Self‐expandable tubular collagen implants

Collagen has been extensively used as a biomaterial, yet for tubular organ repair, synthetic polymers or metals (e.g., stents) are typically used. In this study, we report a novel type of tubular implant solely consisting of type I collagen, suitable to self‐expand in case of minimal invasive implantation. Potential benefits of this collagen scaffold over conventional materials include improved endothelialization, biodegradation over time, and possibilities to add bioactive components to the scaffold, such as anticoagulants. Implants were prepared by compression of porous scaffolds consisting of fibrillar type I collagen (1.0–2.0% (w/v)). By applying carbodiimide cross‐linking to the compressed scaffolds in their opened position, entropy‐driven shape memory was induced. The scaffolds were subsequently crimped and dried around a guidewire. Upon exposure to water, crimped scaffolds deployed within 15–60 s (depending on the collagen concentration used), thereby returning to the original opened form. The scaffolds were cytocompatible as assessed by cell culture with human primary vascular endothelial and smooth muscle cells. Compression force required to compress the open scaffolds increased with collagen content from 16 to 32 mN for 1.0% to 2.0% (w/v) collagen scaffolds. In conclusion, we report the first self‐expandable tubular implant consisting of solely type I collagen that may have potential as a biological vascular implant.     

Topical S-nitrosoglutathione-releasing hydrogel improves healing of rat ischaemic wounds

Topical application of the nitric oxide (NO) donor S-nitrosoglutathione (GSNO) is known to exert beneficial effects on wound healing. The aim of this study was to evaluate, for the first time, the effect of topical application of GSNO on the healing of ischaemic wounds. Wistar rats were submitted to two parallels incisions on their backs; the skin was separated from the underlying tissue, the incisions were sutured and an excisional wound was made between the parallel incisions to create an ischaemic condition surrounding the wound. The animals were separated into a control group, which received a hydrogel vehicle without GSNO, and a GSNO-treated group, which received a GSNO-containing hydrogel. The animals were treated for 7 days consecutively with one daily application. The GSNO-treated group displayed higher rates of wound contraction and re-epithelization, lower amounts of inflammatory cells, an increase in collagen fibre density and organization and a decrease in the neovascularization compared to control. These results show that topical application of GSNO is effective in the treatment of ischaemic wounds, leading to a significant improvement in the wound healing. Therefore, topical GSNO-containing hydrogels have potential for the therapeutic treatment of ischaemic diabetic and venous ulcers.     

Nitric oxide‐sensitive guanylyl cyclase is the only nitric oxide receptor mediating platelet inhibition

See also Gordge MP. Nitric oxide: a one‐trick pony? This issue, pp 1340–2. Summary. Background: The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling cascade is involved in the precise regulation of platelet responses. NO released from the endothelium is known to activate NO‐sensitive guanylyl cyclase (NO‐GC) in platelets. By the generation of cGMP and subsequent activation of cGMP‐dependent protein kinase (PKG), NO‐GC mediates the reduction of the intracellular calcium and inhibits platelet adhesion and aggregation. However, NO has been postulated to influence these platelet functions also via cGMP‐independent mechanisms. Objective: We studied the effect of NO on platelets lacking NO‐sensitive guanylyl cyclase with regards to aggregation, adhesion, calcium mobilization and bleeding time. Methods and results: Here, we show that NO signaling leading to inhibition of agonist‐induced platelet aggregation is totally abrogated in platelets from mice deficient in NO‐GC (GCKO). Even at millimolar concentrations none of the several different NO donors inhibited collagen‐induced aggregation of GCKO platelets. In addition, NO neither affected adenosine 5′‐diphosphate (ADP)‐induced adhesion nor thrombin‐induced calcium release in GCKO platelets. Although the NO‐induced cGMP signal transduction was totally abrogated cyclic adenosine monophosphate (cAMP) signaling was still functional; however, cGMP/cAMP crosstalk was disturbed on the level of phosphodiesterase type 3 (PDE3). These in vitro data are completed by a reduced bleeding time indicating the lack of NO effect in vivo. Conclusions: We conclude that NO‐GC is the only NO receptor in murine platelets mediating the inhibition of calcium release, adhesion and aggregation: lack of the enzyme leads to disturbance of primary hemostasis.     

