Wound Tissue Repair Research Articles

Collagen nano scaffold in tendon repair and its application in the restoration of sports mechanical properties

Tendons are specialised dense connective tissue, which connect bone cartilage and muscle tissue, and play a role in transmitting the tension, movement and stabilising joints produced by muscles. Tendon injury is a common clinical disease, the repair of tendon injury has both exogenous and endogenous healing. Exogenous repair is involved in early repair, which mainly depends on cells infiltrated from external tissues, including synovium. This repair mechanism can lead to the adhesion of tendon and surrounding tissue to form paralysis marks, and damage the activity of muscle and leg, prevention of adhesion is an important link in the treatment of muscle and leg injury. In this paper, the main diaphragm mechanism of collagen scaffolds is used to reduce the participation of exogenous repair, prevent the formation of muscle leg adhesion, and selectively guide the attachment and proliferation of endogenous tendon cells to the damaged site, so as to achieve the purpose of tendon tissue injury repair, to provide a new idea and method for the prevention and treatment of tendon adhesion and injury repair in clinical work.

Proof of Concept Study for Increasing Tenascin-C-Targeted Drug Delivery to Tumors Previously Subjected to Therapy: X-Irradiation Increases Tumor Uptake

Simple SummaryWe hypothesized that an agent recognizing a specific factor, which is involved in tissue injury repair, could achieve the goal of delivering an additional antitumor agent to tumors during tissue repair after initial anticancer therapy. To demonstrate our concept, the present study employed tenascin-C (TNC) as a target molecule and radiation as initial therapy. Increased TNC expression was observed in tumors after radiation exposure in a pancreatic cancer mouse model. Of our three anti-TNC antibodies, the antibody 3–6 showed statistically significant higher tumor uptake compared with non-irradiated tumors in the by biodistribution and single-photon emission computed tomography with computed tomography studies. This finding strongly supports our concept. Our proposed therapeutic strategy could result in better outcomes for patients with treatment-refractory cancer.In treatment-refractory cancers, tumor tissues damaged by therapy initiate the repair response; therefore, tumor tissues must be exposed to an additional burden before successful repair. We hypothesized that an agent recognizing a molecule that responds to anticancer treatment-induced tissue injury could deliver an additional antitumor agent including a radionuclide to damaged cancer tissues during repair. We selected the extracellular matrix glycoprotein tenascin-C (TNC) as such a molecule, and three antibodies recognizing human and murine TNC were employed to evaluate X-irradiation-induced changes in TNC uptake by subcutaneous tumors. TNC expression was assessed by immunohistochemical staining of BxPC-3 tumors treated with or without X-irradiation (30 Gy) for 7 days. Antibodies against TNC (3–6, 12–2–7, TDEAR) and a control antibody were radiolabeled with 111In and injected into nude mice having BxPC-3 tumors 7 days after X-irradiation, and temporal uptake was monitored for an additional 4 days by biodistribution and single-photon emission computed tomography with computed tomography (SPECT/CT) studies. Intratumoral distribution was analyzed by autoradiography. The immunohistochemical signal for TNC expression was faint in nontreated tumors but increased and expanded with time until day 7 after X-irradiation. Biodistribution studies revealed increased tumor uptake of all three 111In-labeled antibodies and the control antibody. However, a statistically significant increase in uptake was evident only for 111In-labeled 3–6 (35% injected dose (ID)/g for 30 Gy vs. 15% ID/g for 0 Gy at day 1, p < 0.01), whereas limited changes in 111In-labeled TDEAR2, 12–2–27, and control antibody were observed (several % ID/g for 0 and 30 Gy). Serial SPECT/CT imaging with 111In-labeled 3–6 or control antibody provided consistent results. Autoradiography revealed noticeably stronger signals in irradiated tumors injected with 111In-labeled 3–6 compared with each of the nonirradiated tumors and the control antibody. The signals were observed in TNC-expressing stroma. Markedly increased uptake of 111In-labeled 3–6 in irradiated tumors supports our concept that an agent, such as an antibody, that recognizes a molecule involved in tissue injury repair, such as TNC, could enhance drug delivery to tumor tissues that have undergone therapy. The combination of antibody 3–6 coupled to a tumoricidal drug and conventional therapy has the potential to achieve better outcomes for patients with refractory cancer.

