An Optimally Designed Engineering Exosome–Reductive COF Integrated Nanoagent for Synergistically Enhanced Diabetic Fester Wound Healing
Baohong SunFan WuXinye WangQiuxian SongZiqiu YeMohsen MohammadniaeiMing ZhangXiaohong ChuSheng XiNinglin ZhouWentao WangCheng YaoJian Shen
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Abstract Oxidative stress and local overactive inflammation have been considered major obstacles in diabetic wound treatment. Although antiphlogistic tactics have been reported widely, they are also challenged by pathogen contamination and compromised angiogenesis. Herein, a versatile integrated nanoagent based on 2D reductive covalent organic frameworks coated with antibacterial immuno‐engineered exosome (PCOF@E‐Exo) is reported to achieve efficient and comprehensive combination therapy for diabetic wounds. The E‐Exo is collected from TNF‐α‐treated mesenchymal stem cells (MSCs) under hypoxia and encapsulated cationic antimicrobial carbon dots (CDs). This integrated nanoagent not only significantly scavenges reactive oxygen species and induces anti‐inflammatory M2 macrophage polarization, but also stabilizes hypoxia‐inducible factor‐1α (HIF‐1α). More importantly, the PCOF@E‐Exo exhibits intriguing bactericide capabilities toward Gram‐negative, Gram‐positive, and drug‐resistant bacteria, showing favorable intracellular bacterial destruction and biofilm permeation. In vivo results demonstrate that the synergetic impact of suppressing oxidative injury and tissue inflammation, promoting angiogenesis and eradicating bacterial infection, could significantly accelerate the infected diabetic fester wound healing with better therapeutic benefits than monotherapy or individual antibiotics. The proposed strategy can inspire further research to design more delicate platforms using the combination of immunotherapy with other therapeutic methods for more efficient ulcerated diabetic wounds treatments.A porous, homogeneous, phosphorous‐enriched oxide nanolayer was realized on the new Ti‐15Ta‐5Zr alloy surface by the anodic galvanostatic electrodeposition in phosphoric acid solution. This nanolayer contains TiO 2 , ZrO 2 oxides, tantalum suboxides, and ions incorporated in the time of the electrodeposition process and has a thickness of 15.5 nm (X‐ray photoelectron spectroscopy data). Atomic force microscopy determined a homogeneous roughness. Scanning electron microscopy evinced a porous microstructure that can stimulate the growth of the bone tissue into pores. The presence of the anions promotes the electrostatic bonds between the nanolayer and different species from the biofluid, namely, osteoinduction. The anodic oxidation nanolayer improved all electrochemical and corrosion parameters conferring superior protection to the substrate by its higher resistance to the ion migration. Impedance spectra showed that the electrodeposited nanolayer is formed by an inner, dense, barrier layer and an outer porous layer. The nanolayer thickened in time, namely, is bioactive. The oxidized nanolayer is able to protect the alloy from ion release, to assure long‐term corrosion resistance, to minimize adverse reactions, to increase alloy bioactivity, to stimulate cell growth, and to favor osseointegration.
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Angiogenesis, a formation of neovessels, is regulated by the local balance between angiogenesis stimulators and inhibitors. A number of such endogenous regulators of angiogenesis have been found in the body. Recently, vasohibin-1 (VASH1) was isolated as a negative feedback regulator of angiogenesis produced by endothelial cells (ECs) and subsequently vasohibin-2 (VASH2) as a homologue of VASH1. It was then explored that VASH1 is expressed in ECs to terminate angiogenesis, whereas VASH2 is expressed in cells other than ECs to promote angiogenesis in the mouse model of angiogenesis. This review will focus on the vasohibin family members, which are novel regulators of angiogenesis.
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Angiogenesis is the process of new blood vessel growth and is a critical biological process under both physiologic and pathologic conditions. Angiogenesis can occur under physiologic conditions that include embryogenesis and the ovarian/menstrual cycle. In contrast, pathologic angiogenesis is associated with chronic inflammation/chronic fibroproliferative disorders and tumorigenesis of cancer. Similarly, aberrant angiogenesis associated with chronic inflammation/fibroproliferative disorders is analogous to neovascularization of tumorigenesis of cancer. Net angiogenesis is determined by a balance in the expression of angiogenic compared with angiostatic factors. CXC chemokines are heparin-binding proteins that display unique disparate roles in the regulation of angiogenesis. Based on their structure, CXC chemokines can be divided into two groups that either promote or inhibit angiogenesis, and they are therefore uniquely placed to regulate net angiogenesis in both physiologic and pathologic conditions.