Promotion of diabetic wound healing by collagen scaffold with collagen‐binding vascular endothelial growth factor in a diabetic rat model

Aims: Studies show that VEGF can promote tissue regeneration in diabetic wounds. The aim of this study was to evaluate the effects of a new composite biomaterial, a collagen scaffold with CBD‐VEGF, for wound healing in a diabetic rat model. Materials and methods: We produced a collagen scaffold loaded with CBD‐VEGF, which allowed VEGF to bind to the collagen scaffold. The diabetic rat model was constructed by injecting streptozocin (STZ) peritoneally and removing a 2 x 2.5 cm thick slice of skin from the back of the animal. Animals were randomly divided into 4 groups: blank control (BC Group, n = 24), collagen scaffold loaded with PBS (PBS Group, n = 24), collagen scaffold loaded with NAT‐VEGF (NAT‐VEGF Group, n = 24), and collagen scaffold loaded with CBD‐VEGF (CBD‐VEGF Group, n = 24). Wounds of the BC Group were covered with gauze and those of the PBS, NAT‐VEGF and CBD‐VEGF Groups were grafted by corresponding collagen scaffolds, respectively. Healing rates were calculated and compared among groups. Wound tissue was evaluated by histologic analysis. Results: The CBD‐VEGF group showed a higher wound healing rate, better vascularization and higher level of VEGF in the granulation tissue wound compared with NAT‐VEGF and PBS groups. Conclusions: The collagen scaffold with CBD‐VEGF promoted wound healing in a diabetic rat model, which could potentially provide better therapeutic options for the treatment of diabetic wounds. Copyright © 2012 John Wiley & Sons, Ltd.     

Therapeutic effects of a recombinant human collagen peptide bioscaffold with human adipose‐derived stem cells on impaired wound healing after radiotherapy

Chronic changes following radiotherapy include alterations in tissue‐resident stem cells and vasculatures, which can lead to impaired wound healing. In this study, novel recombinant human collagen peptide (rhCP) scaffolds were evaluated as a biomaterial carrier for cellular regenerative therapy. Human adipose‐derived stem cells (hASCs) were successfully cultured on rhCP scaffolds. By hASC culture on rhCP, microarray assay indicated that expression of genes related to cell proliferation and extracellular matrix production was upregulated. Pathway analyses revealed that signaling pathways related to inflammatory suppression and cell growth promotion were activated as well as signaling pathways consistent with some growth factors including vascular endothelial growth factor, hepatocyte growth factor, and transforming growth factor beta, although gene expression of these growth factors was not upregulated. These findings suggest the rhCP scaffold showed similar biological actions to cytokines regulating cell growth and immunity. In subsequent impaired wound healing experiments using a locally irradiated (20 Gray) mouse, wound treatment with rhCP sponges combined with cultured hASCs and human umbilical vein endothelial cells accelerated wound closure compared with wounds treated with rhCP with hASCs alone, rhCP only, and control (dressing alone), with better healing observed according to this order. These results indicating the therapeutic value of rhCP scaffolds as a topical biomaterial dressing and a biocarrier of stem cells and vascular endothelial cells for regenerating therapies. The combination of rhCP and functional cells was suggested to be a potential tool for revitalizing stem cell‐depleted conditions such as radiation tissue damage.     

Chronic treatment with taurine ameliorates diabetes‐induced dysfunction of nitric oxide‐mediated neurogenic and endothelium‐dependent corpus cavernosum relaxation in rats

This study was aimed to examine the effect of chronic taurine treatment on corpus cavernosum dysfunction in diabetic rats and to investigate possible underlying mechanisms. Thirty male rats were randomized to three groups of 10 each, including control, diabetic, and taurine‐treated diabetic. Diabetes was induced in rats by streptozotocin (STZ, single intraperitoneal dose of 50 mg/kg body weight). Taurine was administered orally for 12 weeks (1% w/v in drinking water) from the day on which STZ was injected. At the end of the 12th week, strips of corpus cavernosum were suspended in an organ bath system for functional studies. Nitric oxide (NO)‐mediated endothelium‐dependent and neurogenic corpus cavernosum relaxation were evaluated by acetylcholine (ACh, 0.1–100 μm ) and electrical field stimulation (EFS, 30 V, 5 ms, 2–32 Hz), respectively. The expressions of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p‐eNOS) (Ser‐1177), neuronal nitric oxide synthase (nNOS), NADPH oxidase subunit gp91^phox, Rho A, and Rho kinase in corpus cavernosum were semi‐quantitatively assessed by immunohistochemistry. Induction of diabetes resulted in significant inhibition of NO‐mediated endothelium‐dependent and neurogenic corpus cavernosum relaxation. Furthermore, eNOS, p‐eNOS, and nNOS expressions decreased significantly in diabetic rats compared to controls, while gp91^phox, RhoA and Rho kinase expressions increased significantly. The diminished relaxation response to ACh and EFS as well as diabetes‐related changes in expressions of these proteins in corpus cavernosum of diabetic rats was significantly improved by taurine. Taurine treatment improves NO‐mediated relaxations of corpus cavernosum in diabetic rats probably by inhibiting NADPH oxidase/Rho kinase pathways.     

