Understanding platelet–surface activation is of clinical importance because it directly involves the formation of a hemostatic plug or blood clot at sites of vascular injury. Although platelet activation on various structured patterns has been investigated, this behavior on nanoscale groove patterns remains unclear. Here, we fabricated pattern arrays with 100 and 500 nm groove sizes by electron-beam lithography and investigated the response of platelets on these patterns using scanning electron microscopy and atomic force microscopy. Without modification, platelets spread strongest on the unstructured surface and weakest on 100 nm grooves, while the spreading characteristic significantly decreased on laminin-modified surfaces. With a laminin coating, platelets did not spread after contact for 15 min, but the formation of filopodia of different lengths occurred, which is longest on the unstructured surface and shortest on 100 nm grooves. This difference correlated with the adhesion forces because the platelets bound strongest, weaker, and weakest on the corresponding unstructured surface and 500 and 100 nm nanopatterns. Our results show that platelet–surface activation depends on the underlying nanostructured surface, and the findings may have a major impact on medical applications.

Freestanding multilayer films prepared by layer‐by‐layer technique have attracted interest as promising materials for wound dressings. The goal is to fabricate freestanding films using chitosan (CHI) and alginate (ALG) including subsequent crosslinking to improve the mechanical properties of films while maintaining their biocompatibility. Three crosslinking strategies are investigated, namely use of calcium ions for crosslinking ALG, 1‐ethyl‐3‐(‐3‐dimethylaminopropyl) carbodiimide combined with N‐hydroxysuccinimide for crosslinking ALG with CHI, and Genipin for crosslinking chitosan inside the films. Different characteristics, such as surface morphology, wettability, swelling, roughness, and mechanical properties are investigated showing that films became thinner, exhibited rougher surfaces, had lower water uptake, and increased mechanical strength after crosslinking. Changes of wettability are moderate and dependent on the crosslinking method. In vitro cytotoxicity and cell attachment studies with human dermal fibroblasts show that freestanding CHI‐ALG films represent a poorly adhesive substratum for fibroblasts, while studies using incubation of plastic‐adherent fibroblast beneath floating films show no signs of cytotoxicity in a time frame of 7 days. Results from cell experiments combined with film characteristics after crosslinking, indicate that crosslinked freestanding films made of ALG and CHI may be interesting candidates for wound dressings.

Modulation of platelet-surface activation is important for many biomedical applications such as in vivo performance, platelet storage, and acceptance of an implant. Reducing platelet-surface activation is challenging because they become activated immediately after short contact with nonphysiological surfaces. To date, controversies and open questions in the field of platelet-surface activation still remain. Here, we review state-of-the-art approaches in inhibiting platelet-surface activation, mainly focusing on modification, patterning, and methodologies for characterization of the surfaces. As a future perspective, we discuss how the combination of biochemical and physiochemical strategies together with the topographical modulations would assist in the search for an ideal nonthrombogenic surface.

Platelet-surface interaction is of paramount importance in biomedical applications as well as in vitro studies. However, controlling platelet-surface activation is challenging and still requires more effort as they activate immediately when contacting with any nonphysiological surface. As hydrogels are highly biocompatible, in this study, we developed agarose and gelatin-based hydrogel films to inhibit platelet-surface adhesion. We found promising agarose films that exhibit higher surface wettability, better controlled-swelling properties, and greater stiffness compared to gelatin, resulting in a strong reduction of platelet adhesion. Mechanical properties and surface wettability of the hydrogel films were varied by adding magnetite (Fe 3 O 4 ) nanoparticles. While all of the films prevented platelet spreading, films formed by agarose and its nanocomposite repelled platelets and inhibited platelet adhesion and activation stronger than those of gelatin. Our results showed that platelet-surface activation is modulated by controlling the properties of the films underneath platelets and that the bioinert agarose can be potentially translated to the development of platelet storage and other medical applications.

Platelets are cell fragments from megakaryocytes devoid of the cell nucleus. They are highly sensitive and easily activated by nonphysiological surfaces. Activated platelets have an intrinsic mechanism to release various proteins that participate in multiple pathways, initiating the platelet activation cascade. Surface-induced platelet activation is a challenge encountered during platelet storage, which eventually leads to aggregation of platelets and can thereby result in the degradation of the platelet concentrates. We have previously reported that surface-induced platelet activation can be minimized by either modifying their contact surfaces with polymers or introducing nanogroove patterns underneath the platelets. Here, we investigated the response of platelets to various nanotopographical surfaces printed using fluidic force microscopy (FluidFM). We found that the hemispherical array (grid) and hexagonal tile (hive) structures caused a reduction of surface stiffness, which leads to an inhibition of platelet adhesion. Our results reveal that nanopatterns enable the inhibition of platelet activation on surfaces, thus implying that development in nanotexturing of storage bags can extend the lifetime of platelet concentrates.