode of preparation and preservation of PRP for clinical applications. This allows to optimize the product that is delivered to the patients as a treatment for the dysfunctions of the ocular surface, guaranteeing that the conservation does not affect at all the quality of the PRP that it is going to be used.

show abstract

Section: Discussionsupporting

confidence: 91%

Quantification of Growth Factors and Fibronectin in Diverse Preparations of Platelet-Rich Plasma for the Treatment of Ocular Surface Disorders (E-PRP)

Rodrı́guez

Gisbert

Palazón

et al. 2020

Trans. Vis. Sci. Tech.

View full text Add to dashboard Cite

show abstract

“…Therefore, no significant difference was found between the platelet count in these biotechnological products, which coincides with the data of some studies on plateletrich plasma [36,40,43,47]. However, some studies have shown that the number of platelets in leukocyte-poor platelet concentrates is significantly lower than in leukocyte-containing ones [6,39].…”

Section: Resultssupporting

confidence: 85%

The blood cells count in leukocyte and leukocyte-poor platelet-concentrated plasma in patients with musculoskeletal disorders

Yavorovska¹,

Goliuk²,

Магомедов³

et al. 2020

COT

View full text Add to dashboard Cite

The cellular composition significantly affects the properties of platelet concentrates. In particular, leukocyte platelet concentrates due to the increased number of monocytes and granulocytes have increased levels of proinflammatory cytokines, which contribute to the destruction of extracellular matrix, reduce synthesis of its components and enhance inflammation in tissues. The purpose. To determine the blood cells number in leukocyte (L-PCP) or leukocyte-poor platelet-concentrated plasma (LP-PCP) and compare it with whole venous blood, plasma and platelet-poor plasma. Materials and methods. 20 L-PCP and 21 LP-PCP samples were obtained by double centrifugation from the venous blood of 30 donors aged 26 to 78 with local pathology of the musculoskeletal system. In the first stage, plasma was isolated after the separation of whole blood, and in the second stage, platelets were concentrated in a small volume of platelet-poor plasma. The number of blood cells in the test samples was determined by hematology analyzer.

show abstract

“…However, the possibility that VEGF-A released by PRP may affect α-sma expression regardless of modulation of TGF-β1 signaling cannot be excluded. We can speculate that VEGF-A might exert its inhibitory action by cross-talking with other factors contained in PRP capable to act as antifibrotic agents, such as FGF-2 [ 64 , 86 , 87 , 88 ], or profibrotic ones such as PDGF [ 64 , 86 , 87 , 98 ], as reported in other cell types [ 99 , 100 ].…”

Section: Discussionmentioning

confidence: 96%

“…By contrast, other studies proved that PRP promotes the myofibroblastic differentiation process [ 81 , 82 , 83 , 84 , 85 ]. These contradictory PRP-elicited biological responses may be attributed to different cell type responsiveness or, more likely, to the heterogeneity of PRP preparation techniques and formulations containing different concentration of interplaying growth factors [ 64 , 86 , 87 ] exerting, at the same time, profibrotic (such as TGF-β) and antifibrotic actions (such as FGF-2) [ 88 ]. In addition, the different PRP dosages used could be determinant when considering the dose-dependence of some fibroblasts’ responses [ 89 , 90 , 91 ].…”

Section: Discussionmentioning

confidence: 99%

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

Tani

Vallone

et al. 2018

Cells

View full text Add to dashboard Cite

The antifibrotic potential of platelet-rich plasma (PRP) is controversial. This study examined the effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the main drivers of fibrosis, and the involvement of vascular endothelial growth factor (VEGF)-A in mediating PRP-induced responses. The impact of PRP alone on fibroblast differentiation was also assessed. Myofibroblastic phenotype was evaluated by confocal fluorescence microscopy and western blotting analyses of α-smooth muscle actin (sma) and type-1 collagen expression, vinculin-rich focal adhesion clustering, and stress fiber assembly. Notch-1, connexin 43, and VEGF-A expression were also analyzed by RT-PCR. PRP negatively regulated fibroblast-myofibroblast transition via VEGF-A/VEGF receptor (VEGFR)-1-mediated inhibition of TGF-β1/Smad3 signaling. Indeed TGF-β1/PRP co-treated fibroblasts showed a robust attenuation of the myofibroblastic phenotype concomitant with a decrease of Smad3 expression levels. The VEGFR-1 inhibition by KRN633 or blocking antibodies, or VEGF-A neutralization in these cells prevented the PRP-promoted effects. Moreover PRP abrogated the TGF-β1-induced reduction of VEGF-A and VEGFR-1 cell expression. The role of VEGF-A signaling in counteracting myofibroblast generation was confirmed by cell treatment with soluble VEGF-A. PRP as single treatment did not induce fibroblast myodifferentiation. This study provides new insights into cellular and molecular mechanisms underpinning PRP antifibrotic action.

show abstract

Analysis of cytokine profile and growth factors in platelet-rich plasma obtained by open systems and commercial columns

Cited by 37 publications

References 36 publications

Quantification of Growth Factors and Fibronectin in Diverse Preparations of Platelet-Rich Plasma for the Treatment of Ocular Surface Disorders (E-PRP)

Quantification of Growth Factors and Fibronectin in Diverse Preparations of Platelet-Rich Plasma for the Treatment of Ocular Surface Disorders (E-PRP)

The blood cells count in leukocyte and leukocyte-poor platelet-concentrated plasma in patients with musculoskeletal disorders

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 †

Contact Info

Product

Resources

About