Research Article Immunoglobulin G in Platelet-Derived Wound Healing Factors Elisa Seria , 1 Sarah Samut Tagliaferro , 1 Doreen Cutajar , 2 Ruth Galdies , 1 and Alex Felice 1 1 Department of Physiology and Biochemistry, Faculty of Medicine and Surgery, Centre of Molecular Medicine and Biobanking, University of Malta and Division of Pathology, Mater Dei Hospital, Malta MSD2080 2 Department of Surgery, Faculty of Medicine and Surgery, University of Malta Medical School and Mater Dei Hospital, Malta MSD2080 Correspondence should be addressed to Elisa Seria; elisa.seria@um.edu.mt Received 24 August 2020; Revised 3 December 2020; Accepted 13 January 2021; Published 28 January 2021 Academic Editor: Saheem Ahmad Copyright © 2021 Elisa Seria et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We intended to reformulate an existing platelet-derived wound healing formula to target each phase of the healing wound with the appropriate phase-specific molecules. A decreased perfusion of the skin, often associated with conditions such as thalassemia, sickle cell disease, diabetes mellitus, and chronic vascular disease, is the most common etiology of cutaneous ulcers and chronic wounds. We had previously shown that a PDWHF topically applied to a chronic nonhealing ulcer of a β-thalassemia homozygote stimulated and accelerated closure of the wound. The PDWHF was prepared from a pooled platelet concentrate of a matching blood group, consisting of a combination of platelet α-granule-derived factors. Processing of the apheresis-pooled platelets yielded various amounts of proteins (3:36 g/mL ± 0:25 (SD) (N = 10)) by the better lysis buffer method. Immunoglobulin G was found to be the most abundant α-granule-secreted protein. Equally broad quantities of the IgG (10:76 ± 12:66% (SD) (N = 10)) and IgG/albumin ratios (0:6±0:4 (SD) (N = 10)) were quantified. We have developed a method using a reformulated lysis buffer followed by size exclusion chromatography and affinity chromatography to extract, identify, quantify, and purify IgG from activated platelets. IgG purification was confirmed by Western blot and flow cytometry. It was thought unlikely that the platelet IgG could be accounted for by adsorption of plasma protein, though the variable quantities could account for diversity in wound healing rates. The IgG could protect the wound even from subclinical infections and functionally advance healing. It may be useful in the management of skin ulcers in the early phase of wound healing. 1. Introduction Cutaneous wounds are seldomly caused by decreased perfu- sion of the skin that becomes infected. Clinical hemolytic dis- orders such as sickle cell disease (SCD) and beta-thalassemia (β-thalassemia) are associated with indolent leg ulcers, partly caused by peripheral hypoxia [1, 2], but may develop further as a result of low bioavailability of nitric oxide (NO), iron overload, and impaired endothelial function [3]. Hemoglo- bin disorders are frequently observed in Malta, Southern Europe, and the Mediterranean due to several β globin gene mutations [4]. Chronic leg ulcers may also develop in individuals with type 2 diabetes mellitus (T2DM) and long-term venous insufficiency. Irrespective of the different pathophysiology, these ulcers indicate poor skin perfusion, altered metabolism, and chronic inflammation, which impairs repair and closure of the wound [5–7]. Ulcer formation results in the release of danger signals, such as pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), as well as other proinflammatory cytokines, which activate the early inflammatory phase of the wound. Subsequently, neutrophil apoptosis triggers macrophages to transition to an anti- inflammatory cellular phenotype. In combination with other local immune signals, this leads to the fundamental steps for the resolution of the inflammation [8]. Iron overload, hyp- oxia, and hyperglycemia inhibit this physiological transition. Hindawi BioMed Research International Volume 2021, Article ID 4762657, 16 pages https://doi.org/10.1155/2021/4762657