scholarly journals Leucocyte-Rich Platelet-Rich Plasma Enhances Fibroblast and Extracellular Matrix Activity: Implications in Wound Healing

2020 ◽  
Vol 21 (18) ◽  
pp. 6519
Author(s):  
Jeannie Devereaux ◽  
Narges Dargahi ◽  
Sarah Fraser ◽  
Kulmira Nurgali ◽  
Dimitrios Kiatos ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Autologous Blood ◽  
Human Fibroblasts ◽  
White Blood Cells ◽  
High Concentration ◽  
Gene Expressions

Background: Platelet-rich plasma (PRP) is an autologous blood product that contains a high concentration of platelets and leucocytes, which are fundamental fibroblast proliferation agents. Literature has emerged that offers contradictory findings about leucocytes within PRP. Herein, we elucidated the effects of highly concentrated leucocytes and platelets on human fibroblasts. Methods: Leucocyte-rich, PRP (LR-PRP) and leucocyte-poor, platelet-poor plasma (LP-PPP) were compared to identify their effects on human fibroblasts, including cell proliferation, wound healing and extracellular matrix and adhesion molecule gene expressions. Results: The LR-PRP exhibited 1422.00 ± 317.21 × 103 platelets/µL and 16.36 ± 2.08 × 103 white blood cells/µL whilst the LP-PPP demonstrated lower concentrations of 55.33 ± 10.13 × 103 platelets/µL and 0.8 ± 0.02 × 103 white blood cells/µL. LR-PRP enhanced fibroblast cell proliferation and cell migration, and demonstrated either upregulation or down-regulation gene expression profile of the extracellular matrix and adhesion molecules. Conclusion: LR-PRP has a continuous stimulatory anabolic and ergogenic effect on human fibroblast cells.

The Effect of Red Blood Cells on the ADP-induced Aggregation of Human Platelets in Flow Through Tubes

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Mean Transit Time ◽  
White Blood Cells ◽  
Aggregate Size ◽  
Human Platelets ◽  
Induced Aggregation

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

scholarly journals Platelet rich plasma in dermatology and cosmetology

2020 ◽  
Vol 6 (2) ◽  
pp. 288
Author(s):  
Shobhit Mohan ◽  
Lalit Mohan ◽  
Renu Sangal ◽  
Neelu Singh
Keyword(s):  
Wound Healing ◽  
Tissue Regeneration ◽  
Blood Product ◽  
Platelet Rich Plasma ◽  
Autologous Blood ◽  
Detailed Knowledge ◽  
Skin Rejuvenation ◽  
Scar Revision ◽  
Current Review

<p class="abstract">Platelet rich plasma (PRP) therapies in medicine has become increasing popular during the last decade. The interest in in the application of PRP in dermatology and cosmetology has increased recently in different applications such as alopecia, skin rejuvenation, wound healing, scar revision, and tissue regeneration. PRP is an autologous blood product obtained from the blood of the patients. The detailed knowledge about PRP should help clinicians better understand this therapy. In this view, the current review was done for a better understanding of what pathologies can be corrected with PRP.</p>

scholarly journals Roles of Proteoglycans and Glycosaminoglycans in Wound Healing and Fibrosis

2015 ◽  
Vol 2015 ◽  
pp. 1-20 ◽  
Author(s):  
Shibnath Ghatak ◽  
Edward V. Maytin ◽  
Judith A. Mack ◽  
Vincent C. Hascall ◽  
Ilia Atanelishvili ◽  
...  
Keyword(s):  
Wound Healing ◽  
Blood Cells ◽  
White Blood Cells ◽  
Cell Types ◽  
Repair Process ◽  
Epithelial Layer ◽  
Extracellular Molecules ◽  
Living Tissues ◽  
Type Of Injury

A wound is a type of injury that damages living tissues. In this review, we will be referring mainly to healing responses in the organs including skin and the lungs.Fibrosisis a process of dysregulated extracellular matrix (ECM) production that leads to a dense and functionally abnormal connective tissue compartment (dermis). In tissues such as the skin, the repair of the dermis after wounding requires not only thefibroblaststhat produce the ECM molecules, but also the overlying epithelial layer (keratinocytes), theendothelial cells, andsmooth muscle cellsof the blood vessel and white blood cells such asneutrophilsandmacrophages, which together orchestrate the cytokine-mediated signaling and paracrine interactions that are required to regulate the proper extent and timing of the repair process. This review will focus on the importance of extracellular molecules in the microenvironment, primarily the proteoglycans and glycosaminoglycan hyaluronan, and their roles in wound healing. First, we will briefly summarize the physiological, cellular, and biochemical elements of wound healing, including the importance of cytokine cross-talk between cell types. Second, we will discuss the role of proteoglycans and hyaluronan in regulating these processes. Finally, approaches that utilize these concepts as potential therapies for fibrosis are discussed.