Controlled collagen crosslinking process in tissue‐engineered fibroblast sheets for preventing scar contracture on the surface of lungs

For preventing the scar contracture of host tissue and adjusting the tensile strength of covering cell sheets, a controlled collagen crosslinking step process in the preparation of skin‐fibroblast sheets for repairing wound was investigated by using β‐aminopropionitrile (BAPN), a collagen crosslinking inhibitor, in the culture medium. Skin fibroblasts obtained from neonatal rats were cultured in medium with and without 0.25 mm BAPN for 7 days and seeded on temperature‐responsive culture dishes. After the confluent cells were non‐invasively harvested as a monolithic cell sheet, two cell sheets were transplanted to a lung‐injury site of athymic rats, which was closed by neither fibrin glue nor suturing. Four weeks after the transplantation the animals were sacrificed and the lungs with the transplanted cell sheets were examined. Although the control cell sheet‐transplanted lungs contracted the surrounding tissue, BAPN‐treated cell sheet‐transplanted lungs showed no contraction of the tissue. Collagen fibres of control cell sheets were more dense and thick than those of BAPN‐treated cell sheets, where the crosslinking of collagen fibres was clearly inhibited. Sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS–PAGE) showed that BAPN‐treated cell sheets gave no β‐chain band, indicating that the collagen crosslinkings of the fibroblast sheets were able to be controlled by BAPN. BAPN‐treated fibroblast sheets promise to allow wound clefts to be repaired without scar contractures. Copyright © 2012 John Wiley & Sons, Ltd.     

Fetal dermal fibroblasts exhibit enhanced growth and collagen production in two‐ and three‐dimensional culture in comparison to adult fibroblasts

The high morbidity of tendon injuries and the poor outcomes observed following repair or replacement have stimulated interest in regenerative approaches to treatment and, in particular, the use of cell‐based analogues as alternatives to autologous and allogeneic graft repair. Given the known regenerative properties of fetal tissues, the objective of this study was to assess the biological and mechanical properties of tissue‐engineered three‐dimensional (3D) composites seeded with fetal skin cells. Dermal fibroblasts were isolated from pregnant rats and their fetuses and characterized in monolayer culture and on 3D resorbable polyester scaffolds. To determine the differences between fetal and adult fibroblasts, DNA, total protein and types I and III collagen production were measured. In addition, morphology and mechanical properties of the 3D constructs were examined. In monolayer culture, fetal fibroblasts produced significantly more types I and III collagen and displayed serum‐independent growth, while adult fibroblasts elaborated less collagen and exhibited reduced cell spreading and attachment under low‐serum conditions. In 3D culture, fetal constructs appeared more developed based on gross examination, with significantly more total DNA, total protein and normalized type I collagen production compared to adult specimens. Finally, after 35 days, fetal fibroblast‐seeded constructs possessed superior mechanical properties compared to adult samples. Taken together, these findings indicate that fetal dermal fibroblasts may be an effective source of cells for fabricating tissue equivalents to regenerate injured tendons. Copyright © 2009 John Wiley & Sons, Ltd.     

The effectiveness of silver‐releasing dressings in the management of non‐healing chronic wounds: a meta‐analysis

