Men and Women Differ in the Biochemical Composition of Platelet-Rich Plasma

Xiong, Grace; Lingampalli, Nithya; Koltsov, Jayme; Leung, Lawrence L.K.; Bhutani, Nidhi; Robinson, William H.; Chu, Constance R.

doi:10.1177/0363546517740845

Cited by 89 publications

(79 citation statements)

References 79 publications

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“…Batch‐to‐batch consistency in HPL batches seems to require the pooling of 40 to 50 PC donations, corresponding to approximately 250 donors when using “random‐donor” PCs. Pooling minimizes inherent donor‐to‐donor variability due to impact of age or sex, such as the content in growth factors and other cell growth–promoting molecules, which are important components for growth medium supplementation . However, pooling increases the risk of contamination by 1) window period donations, 2) viruses that are not tested for, or 3) emerging agents, making the implementation of virus/pathogen inactivation procedures required .…”

Section: Discussionmentioning

confidence: 99%

A double‐virally‐inactivated (Intercept–solvent/detergent) human platelet lysate for in vitro expansion of human mesenchymal stromal cells

Barro

Nebie

et al. 2019

Transfusion

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BACKGROUND: Pooled human platelet lysate (HPL) can replace fetal bovine serum (FBS) as xeno-free supplement for ex vivo expansion of mesenchymal stromal cells (MSCs). We evaluate here whether a double-virallyinactivated HPL (DVI-HPL) prepared from expired Intercepttreated platelet concentrates (PCs) and treated by solvent/detergent (S/D) can be used for MSC expansion.STUDY DESIGN AND METHODS: Expired Intercepttreated PCs in 65% platelet (PLT) additive solution were pooled and subjected to a 1% tri-n-butyl phosphate/1% Triton X-45 treatment followed by soybean oil, hydrophobic interaction chromatography purification, and sterile filtration. Bone marrow-derived MSCs (BM-MSCs) were expanded for four passages in growth medium containing 10% DVI-HPL, I-HPL (from Intercept-PC only), untreated HPL, and FBS. MSC morphology, doubling time, immunophenotype, immunosuppressive activity, and differentiation capacity were compared. RESULTS:Expanded cells had typical spindle morphology and showed higher viability in all HPL conditions than in FBS. The DVI-HPL and FBS-expanded cells were morphologically larger than in I-HPL and HPL supplements. The cumulative population doubling was lower using DVI-HPL than with HPL and I-HPL, but significantly higher than using FBS. Immunophenotype was not affected by the supplements used. Immunosuppressive activity was maintained with all supplements. Differentiation capacity into chondrocytes and osteocytes was more effective in DVI-HPL but less toward adipocytes compared to other supplements. CONCLUSIONS: Human PLT lysate made fromIntercept-PCs subjected to S/D treatment may be an alternative to untreated HPL and to I-HPL for BM-MSC expansion. This finding reinforces the potential of HPL as a virally safe alternative to FBS for clinical grade MSC expansion protocols. ABBREVIATIONS: BDNF = brain-derived neurotrophic factor; BM-MSC(s) = bone marrow-derived mesenchymal stromal cells; BrdU = bromodeoxyuridine/5-bromo-2 0 -deoxyuridine; CCK-8 = cell counting kit-8; DVI = double-virally-inactivated; DVI-HPL = doublevirally-inactivated (intercept-solvent/detergent) human platelet lysate; ECM = extracellular matrix; EGF = epidermal growth factor FBS = fetal bovine serum; HGF = hepatocyte growth factor HLA-DR = human leukocyte antigen DR; HPL = human platelet lysate; IGF = insulin-like growth factor-1; I-HPL = Intercept human platelet lysate; MSC(s) = mesenchymal stromal cells; PAS = platelet additive solution; PB19V = parvovirus B19; PC(s) = platelet concentrate(s); PD (s) = population doubling(s); PDGF-AB = platelet-derived growth factor-AB; PF4 = platelet factor 4; PHA = phytohemagglutinin; PPARG = peroxisome proliferator-activated receptor gamma; SOX9 = SRY (sex-determining region Y)-box 9; SPP1 = secreted phosphoprotein 1. From the

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Section: Discussionmentioning

confidence: 99%

A double‐virally‐inactivated (Intercept–solvent/detergent) human platelet lysate for in vitro expansion of human mesenchymal stromal cells

Barro

Nebie

et al. 2019

Transfusion

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“…Conversely, another study of plateletrich plasma found that PDGF-BB was higher in men and found no sex differences in IGF-1 levels [374]. The same study also found that interleukin-1 beta (IL-1β) and several angiogenic growth factors, including tumor necrosis factor-alpha (TNF-α), basic fibroblast growth factor (bFGF), and transforming growth factor-beta 1(TGF-β1) were higher in males [374]. Further studies do not show a strict pro-angiogenic correlation in females versus males in serum; anti-angiogenic factor angiopoietin-2 and pro-angiogenic factor IL-3 were higher in females, while anti-angiogenic thrombospondin (TSP) and several pro-angiogenic endothelial adhesion molecules (E-selectin, VCAM-1) were higher in males [375].…”