scholarly journals Gene expressions involved in immune system control and serum CA125 content in polycythemia vera. Tap

2020 ◽  
Vol 42 (1) ◽  
Author(s):  
Do Thi Trang ◽  
Nguyen Thi Xuan
Keyword(s):  
Immune System ◽  
Polycythemia Vera ◽  
Immune Tolerance ◽  
Blood Cells ◽  
Myeloproliferative Neoplasms ◽  
Tyrosine Phosphatase ◽  
White Blood Cells ◽  
System Control ◽  
Gene Expressions ◽  
Gene Group

Polycythemia Vera (PV) is a slowly progressing blood cancer associated with myeloproliferative neoplasms. The disease is characterized by an abnormal proliferation of three cell types including red blood cells, white blood cells and platelets and a symptom of pruritus caused by release of itching agents of activated mast cells. The enhanced expression of several genes involved in immune system control including CTLA-4, PD-1 and LAG3 are linked to activation immune tolerance. Klotho gene has anti-aging, anti-inflammation and anti-cancer functions. The SHP gene group belongs to the tyrosine phosphatase protein signaling family that regulates cancer cell proliferation through maturation, migration and apoptosis and includes two main genes, SHP-1 and SHP-2. The increased serum content of cancer antigen CA125 is considered as a cancer marker of several blood and hematopoietic disorders. In this study, we conducted experiments to determine mRNA expression of above genes in PV patients by realtime-PCR and CA125 concentration by ELISA. Results showed that expression of klotho, LAG3, CTLA-4 and PD-1 genes was decreased in PV patients, indicating that the immune tolerance was inactivated in PV patients. CA125 concentration was significantly increased in PV patients compared to healthy individuals and interestingly, there was a positive association among three patients, who having increased CA125 concentration and biochemical indicators including LDH, AST and ALT. The results in this study provide an important reference document for further studies that serve for the early detection of PV disease. 

scholarly journals Plasma-Coated Polycaprolactone Nanofibers with Covalently Bonded Platelet-Rich Plasma Enhance Adhesion and Growth of Human Fibroblasts

Nanomaterials ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 637 ◽  
Author(s):  
Svetlana Miroshnichenko ◽  
Valeriia Timofeeva ◽  
Elizaveta Permyakova ◽  
Sergey Ershov ◽  
Philip Kiryukhantsev-Korneev ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Wound Healing ◽  
Biological Activity ◽  
Photoelectron Spectroscopy ◽  
Platelet Rich Plasma ◽  
Low Cost ◽  
Human Fibroblasts ◽  
Covalent Binding ◽  
Covalent Bonding ◽  
Plasma Modification

Biodegradable nanofibers are extensively employed in different areas of biology and medicine, particularly in tissue engineering. The electrospun polycaprolactone (PCL) nanofibers are attracting growing interest due to their good mechanical properties and a low-cost structure similar to the extracellular matrix. However, the unmodified PCL nanofibers exhibit an inert surface, hindering cell adhesion and negatively affecting their further fate. The employment of PCL nanofibrous scaffolds for wound healing requires a certain modification of the PCL surface. In this work, the morphology of PCL nanofibers is optimized by the careful tuning of electrospinning parameters. It is shown that the modification of the PCL nanofibers with the COOH plasma polymers and the subsequent binding of NH2 groups of protein molecules is a rather simple and technologically accessible procedure allowing the adhesion, early spreading, and growth of human fibroblasts to be boosted. The behavior of fibroblasts on the modified PCL surface was found to be very different when compared to the previously studied cultivation of mesenchymal stem cells on the PCL nanofibrous meshes. It is demonstrated by X-ray photoelectron spectroscopy (XPS) that the freeze–thawed platelet-rich plasma (PRP) immobilization can be performed via covalent and non-covalent bonding and that it does not affect biological activity. The covalently bound components of PRP considerably reduce the fibroblast apoptosis and increase the cell proliferation in comparison to the unmodified PCL nanofibers or the PCL nanofibers with non-covalent bonding of PRP. The reported research findings reveal the potential of PCL matrices for application in tissue engineering, while the plasma modification with COOH groups and their subsequent covalent binding with proteins expand this potential even further. The use of such matrices with covalently immobilized PRP for wound healing leads to prolonged biological activity of the immobilized molecules and protects these biomolecules from the aggressive media of the wound.