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Angiogenesis is regulated by a local balance between the levels of endogenous stimulators and inhibitors of angiogenesis. Understanding of the mechanism of angiogenesis has advanced significantly since the discovery of two members of the family of angiogenesis stimulators, i.e., vascular endothelial growth factor family proteins and angiopoietins. These factors act on endothelial cells to stimulate angiogenesis. In contrast, most of angiogenesis inhibitors do not seem to have such characteristics. Very few genes encoding molecules that selectively inhibit angiogenesis have been discovered. This review will focus on our current understanding of endogenous inhibitors of angiogenesis.
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Angiogenesis plays an important role in tumour progression. However, anti-angiogenesis therapy of inhibiting pro-angiogenic factors failed to meet expectations in certain types of tumour in clinical trials. Recent studies reveal that tumour-derived extracellular vesicles (EVs) are essential in tumour angiogenesis and anti-angiogenesis drug resistance. This function has most commonly been attributed to EV contents including proteins and non-coding RNAs. Here, we summarize the recent findings of tumour-derived EV contents associated with regulating angiogenesis and illustrate the underlying mechanisms. In addition, the roles of EVs in tumour microenvironmental cells are also illustrated with a focus on how EVs participate in cell-cell communication, contributing to tumour-mediated angiogenesis. It will help offer new perspectives on developing targets of anti-angiogenesis drugs and improve the efficacy of anti-angiogenesis therapies based on tumour-derived EVs.
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Бұл зерттеужұмысындaКaно моделітурaлы жәнеоғaн қaтыстытолықмәліметберілгенжәнеуниверситетстуденттерінебaғыттaлғaн қолдaнбaлы (кейстік)зерттеужүргізілген.АхметЯссaуи университетініңстуденттеріүшін Кaно моделіқолдaнылғaн, олaрдың жоғaры білімберусaпaсынa қоятынмaңыздытaлaптaры, яғнисaпaлық қaжеттіліктері,олaрдың мaңыздылығытурaлы жәнесaпaлық қaжеттіліктерінеқaтыстыөз университетінқaлaй бaғaлaйтындығытурaлы сұрaқтaр қойылғaн. Осы зерттеудіңмaқсaты АхметЯсaуи университетіндетуризмменеджментіжәнеқaржы бaкaлaвриaт бaғдaрлaмaлaрыныңсaпaсынa қaтыстыстуденттердіңқaжеттіліктерінaнықтaу, студенттердіңқaнaғaттaну, қaнaғaттaнбaу дәрежелерінбелгілеу,білімберусaпaсын aнықтaу мен жетілдіружолдaрын тaлдaу болыптaбылaды. Осы мaқсaтқaжетуүшін, ең aлдыменКaно сaуaлнaмaсы түзіліп,116 студенткеқолдaнылдыжәнебілімберугежәнеоның сaпaсынa қaтыстыстуденттердіңтaлaптaры мен қaжеттіліктерітоптықжұмыстaрaрқылыaнықтaлды. Екіншіден,бұл aнықтaлғaн тaлaптaр мен қaжеттіліктерКaно бaғaлaу кестесіменжіктелді.Осылaйшa, сaпa тaлaптaры төрт сaнaтқa бөлінді:болуытиіс, бір өлшемді,тaртымдыжәнебейтaрaп.Соңындa,қaнaғaттaну мен қaнaғaттaнбaудың мәндеріесептелдіжәнестуденттердіңқaнaғaттaну мен қaнaғaттaнбaу деңгейлерінжоғaрылaту мен төмендетудеосытaлaптaр мен қaжеттіліктердіңрөліaйқын aнықтaлды.Түйінсөздер:сaпa, сaпaлық қaжеттіліктер,білімберусaпaсы, Кaно моделі.
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