Aim. The purpose of this study was to examine the efficacy of silver‐releasing dressings in the management of non‐healing chronic wounds. Background. Non‐healing chronic wounds often have a negative physical impact on patients and place a financial burden on healthcare systems. Silver dressings are wound products designed to control infection and provide a wound environment conducive to healing. However, validation of the clinical efficacy of these dressings is lacking. Design. Systematic review and meta‐analysis. Methods. A systematic search of the major electronic databases PubMed, CINAHL, Cochrane, MEDLINE, British Nursing Index, EBSCO, OCLC and Proquest between 1950–June 2007 was conducted. Hand searches of selected periodicals, textbooks and checking reference lists and contacting experts was also performed. Results. Eight studies were selected from a potentially relevant 1957 references screened. Analysis incorporated data from 1399 participants in the eight randomised control trials. We found that silver dressings significantly improved wound healing (CI₉₅: 0·16–0·39, p < 0·001), reduced odour (CI₉₅: 0·24–0·52, p < 0·001) and pain‐related symptoms (CI₉₅: 0·18–0·47, p < 0·001), decreased wound exudates (CI₉₅: 0·17–0·44, p < 0·001) and had a prolonged dressing wear time (CI₉₅: 0·19–0·48, p = 0·028) when compared with alternative wound management approaches. An analysis of sensitivity in these studies by subgroup analysis generally supported these associations. Furthermore, studies indicated an improvement in quality of life (CI₉₅: 0·04–0·33, p = 0·013) using silver dressings in wound management with no associated severe adverse events. Conclusion. This meta‐analysis confirms the effectiveness of silver dressings in wound healing and improving patients’ quality of life. However, it also highlights the need for additional well‐designed randomised controlled trials to evaluate the effectiveness of silver‐related dressings further. Relevance to clinical practice. The results of this study provide objective data on the effectiveness of silver‐related dressing when applied to non‐healing chronic wounds.     

The dual delivery of KGF and bFGF by collagen membrane to promote skin wound healing

The major challenges associated with skin regeneration can include hindered vascularization and an insufficient degree of epithelization. In view of the complexity of these processes and the control signals on which they depend, one possible solution to these limitations could be simulating normal skin development and wound repair via the exogenous delivery of multiple cytokines. Here, we report the use of keratinocyte growth factor (KGF or FGF‐7) and basic fibroblast growth factor (bFGF or FGF‐2) released chemically modified collagen membranes to facilitate skin wound healing. The results from in vitro studies confirmed that this system resulted in higher cellular proliferation and faster cell migration. After transplanting the biomaterial onto an excisional wound healing model, the dual growth factor group, compared with the single growth factor groups and empty control group, showed more highly developed vascular networks and organized epidermal regeneration in the wounds. As a consequence, this experimental group showed mature epidermal coverage. Overall, this novel approach of releasing growth factors from a collagen membrane opens new avenues for fulfilling unmet clinical needs for wound care.     

Wound healing grafts: Omega‐3 fatty acid lipid content differentiates the lipid profiles of acellular Atlantic cod skin from traditional dermal substitutes

Acellular fish skin (ACS) has emerged as a dermal substitute used to promote wound healing with decreased scar formation and pain relief that may be due to polyunsaturated fatty acid (PUFA) content. However, the PUFA content of ACS is still unknown. The aim of this study was to compare the total fatty acids and lipid profiles of ACS to two bovine‐based grafts and standard of care human cadaver skin (HCS). Furthermore, there was also the goal to assess the capability of ACS lipid content to enhance wound healing. The fatty acid analysis was performed with GC–FID, and an LC–MS untargeted method was developed in order to the analyse the lipid profiles of the grafts was. The enhancement of wound healing by the ACS extract was investigated in vitro on HaCat cells. Our results showed that ACS had the highest content of PUFA (27.0 ± 1.43% of their total fatty acids), followed by HCS (20.6 ± 3.9%). The two grafts of bovine origin presented insignificant PUFA amounts. The majority of the PUFAs found in ACS were omega‐3, and in HCS, they were omega‐6. The untargeted lipidomics analysis demonstrated that ACS grafts were characterized by phosphatidylcholine containing either 20:5 or 22:6 omega‐3 PUFA. The ACS lipid extract increased the HaCat cells migration and enhanced wound closure 4 hr earlier versus control. Our study demonstrated that ACS has a lipid profile that is distinct from other wound healing grafts, that PUFAs are maintained in ACS post‐processing as phosphatidylcholine, and that ACS lipid content influences wound healing properties.     

Engineered skin graft with stromal vascular fraction cells encapsulated in fibrin–collagen hydrogel: A clinical study for diabetic wound healing