scholarly journals LncRNA XIST promotes extracellular matrix synthesis, proliferation and migration by targeting miR-29b-3p/COL1A1 in human skin fibroblasts after thermal injury

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Wei Cao ◽  
Youping Feng
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Western Blot ◽  
Thermal Injury ◽  
Human Skin Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). Methods The wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay. Results The expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function. Conclusion XIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.

scholarly journals Role of White Blood Cells in Blood- and Bone Marrow-Based Autologous Therapies

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
William King ◽  
Krista Toler ◽  
Jennifer Woodell-May
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Growth Factors ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Complex Mixture ◽  
Negative Results

There has been significant debate over the role of white blood cells (WBCs) in autologous therapies, with several groups suggesting that WBCs are purely inflammatory. Misconceptions in the practice of biologic orthopedics result in the simplified principle that platelets deliver growth factors, WBCs cause inflammation, and the singular value of bone marrow is the stem cells. The aim of this review is to address these common misconceptions which will enable better development of future orthopedic medical devices. WBC behavior is adaptive in nature and, depending on their environment, WBCs can hinder or induce healing. Successful tissue repair occurs when platelets arrive at a wound site, degranulate, and release growth factors and cytokines which, in turn, recruit WBCs to the damaged tissue. Therefore, a key role of even pure platelet-rich plasma is to recruit WBCs to a wound. Bone marrow contains a complex mixture of vascular cells, white blood cells present at much greater concentrations than in blood, and a small number of progenitor cells and stem cells. The negative results observed for WBC-containing autologous therapies in vitro have not translated to human clinical studies. With an enhanced understanding of the complex WBC biology, the next generation of biologics will be more specific, likely resulting in improved effectiveness.

Wound Healing In Glaucoma

2013 ◽  
Author(s):  
Kimberly A. Mankiewicz ◽  
Leonard K. Seibold
Keyword(s):  
Wound Healing ◽  
Blood Cells ◽  
Healing Process ◽  
White Blood Cells ◽  
Glaucoma Surgery ◽  
Scar Formation ◽  
Wound Site ◽  
Normal Wound Healing ◽  
Inflammatory Phase ◽  
Repair Phase

The goal of wound healing in most surgeries is to bring the injured tissue back to its original state to prevent the wound from reopening. However, in glaucoma surgery, the goal is to have incomplete wound healing. Scar formation prevents the filtering mechanism and bleb from functioning properly, leading to poor pressure control and failure of the surgery. However, if there is too little wound healing, surgical failure may be marked by overfiltration and hypotony. Several modulators are currently used in conjunction with glaucoma surgery, and new targets are under investigation to improve our ability to control the healing process. Normal wound healing occurs in 3 phases: the inflammatory phase, the proliferative/repair phase, and the remodeling phase. In the inflammatory phase, blood cells and plasma proteins are released around the wound site. These proteins attract other wound healing factors, such as cytokines and growth factors. White blood cells are also recruited to the site, clearing out undesired cellular debris through phagocytosis. Additionally, platelet aggregation and fibrin clot formation occur. In the proliferative/repair phase, fibroblasts, crucial cells for tissue repair and scarring, begin reforming the extracellular matrix (ECM) and other components of connective tissue. Angiogenesis also occurs, and the wound begins to close. In the final phase, blood vessels are resorbed and fibroblasts disperse. Fibroblasts produce matrix metalloproteinases that, along with collagen and elastin, allowing for wound remodeling and scar formation. The modulators used in glaucoma surgery, as well as new agents in development, disrupt various aspects of this cycle. Use of topical corticosteroids in conjunction with filtering surgery is a routine part of postoperative management and has been for many decades. Corticosteroids blunt the wound healing response by altering the inflammatory phase through reducing the amount of inflammatory cells and cytokines that migrate to the wound site. Corticosteroids also prevent the complexing and conversion of inflammatory mediators, as well as reduce vascular permeability to limit mobility of wound healing factors to the wound site.