Compatibility of Carbon Composite Biomaterials for Repairing Bone Tissue Injury in Wushu Training

With the improvement of economic level, more and more people begin to pursue a healthy lifestyle, among which sports have become an important way of modern people’s sports, but in the process of sports, there will inevitably be some injuries, especially in martial arts training, and bone is the most vulnerable part. Because of the special physiological characteristics of cartilage tissue, it is difficult to recover after injury. This problem has become the main health problem in real life, which greatly affects people’s health and quality of life. At present, the technology of carbon composite biological nanomaterials is more and more mature, and the bioactive composite materials are composed of polymers and bioactive components, which have very good biocompatibility. In recent years, the bioactive composite materials have been applied to clinical practice and achieved very good results. Based on this, this paper considers linking the bioactive carbon composite biomaterials with the recovery of bone tissue damage, and according to the biocompatibility of bioactive composite materials, it is applied to the repair of bone tissue injury in clinical practice. In this paper, two kinds of carbon composite biomaterials, calcium carbonate composite and graphene composite, were synthesized by electrochemical method and photocatalytic reduction method. The crystal of calcium carbonate complex and graphene composite was extracted by changing the experimental time and the parameters of the solution in the experiment, and then the two carbon composite materials were analyzed as biomineralization complex biocompatibility, cell growth, and cell activity of the complex as a drug carrier for bone tissue injury. The experimental results show that the two kinds of carbon composite biomaterials can provide a very good interface for cell adhesion and spreading. This experiment proves that the artificial bone made of carbon composite biological nanomaterials has good biocompatibility, and the biocompatibility of carbon composite biological nanomaterials can be directly applied to clinical bone tissue repair surgery.

Human amniotic membrane mesenchymal stem cells-conditioned medium attenuates myocardial ischemia-reperfusion injury in rats by targeting oxidative stress.

Objective(s):Ischemic heart diseases (IHD) are one of the major causes of death worldwide. Studies have shown that mesenchymal stem cells can secrete and release conditioned medium (CM) which has biological activities and can repair tissue injury. This study aimed to investigate the effects of human amniotic membrane mesenchymal stem cells (hAMCs)-CM on myocardial ischemia/reperfusion (I/R) injury in rats by targeting oxidative stress. Materials and Methods:Male Wistar rats (40 rats, weighing 200–250 g) were randomly divided into four groups: Sham, myocardial infarction (MI), MI + culture media, and MI + conditioned medium. MI was induced by ligation of the left anterior descending coronary artery for 30 min. After 15 min of reperfusion, intramyocardial injections of hAMCs-CM or culture media (150 μl) were performed. At the end of the experiment, serum levels of cardiac troponin-I (cTn-I), myocardial levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as cardiac histological changes were evaluated.Results:HAMCs-CM significantly decreased cTn-I and MDA levels and increased SOD and GPx activities (P<0.05). In addition, hAMCs-CM improved cardiac histological changes and decreased myocardial injury percentage (P<0.05). Conclusion:This study showed that hAMCs-CM has cardioprotective effects in the I/R injury condition. Reduction of oxidative stress by hAMCs-CM plays a significant role in this context. Based on the results of this study, it can be concluded that hAMCs-CM can be offered as a therapeutic candidate for I/R injury in the future, but more research is needed.

Ozonized solutions favor the repair of experimentally induced skin wounds in rats

ABSTRACT: This study aimed to evaluate and compare the effects of ozonized solutions on tissue wound repair in rats. Treatments consisted of ozonized water (GA), 0.9% sodium chloride (GCL), ozonized oil (GO), and 0.2% allantoin cream (GAL). The morphometric evaluation showed that wounds of the GA group presented a higher degree of retraction (p&lt;0.05) at three and eight days of treatment (37.96 and 84.81%, respectively). Picrosirius red staining showed that groups GA and GO presented higher deposition (p&lt;0.05) of type I collagen at 15 and 22 days of treatment, respectively. The neovascularization was higher in wounds of group GO on days 3, 8, and 15 (p&lt;0.05), with higher VEGF immunostaining. (p&lt;0.05). Thus, ozonized water enhances wound retraction and assists in the maturation and remodeling phase, while ozonized oil promotes higher neovascularization during tissue repair and higher deposition of type I collagen from the third week of treatment.