Despite the abundance of skin substitutes in the worldwide market, major hurdles in developing more complex tissues include the addition of skin appendages and vascular networks as the most important structure. The aim of this research was a clinical feasibility study of a novel prevascularized skin grafts containing the dermal and epidermal layer using the adipose stromal vascular fraction (SVF)‐derived endothelial cell population for vascular network regeneration. Herein, we characterized hydrogel with emphasis on biological compatibility and cell proliferation, migration, and vitality. The therapeutic potential of the prevascularized hydrogel transplanted on five human subjects as an intervention group with diabetic wounds was compared with nonvascularized skin grafts as the control on five patients. Wound planimetric and biometric analysis was performed using a Mann–Whitney nonparametric t‐test (p ≤ .05). The fibrin–collagen hydrogel was suitable for skin organotypic cell culture. There was a significant (p ≤ .05) increased in skin thickness and density in the vascular beds of the hypodermis measured with skin scanner compared with that in the control group. No significant macroscopic differences were observed between the intervention and control groups (p ≤ .05). In summary, we report for the first time the use of autologous dermal–epidermal skin grafts with intrinsic vascular plexus in a clinical feasibility study. The preliminary data showed that SVF‐based full‐thickness skin grafts are safe and accelerate the wound healing process. The next stage of the study is a full‐scale randomized clinical trial for the treatment of patients with chronic wounds.     

Recombinant human collagen III gel for transplantation of autologous skin cells in porcine full‐thickness wounds

Complex skin wounds, such as chronic ulcers and deep burns, require lengthy treatments and cause extensive burdens on healthcare and the economy. Use of biomaterials and cell transplantation may improve traditional treatments and promote the healing of difficult‐to‐treat wounds. In this study, we investigated the use of recombinant human collagen III (rhCol‐III) gel as a delivery vehicle for cultured autologous skin cells (keratinocytes only or keratinocyte–fibroblast mixtures). We examined its effect on the healing of full‐thickness wounds in a porcine wound‐healing model. Two Landrace pigs were used for the study. Fourteen deep dermal wounds were created on the back of each pig with an 8 mm biopsy punch. Syringes containing acellular rhCol‐III gel (n = 8) or rhCol‐III gel with autologous keratinocytes (n = 8) or rhCol‐III gel with autologous keratinocytes and fibroblasts (n = 8) were applied into wounds. Untreated wounds were used as controls for the treatment groups (n = 4). We used rhCol‐III gel to manufacture a cell‐delivery syringe containing autologous skin cells. In a full‐thickness wound‐healing model, we observed that rhCol‐III gel enhances early granulation tissue formation. Interestingly, we found cell type‐dependent differences in the stability of rhCol‐III in vivo. Fibroblast‐containing gel was effectively removed from the wound, whereas gels without cells or with keratinocytes only remained intact. Our results demonstrate that the properties of rhCol‐III gel for skin cell transplantation can be significantly altered in a cell type‐dependent manner. Copyright © 2013 John Wiley & Sons, Ltd.     

Combination therapy of autologous adipose mesenchymal stem cell‐enriched,high‐density lipoaspirate and topical timolol for healing chronic wounds

Chronic venous leg ulcers are profoundly debilitating and result in billions in health care expenditure. Thus, there is a quest for engineered and innovative approaches. Herein we present a 63‐year‐old patient with a 30 year history of venous stasis and left lower extremity ulcers, which have been refractory to standard of care, anticoagulation and venous stripping. The medial ulcer was treated with transplantation of autologous adipose mesenchymal stem cell (AMSC)‐enriched, high‐density lipoaspirate (HDL) on OASIS wound matrix and compression therapy. The lateral ulcer was treated as a control with standard debridement and compression therapy. Four weeks later, both ulcers received daily topical timolol. Three months later, the test ulcer was completely epithelized and remains healed for over 15 months. However, the control showed minimal signs of improvement. In companion studies in our laboratory, human AMSC were cultured in Minimum Essential Medium Eagle Alpha Modifications (MEMα) with fetal bovine serum (FBS). Timolol was administered to AMSC prior to treatment with epinephrine and 104 bacteria/ml heat‐killed Staphylococcus aureus. The MEMα with FBS devoid of AMSC served as a background control. After 24 h, cell culture supernatants and protein lysates were collected to determine cytokine production. There was a statistical significant decrease in pro‐inflammatory interleukin‐6 and ‐8 induced by the bacteria (to model the wound environment) in AMSC in the presence of timolol compared with control (p < 0.5). This is the first case of a successful combination of autologous AMSC‐enriched, HDL with topical timolol for the healing of chronic venous leg ulcers. Copyright © 2016 John Wiley & Sons, Ltd.     