Section: Sex Differences In Angiogenesismentioning

confidence: 94%

“…Finally, females and males have different amounts of circulating pro-angiogenic and anti-angiogenic factors, which may further contribute to the sex differences in tumor angiogenesis epidermal growth factor (EGF), insulin growth factor-1 (IGF-1), PDGF-BB, and VEGF, were significantly higher in women [373]. Conversely, another study of plateletrich plasma found that PDGF-BB was higher in men and found no sex differences in IGF-1 levels [374]. The same study also found that interleukin-1 beta (IL-1β) and several angiogenic growth factors, including tumor necrosis factor-alpha (TNF-α), basic fibroblast growth factor (bFGF), and transforming growth factor-beta 1(TGF-β1) were higher in males [374].…”

Section: Sex Differences In Angiogenesismentioning

confidence: 99%

Sex differences in cancer mechanisms

et al. 2020

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We now know that cancer is many different diseases, with great variation even within a single histological subtype. With the current emphasis on developing personalized approaches to cancer treatment, it is astonishing that we have not yet systematically incorporated the biology of sex differences into our paradigms for laboratory and clinical cancer research. While some sex differences in cancer arise through the actions of circulating sex hormones, other sex differences are independent of estrogen, testosterone, or progesterone levels. Instead, these differences are the result of sexual differentiation, a process that involves genetic and epigenetic mechanisms, in addition to acute sex hormone actions. Sexual differentiation begins with fertilization and continues beyond menopause. It affects virtually every body system, resulting in marked sex differences in such areas as growth, lifespan, metabolism, and immunity, all of which can impact on cancer progression, treatment response, and survival. These organismal level differences have correlates at the cellular level, and thus, males and females can fundamentally differ in their protections and vulnerabilities to cancer, from cellular transformation through all stages of progression, spread, and response to treatment. Our goal in this review is to cover some of the robust sex differences that exist in core cancer pathways and to make the case for inclusion of sex as a biological variable in all laboratory and clinical cancer research. We finish with a discussion of lab-and clinic-based experimental design that should be used when testing whether sex matters and the appropriate statistical models to apply in data analysis for rigorous evaluations of potential sex effects. It is our goal to facilitate the evaluation of sex differences in cancer in order to improve outcomes for all patients.

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“…PRP contains a mixture of growth factors (GFs), cytokines, and other proteins. Recent studies show high variability in the levels of GFs and inflammatory mediators (IMs) between males and females, between different individuals, and between samples from the same individual depending on timing and method of preparation . The multiple sources of variability in PRP composition substantially complicate understanding mechanisms of action and evaluation of clinical effectiveness …”

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confidence: 99%

Platelet‐Rich Plasma (PRP) From Older Males With Knee Osteoarthritis Depresses Chondrocyte Metabolism and Upregulates Inflammation

O’Donnell

Migliore

Grandi

et al. 2019

Journal Orthopaedic Research

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There is intense clinical interest in the potential effects of platelet-rich plasma (PRP) for the treatment of osteoarthritis (OA). This study tested the hypotheses that (i) "lower" levels of the inflammatory mediators (IMs), interleukin-1β, and tumor necrosis factor α (TNF-α) and (ii) "higher" levels of the growth factors (GFs), insulin-like growth factor 1, and transforming growth factor β1 within leukocyte-poor PRP correlate with more favorable chondrocyte and macrophage responses in vitro. Samples were collected from 10 "healthy" young male (23-33 years old) human subjects (H-PRP) and nine older (62-85 years old) male patients with severe knee OA (OA-PRP). The samples were separated into groups of "high" or "low" levels of IM and GF based on multiplex cytokine and enzyme-linked immunosorbent assay data. Three-dimensional (3D) alginate bead chondrocyte cultures and monocyte-derived macrophage cultures were treated with 10% PRP from donors in different groups. Gene expression was analyzed by quantitative polymerase chain reaction. Contrary to our hypotheses, the effect of PRP on chondrocytes and macrophages was mainly influenced by the age and disease status of the PRP donor as opposed to the IM or GF groupings. While H-PRP showed similar effects on expression of chondrogenic markers (Col2a1 and Sox9) as the negative control group (p > 0.05), OA-PRP decreased chondrocyte expression of Col2a1 and Sox-9 messenger RNA by 40% and 30%, respectively (Col2a1, p = 0.015; Sox9, p = 0.037). OA-PRP also upregulated TNF-α and matrix metallopeptidase 9 (p < 0.001) gene expression in macrophages while H-PRP did not. This data suggests that PRP from older individuals with OA contain factors that may suppress chondrocyte matrix synthesis and promote macrophage inflammation in vitro.

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Men and Women Differ in the Biochemical Composition of Platelet-Rich Plasma

Abstract: Variability in the proteomic profile of PRP may affect tissue and clinical responses to treatment. These data suggest that clinical studies should account for the composition of PRP used.

Cited by 89 publications

References 79 publications

A double‐virally‐inactivated (Intercept–solvent/detergent) human platelet lysate for in vitro expansion of human mesenchymal stromal cells

A double‐virally‐inactivated (Intercept–solvent/detergent) human platelet lysate for in vitro expansion of human mesenchymal stromal cells

Sex differences in cancer mechanisms

Platelet‐Rich Plasma (PRP) From Older Males With Knee Osteoarthritis Depresses Chondrocyte Metabolism and Upregulates Inflammation

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