CD9 promotes TβR2-TβR1 association driving the transition of human dermal fibroblasts to myofibroblast under hypoxia.

Background: During wound healing, fibroblast to myofibroblast transition is required for wound contraction and remodeling. While hypoxia is an important biophysical factor in wound microenvironment, the exact regulatory mechanism underlying hypoxia and fibroblast-to-myofibroblast transition remains unclear. We previously found that tetraspanin CD9 plays an important role in oxygen sensing and wound healing.

Electric fields reverse the differentiation of keratinocyte monolayer by down-regulating E-cadherin through PI3K/AKT/Snail pathway.

Re-epithelialization is an important step in skin wound healing, referring to the migration, proliferation, and differentiation of keratinocytes around the wound. During this process, the edges of the wound begin to form new epithelial cells, which migrate from the periphery of the wound towards the center, gradually covering the entire wound area. These newly formed epithelial cells proliferate and differentiate, ultimately forming a protective layer over the exposed dermal surface.

Ultra-Hydrophobic Gauze Driving Super-Haemostasis.

Controlling bleeding by applying pressing cotton gauze is the most facile treatment in prehospital emergencies. However, the wettable nature of cotton fibers leads to unnecessary blood loss due to excessive blood absorption, inseparable adhesion-induced pain, and pliable to infection. Here, a kind of ultra-hydrophobic haemostatic anti-adhesive gauze whose surface is loaded with polydimethylsiloxane (PDMS) and hydrophobic-modified cellulose nanocrystals (CNCs), achieving a water contact angle of ≈160° is developed.

A Network Meta-analysis to Explore the Effectiveness of the Different Treatment Modalities in Acne Scars.

Background: Multiple treatments are used to treat acne scars, but comparing the effectiveness of these treatments have not been studied yet. This research aimed to conduct a complete analysis of the effectiveness of commonly used therapies in acne scars.

Methods: PubMed, Embase, and Cochrane's Library (Cochrane Center Register of Controlled Trials) databases were searched through May 2023.

Paxillin/HDAC6 regulates microtubule acetylation to promote directional migration of keratinocytes driven by electric fields.

Endogenous electric fields (EFs) have been demonstrated to facilitate wound healing by directing the migration of epidermal cells. Despite the identification of numerous molecules and signaling pathways that are crucial for the directional migration of keratinocytes under EFs, the underlying molecular mechanisms remain undefined. Previous studies have indicated that microtubule (MT) acetylation is linked to cell migration, while Paxillin exerts a significant influence on cell motility.

Electric field promotes dermal fibroblast transdifferentiation through activation of RhoA/ROCK1 pathway.

With the increased incidence of age-related and lifestyle-related diseases, chronic wounds are sweeping the world, where recent studies reveal that dysfunction of fibroblast plays an indispensable role. Endogenous electric field (EF) generated by skin wound disrupting an epithelial layer has been used as an alternative clinical treatment in chronic wound by modulating cellular behaviours, including fibroblasts transdifferentiation. Although many molecules and signaling pathways have been reported associated with fibroblasts transdifferentiation, studies investigating how the electric field affects the cellular pathways have been limited.

CD9 negatively regulates collective electrotaxis of the epidermal monolayer by controlling and coordinating the polarization of leader cells.

Background: Endogenous electric fields (EFs) play an essential role in guiding the coordinated collective migration of epidermal cells to the wound centre during wound healing. Although polarization of leadercells is essential for collective migration, the signal mechanisms responsible for the EF-induced polarization of leader cells under electrotactic collective migration remain unclear. This study aims to determine how the leader cells are polarized and coordinated during EF-guided collective migration of epidermal cell sheets.

The role of mesenchymal stem cell-derived EVs in diabetic wound healing.

Diabetic foot is one of the most common complications of diabetes, requiring repeated surgical interventions and leading to amputation. In the absence of effective drugs, new treatments need to be explored. Previous studies have found that stem cell transplantation can promote the healing of chronic diabetic wounds.

Reshaping the Endogenous Electric Field to Boost Wound Repair via Electrogenerative Dressing.

The endogenous electric field (EF) generated by transepithelial potential difference plays a decisive role in wound reepithelialization. For patients with large or chronic wounds, negative-pressure wound therapy (NPWT) is the most effective clinical method in inflammation control by continuously removing the necrotic tissues or infected substances, thus creating a proproliferative microenvironment beneficial for wound reepithelialization. However, continuous negative-pressure drainage causes electrolyte loss and weakens the endogenous EF, which in turn hinders wound reepithelialization.

Hypoxic preconditioning promotes galvanotaxis of human dermal microvascular endothelial cells through NF-κB pathway.

Angiogenesis plays an important role in wound healing, especially in chronic wound. The directional migration of the human dermal microvascular endothelial cells (HDMECs) is the key regulation of angiogenesis. The wound healing can be regulated by numerous microenvironment factors including the electric fields, hypoxia and chemotaxis.

Autophagy promotes directed migration of HUVEC in response to electric fields through the ROS/SIRT1/FOXO1 pathway.

Endogenous electric fields (EFs) have been confirmed to facilitate angiogenesis through guiding directional migration of endothelial cells (ECs), but the underlying mechanisms remain obscure. Recent studies suggest that the directed migration of ECs in angiogenesis is correlated with autophagy, and the latter of which could be augmented by EFs. We hypothesize that autophagy may participate in the EFs-guided migration of ECs during angiogenesis.

Bioelectric fields coordinate wound contraction and re-epithelialization process to accelerate wound healing via promoting myofibroblast transformation.

Electric fields (EFs) are thought to play a decisive role in wound healing. However, most studies focused on the effects of EF on single species of cells in vitro. Here, we aimed to investigate the coordination function of EFs on wound healing.