Allogeneic platelet‐rich plasma affects monocyte differentiation to dendritic cells causing an anti‐inflammatory microenvironment,putatively fostering wound healing

Autologous platelet‐rich plasma (PRP) is used clinically to induce repair of different tissues through the release of bioactive molecules. In some patients, the production of efficient autologous PRP is unfeasible due to their compromised health. Allogeneic PRP mismatched for AB0 and Rh antigens was developed. The effect of allogeneic PRP on immune response should be defined to use it in clinical practice avoiding side effects. Thus, whether PRP affects the differentiation of peripheral blood monocytes to dendritic cells upon stimulation with granulocyte monocyte colony stimulating factor and interleukin‐4 was investigated. Indeed, these cells are the main players of immune response and tissue repair. PRP inhibited the differentiation of monocytes to CD1a⁺ dendritic cells and favoured the expansion of phagocytic CD163⁺CD206⁺ fibrocyte‐like cells. These cells produced interleukin‐10 and prostaglandin‐E₂, but not interferon‐γ, upon stimulation with lipopolysaccharides. Moreover, they promoted the expansion of regulatory CD4⁺CD25⁺FoxP3⁺ T cells upon allostimulation or antigen specific priming. Finally, the conditioned medium harvested from monocytes differentiated with PRP triggered a strong chemotactic effect on mesenchymal cells in both scratch and transwell migration assays. These results strongly suggest that allogeneic PRP can foster the differentiation of monocytes to a regulatory anti‐inflammatory population, possibly favouring wound healing. Copyright © 2016 John Wiley & Sons, Ltd.     

Life‐threatening hemorrhage and prolonged wound healing are remarkable phenotypes manifested by complete plasminogen activator inhibitor‐1 deficiency in humans

Summary. Background: Plasminogen activator inhibitor‐1 (PAI‐1) is the primary physiological regulator of urokinase plasminogen activator (uPA) and tissue plasminogen activator (tPA) activity. A number of studies have shown that elevated levels of PAI‐1 are related to pathological states such as an increased risk of arterial thrombotic events and a poor prognosis for cancer patients; however, there are few reports about PAI‐1 deficiency in humans because the disorder is very rare. Objective: To understand the in vivo impact of a complete PAI‐1 deficiency, Serpine1^?/? mice were generated; a number of in vivo studies have been conducted to elucidate the function of PAI‐1 using Serpine1^?/? mice. The phenotypes demonstrated in Serpine1^?/? mice, however, were quite different from those in humans. Therefore, it is necessary to find out and analyze SERPINE1 deficiency in humans. Patient and methods: The patient is a 47‐year‐old woman who has had multiple episodes of major bleeding. Although most of the patient’s blood coagulation factors were functionally normal, her PAI‐1 antigen levels were undetectable. Therefore, DNA sequencing of the SERPINE1 gene were analyzed. Results: The proband had a homozygous 1‐bp duplication (C) at exon 3 (c.356dupC; p.Ile120AspfsX42). Both wild‐type PAI‐1 (42.7 kDa) and mutated (Mut) PAI‐1 (14.7 kDa) were expressed in COS‐1 cells, although the level of Mut PAI‐1 expressed in the cell lysates was much lower. Wild‐type PAI‐1 was observed in the culture supernatant, whereas no Mut PAI‐1 was detected in the supernatant. Conclusions: Considering the results of the present study, the translation of mouse studies to humans must be performed with great care.     

Platelet‐derived transforming growth factor‐β1 promotes keratinocyte proliferation in cutaneous wound healing

Platelets are a recognised potent source of transforming growth factor‐β1 (TGFβ1), a cytokine known to promote wound healing and regeneration by stimulating dermal fibroblast proliferation and extracellular matrix deposition. Platelet lysate has been advocated as a novel personalised therapeutic to treat persistent wounds, although the precise platelet‐derived growth factors responsible for these beneficial effects have not been fully elucidated. The aim of this study was to investigate the specific role of platelet‐derived TGFβ1 in cutaneous wound healing. Using a transgenic mouse with a targeted deletion of TGFβ1 in megakaryocytes and platelets (TGFβ1^fl/fl.PF4‐Cre), we show for the first time that platelet‐derived TGFβ1 contributes to epidermal and dermal thickening and cellular turnover after excisional skin wounding. In vitro studies demonstrate that human dermal fibroblasts stimulated with platelet lysate containing high levels of platelet‐derived TGFβ1 did not exhibit enhanced collagen deposition or proliferation, suggesting that platelet‐derived TGFβ1 is not a key promoter of these wound healing processes. Interestingly, human keratinocytes displayed enhanced TGFβ1‐driven proliferation in response to platelet lysate, reminiscent of our in vivo findings. In summary, our novel findings define and emphasise an important role of platelet‐derived TGFβ1 in epidermal remodelling and regeneration processes during cutaneous wound healing.