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Platelet-rich plasma and platelet-derived lipid factors induce different and similar gene expression responses for selected genes related to wound healing in rat dermal wound environment | ||
| Molecular Biology Research Communications | ||
| دوره 9، شماره 4، 2020، صفحه 145-153 اصل مقاله (430.32 K) | ||
| نوع مقاله: Original article | ||
| شناسه دیجیتال (DOI): 10.22099/mbrc.2020.37181.1500 | ||
| نویسندگان | ||
| Fahri Akbas1؛ Busra Ozdemir1؛ Nurten Bahtiyar* 2؛ Hulya Arkan3؛ Ilhan Onaran3 | ||
| 1Department of Medical Biology, Faculty of Medicine, Bezmialem Vakif University, Istanbul, Turkey | ||
| 2Department of Biophysics, Cerrahpasa Faculty of Medicine, Istanbul University- Cerrahpasa, Istanbul, Turkey | ||
| 3Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey | ||
| چکیده | ||
| Although platelet-rich plasma (PRP) is the plasma fraction that contains higher levels of platelet-sequestered proteins such as growth factors and chemokines, it is also abundant in bioactive lipids whose role in wound healing has not been well characterized. This study provides a preliminary evaluation for the effect of the lipid component of PRP on selected genes related to wound healing. Sprague-Dawley rats were classified into four groups after induction of full thickness excisional wounds: the lipid fraction (LF) (lipid extract from PRP) group, PRP group, dimethyl sulfoxide group, and sham group. Subsequently, relevant groups were topically treated with test preparations. Healing wounds were collected on 3rd, 7th and 14th days, and expression levels of 12 genes were determined using qPCR. LF treatment-induced gene expression signature distinct from that induced by PRP treatment, although there are some overlaps in LF- and PRP-responsive genes. Differentially expressed all eight genes (Cxcl5, Cxc11, Egfr, Tgfb1, IL10, Tgfa, Mmp1, and Mmp7) to LF response were significantly down-regulated at either 3rd, 7th, or 14th days. Also, the comparison between LF- and PRP-treatment groups showed that the LF significantly decreased expression of Cxcl11, Mmp7, and Tgfa mRNA on day 7 of healing. This study revealed that PRP and its LF induced different and similar gene expression responses of the skin during the repair of full thickness excisional wounds. Identifying mRNA response to LF treatment at whole transcriptome level can be beneficial for comprehensive understanding of the role of platelet-derived lipid factors in wound healing processes. | ||
| کلیدواژهها | ||
| Platelet-rich plasma؛ Lipid fraction؛ Wound healing؛ Gene expression | ||
| مراجع | ||
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1. McAleer JP, Kaplan E, Persich G. Efficacy of concentrated autologous platelet-derived growth factors in chronic lower-extremity wounds. J Am Podiat Med Assoc 2006;96:482-488. 2. Prabhu R, Vijayakumar C, Chandra AAB, Balagurunathan K, Kalaiarasi R, Venkatesan K, Raja SE, Swetha T. Efficacy of homologous, platelet-rich plasma dressing in chronic non-healing ulcers: an observational study. Cureus 2018;10:e2145. 3. Suthar M, Gupta S, Bukhari S, Ponemone V. Treatment of chronic non-healing ulcers usingautologous platelet rich plasma: a case series. J Biomed Sci 2017;24:16. 4. Pierce GF, Mustoe TA, Altrock BW, Deuel TF, Thomason A. Role of platelet‐derived growth factor in wound healing. J Cell Biochem 1991;45:319-326. 5. O’Donnell VB, Murphy RC, Watson SP. Platelet lipidomics: modern day perspective on lipid discovery and characterization in platelets. Circ Res 2014;114:1185-1203. 6. Snyder F. Platelet-activating factor and related acetylated lipids as potent biologically active cellular mediators. Am J Physiol 1990;259:C697-C708. 7. Calder PC. Polyunsaturated fatty acids and inflammation. Prostag Leukotr Essent Fatty Acids 2006;75:197-202. 8. Jump DB. Fatty acid regulation of gene transcription. Crit Rev Cl Lab Sci 2004;41:41-78. 9. Trengove NJ, Stacey MC, MacAuley S, Bennett N, Gibson J, Burslem F, Murphy G, Schultz G. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Repair Regen1999;7:442-452. 10. Yager DR, Zhang LY, Liang HX, Diegelmann RF, Cohen IK. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Dermatol 1996;107:743-748. 11. Hoeferlin LA, Huynh QK, Mietla JA, Sell SA, Tucker J, Chalfant ChE, Wijesinghe DSh. The lipid portion of activated platelet-rich plasma significantly contributes to its wound healing properties. Adv Wound Care2015;4:100-109. 12. Cakin MC, Ozdemir B, Kaya-Dagistanli F, Arkan H, Bahtiyar N, Anapali M, Akbas F, Onaran I. Evaluation of the in vivo wound healing potential of the lipid fraction from activated platelet-rich plasma. Platelets 2020;31:513-520. 13. Karna SR, D’Arpa P, Chen T, Qian LW, Fourcaudot AB, Yamane K, Chen P, Abercrombie JJ, You T, Leung KP. RNA-Seq transcriptomic responses of full-thickness dermal excision wounds to Pseudomonas aeruginosa acute and biofilm infection. PLoS One 2016;11: e0165312. 14. Cooper L, Johnson C, Burslem F, Martin P. Wound healing and inflammation genes revealed by array analysis of’macrophageless’ PU.1 null mice. Genome Biol 2005;6:R5. 15. Cha J, Kwak T, Butmarc J, Kim TA, Yufit T, Carson P, Kim SJ, Falanga V. Fibroblasts from non-healing human chronic wounds show decreased expression of beta ig-h3, a TGF-beta inducible protein. J Dermatol Sci 2008;50:15-23. 16. Seifert O, Bayat A, Geffers R, Dienus K, Buer J, Löfgren S, Matussek A. Identification of unique gene expression patterns within different lesional sites of keloids. Wound Repair Regen 2008;16:254-265. 17. Smith JC, Boone BE, Opalenik SR, Williams SM, Russell SB. Gene profiling of keloid fibroblasts shows altered expression in multiple fibrosis-associated pathways. J Invest Dermatol 2008;128:1298-1310. 18. Wall IB, Moseley R, Baird DM, Kipling D, Giles P, Laffafian I, Price PE, Thomas DW, Stephens P. Fibroblast dysfunction is a key factor in the non-healing of chronic venous leg ulcers. J Invest Dermatol 2008;128:2526-2540. 19. Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative CT method. Nat Protoc 2008;3:1101-1108. 20. Romagnani P, Lasagni L, Annunziato F, Serio M, Romagnani S. CXC chemokines: the regulatory link between inflammation and angiogenesis. Trends Immunol 2004;25:201-209. | ||
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