Elastic Silicone Occlusive Sheeting Versus Silicone Occlusive Sheeting in the Treatment of Scars: A Randomized Controlled Trial.

Introduction: Hypertrophic scarring caused by conventional open thyroidectomy is prevalent among Asians and published trials have proved that silicone occlusive sheeting is a useful treatment for hypertrophic scarring. However, silicone occlusive sheeting does not effectively prevent scar widening. Here, we report elastic silicone occlusive sheeting as a new type of silicone application.

Impaired Retrograde Transport Due to Lack of TBC1D5 Contributes to the Trafficking Defect of Lysosomal Cathepsins in Ischemic/Hypoxic Cardiomyocytes.

Lysosomal dysfunction has been found in many pathological conditions, and methods to improve lysosomal function have been reported to be protective against infarcted hearts. However, the mechanisms underlying lysosomal dysfunction caused by ischemic injury are far less well-established. The retromer complex is implicated in the trafficking of cation-independent mannose 6-phosphate receptor (CI-MPR), which is an important protein tag for the proper transport of lysosomal contents and therefore is important for the maintenance of lysosomal function.

Autophagy-Related LC3 Accumulation Interacted Directly With LIR Containing RIPK1 and RIPK3, Stimulating Necroptosis in Hypoxic Cardiomyocytes.

The exact relationships and detailed mechanisms between autophagy and necroptosis remain obscure. Here, we demonstrated the link between accumulated autophagosome and necroptosis by intervening with autophagic flux. We first confirmed that the LC3 interacting region (LIR) domain is present in the protein sequences of RIPK1 and RIPK3.

CD38 Causes Autophagic Flux Inhibition and Cardiac Dysfunction Through a Transcriptional Inhibition Pathway Under Hypoxia/Ischemia Conditions.

Induced autophagy is protective against myocardial hypoxia/ischemia (H/I) injury, but evidence regarding the extent of autophagic clearance under H/I and the molecular mechanisms that influence autophagic flux has scarcely been presented. Here, we report that CD38 knockout improved cardiac function and autophagic flux in mice and neonatal cardiomyocytes (CMs) under H/I conditions. Mechanistic studies demonstrated that overexpression of CD38 specifically downregulated the expression of Rab7 and its adaptor protein pleckstrin homology domain-containing protein family member 1 (PLEKHM1) through nicotinamide adenine dinucleotide (NAD)-dependent and non-NAD-dependent pathways, respectively.

Electric field down-regulates CD9 to promote keratinocytes migration through AMPK pathway.

Endogenous electric field (EF)-directed keratinocytes migration is known to play a key role in the wound re-epithelialization process. Although many molecules and signaling pathways are reported important for directional keratinocytes migration under EF, the underlying mechanism remains unclear. Our previous research found that CD9, a trans-membrane protein, is involved in wound re-epithelialization and CD9 downregulation contributes to keratinocytes migration.

The Lysosomal Membrane Protein Lamp2 Alleviates Lysosomal Cell Death by Promoting Autophagic Flux in Ischemic Cardiomyocytes.

Lysosomal membrane permeabilization (LMP) has recently been recognized as an important cell death pathway in various cell types. However, studies regarding the correlation between LMP and cardiomyocyte death are scarce. Lysosomal membrane-associated protein 2 (Lamp2) is an important component of lysosomal membranes and is involved in both autophagy and LMP.

CD9 regulates keratinocyte differentiation and motility by recruiting E-cadherin to the plasma membrane and activating the PI3K/Akt pathway.

During keratinocyte stratification and wound healing, keratinocytes undergo a switch between differentiation and motility. However, limited knowledge exists on the mechanisms of the switch. We have previously demonstrated that the expression of CD9 was changed in different wound stages and involved in the regulation of keratinocyte migration.

Author Correction: Involvement of autophagy in hypoxia-BNIP3 signaling to promote epidermal keratinocyte migration.

Following publication of the original article, it has come to our attention that the Materials and Methods section of the paper was missing. This is because this section was accidentally omitted from the final version of the manuscript when it was submitted to production. Both the PDF and HTML versions of the article have been updated with the missing section and references.

Involvement of autophagy in hypoxia-BNIP3 signaling to promote epidermal keratinocyte migration.

BNIP3 is an atypical BH3-only member of the Bcl-2 family with pro-death, pro-autophagic, and cytoprotective functions, depending on the type of stress and cellular context. Recently, we demonstrated that BNIP3 stimulates the migration of epidermal keratinocytes under hypoxia. In the present study found that autophagy and BNIP3 expression were concomitantly elevated in the migrating epidermis during wound healing in a hypoxia-dependent manner.

Keratinocyte electrotaxis induced by physiological pulsed direct current electric fields.

Endogenous electric fields (EFs) direct the migration (electrotaxis) of keratinocytes in skin wounds, and the exogenous application of EFs may therefore improve wound healing, but the potential benefits are limited by the side effects of constant direct current (DC) passing through tissues. In contrast, with pulsed DC (characterized by intermittent output), parameters can be adjusted to minimize the adverse effects of electric currents. However, it remains unknown whether pulsed DC can reliably induce keratinocyte electrotaxis.

Decreased α-tubulin acetylation induced by an acidic environment impairs autophagosome formation and leads to rat cardiomyocyte injury.

Extracellular pH strongly affects cellular metabolism and function. An acidic environment induced under pathological conditions leads to cardiomyocyte injury and dysfunction, but the underlying mechanisms are still poorly understood. Autophagy has been reported as a cytoprotective mechanism that maintains cellular metabolism and viability by removing misfolded proteins and damaged organelles.