scholarly journals Targeting CCN Proteins in Rheumatoid Arthritis and Osteoarthritis

2021 ◽  
Vol 22 (9) ◽  
pp. 4340
Author(s):  
Iona J. MacDonald ◽  
Chien-Chung Huang ◽  
Shan-Chi Liu ◽  
Yen-You Lin ◽  
Chih-Hsin Tang
Keyword(s):  
Rheumatoid Arthritis ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Evidence Base ◽  
Ccn Proteins ◽  
Matricellular Proteins ◽  
Substantial Evidence ◽  
Ccn Family ◽  
Cellular Processes

The CCN family of matricellular proteins (CYR61/CCN1, CTGF/CCN2, NOV/CCN3 and WISP1-2-3/CCN4-5-6) are essential players in the key pathophysiological processes of angiogenesis, wound healing and inflammation. These proteins are well recognized for their important roles in many cellular processes, including cell proliferation, adhesion, migration and differentiation, as well as the regulation of extracellular matrix differentiation. Substantial evidence implicates four of the proteins (CCN1, CCN2, CCN3 and CCN4) in the inflammatory pathologies of rheumatoid arthritis (RA) and osteoarthritis (OA). A smaller evidence base supports the involvement of CCN5 and CCN6 in the development of these diseases. This review focuses on evidence providing insights into the involvement of the CCN family in RA and OA, as well as the potential of the CCN proteins as therapeutic targets in these diseases.

Differential Stability Of Prostacyclin (PGI2) In Whole Blood And Plasma

1981 ◽  
Author(s):  
S Krishnamurthi ◽  
J Westwick ◽  
V V Kakkar
Keyword(s):  
Whole Blood ◽  
Blood Cells ◽  
Time Course ◽  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Platelet Inhibition ◽  
Solvent Systems ◽  
Differential Stability ◽  
Significant Uptake ◽  
The Stability

The stability of PGI2 in human whole blood (WB) , platelet- rich plasma (PRP) and platelet-poor plasma (PPP) was studied. Following incubation of PGI2(60nM) in the three media, it was found that the half life (t 1/2) of PGI2 (as measured) by the rate of loss of PGI2 equivalents causing platelet inhibition in the supernatant of the incubates) was longer in PPP ᶓ PRP (t 1/2 49±4 ᶓ 42.5±5 min respectively, n=10). On investigation this was found to be largely due to the pH difference observed between PPPᶓPRP (both pH 7.8±1) and WB (pH 7.4±1). Addition of NaHCO3 to raise the pH of WB to 7.8 prolonged the stability of PGI2 with a th of 35±4 min and addition of HC1 to lower the pH of PPP to 7.4 shortened the th to 18.5±4 min. However, incubation of PGI2 in either Hanks buffer or washed red blood cells (WRBC) at pH 7.8 did not increase PG2 stability. Since addition of a mixed population of white blood cells (7xl06cells/ml in PBS pH 7.8) to PPP (pH7.8) did not alter the rate of loss of PGI2 activity and there was found to be no significant uptake (<15%) of 3H PGI2 in WRBC, the possibility of PGI2 conversion to a more stable and platelet-active metabolite such as 6-oxo-PGE2 in plasma was studied by extraction and TLC of the PPP and WB incubates. 3H PGI 2 was found to be converted to % 6-oxo-PGF2 in both WB (pH7.4) and PPP (pH 7.8) with no other detectable metabolites in three different solvent systems. Treatment of the incubates prior to extraction and TLC with NaBH4 (which by reducing free keto groups can distinguish between PGI2 and 6-oxo-PGF1α) showed that 10-20% of the added 3H PGI2 in PPP (pH 7.8) was unchanged even after 120 mins incubation while virtually all the added 3H PGI2 in WB (pH7.4) was converted to 3H 6-oxo-PGFlaby 50 min with a time course (% PGI2 60nM; 1/2 WB-14 min, PPP-35min) similar to the loss of PGI2 activity in WB and PPP on bioassay. We conclude that the prolonged platelet inhibitory activity following incubation of PGI2 in plasma compared to that in whole blood is due to unchanged PGI2 and not the formation of a 6-oxo-PGE1, like substance as suggested by Borda and Gimeno in Prostaglandins 19 pp 899 (1979).

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