Enhancement of nutritional soy protein and peptide supplementation on skin repair in rats

• Protein supplements play a vital role during the inflammatory phase of skin repair. • Soy peptide performed better on fibroblast proliferation than the soy protein. • Soy peptide performed better on collagen synthesis than the soy protein. • Soy peptide showed a better performance of wound tissue repair. The aim of this study was to assess the effect of soy protein and soy peptide on skin repair process in male Wistar rats. Soy protein and soy peptide were administered orally by gavage to the rats post-operatively for 16 days. The supplementation of soy protein and soy peptide resulted in improvement of leucocytes production, decrease in serum inflammation index (IL-1β, IL-6, TNF-α) as well as increase of plasma protein concentration. Additionally, the excessive production of inflammatory factors in peptide group were significantly suppressed compared with the protein group at day 4, which indicated that soy peptide had a better impact on promoting the process of skin repair. Histopathological analysis indicated that peptide group performed better on fibroblast proliferation and collagen synthesis than the protein group, and eventually manifests as more collagen deposition and a better skin repair rate. In conclusion, soy peptide displayed the potential to promote skin regeneration.

Washed Equine Platelet Extract as an Anti-Inflammatory Biologic Pharmaceutical

Mammalian platelets participate in the immediate tissue injury response by initiating coagulation and further promoting tissue injury mitigation and repair. The latter properties are deployed following platelet release of presynthetized morphogens, cytokines, and growth and chemotactic factors, which launch a tissue regenerative, angiogenic, and anti-inflammatory program. Several blood-derived biologic products, like platelet-rich plasma (PRP) and platelet lysate (PL), are currently on the market to allow proper healing and tissue regeneration. However, not all growth factors are released from the platelets and the final products contain plasma proteins such as albumin, fibrinogen, complement, and immunoglobulins, increasing the risks of serum sickness or allergic reaction. To address this problem, we developed a new platelet extract where equine blood platelets are concentrated, washed, and thereafter lysed by detergent Triton X-114. Distinct from PRP, this extract is devoid of albumin, fibrinogen, and immunoglobulins and is 266-fold enriched in platelet-derived growth factor content relative to PRP. Washed equine platelet extract (WEPLEX) is amenable to lyophilization without loss of biological activity. In vitro, WEPLEX significantly inhibits human and equine T cell proliferative response to phytohemagglutinin and also polarizes murine CD45+/CD11b+ peritoneal macrophages to an IL-10+ M2-like phenotype. In vivo, WEPLEX substantially improves clinical outcome of murine experimental dextran sulfate sodium colitis. We propose that equine-sourced, zoonosis-free WEPLEX may serve as an anti-inflammatory biological therapy across mammalian species.

Ear, nose and throat emergencies: an experience in rural area

&lt;p class="abstract"&gt;&lt;strong&gt;Background:&lt;/strong&gt; Ear, nose and throat (ENT) emergencies are very common throughout the world. Early diagnosis and prompt treatment in the hands of expert will result in reduction of morbidity, mortality and referrals.&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Methods:&lt;/strong&gt; This retrospective study was conducted on 352 patients reporting in out-patient department (OPD) and emergency of District Hospital Ramban from June 2016 to May 2017. Demographic data as well as diagnosis were studied. The type of anaesthesia and type of procedure and outcome of emergency case were recorded. Patients with terminal cancer care admitted were excluded from the study. &lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Results:&lt;/strong&gt; A total of 352 patients, 204 males and 148 females were included in present study. The commonest emergency was foreign body (69.03%), trauma (11.9%), epistaxis (9.6%), and abscess (6.8%). Procedures done were foreign body removal, fracture reductions, soft tissue injury repair, incision and drainage, packing and cauterisation.&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; Foreign body is the most common cause of ENT emergency and it is a preventable accident. Education of parents and public at large will go a long way in reducing these preventable mishaps in children. Timely management of emergencies in the hand of experts reduces the mortality and complication rate.&lt;/p&gt;

Gastric Stem Cells: Physiological and Pathological Perspectives.

Gastric epithelium operates in a hazardous environment that curtails the lifespan of the constituent cells, imposing a requirement for continuous epithelial renewal. Stem cells that reside in the stomach are thus essential for regulating physiological tissue renewal and injury repair because of their self-renewal, high proliferation capacity and multiple differentiation potentials. Recent investigations using lineage tracing models have identified diverse populations of gastric stem cells and even fully differentiated cells that can regain stem cell capacity, so enriching our understanding on the identity and plasticity of gastric stem cells. These cell populations include the Villin promotor, Lgr5+, CCKR2+, Axin2+ and AQP5+ stem cells in the antrum, TFF2 mRNA, Mist1+ cells and Troy+ mature chief cells in the corpus, as well as Sox2, eR1, Lrig1, Bmi1-marked cell in both the antrum and the corpus. Establishment of gastric organoids derived from primary gastric tissues and pluripotent stem cells or embryonic stem cells characterizes niche factors required by the gastric stem cell populations, and further provides new insights into stomach development, host-Helicobacter pylori interactions and malignant transformation. Furthermore, focus on the gastric stem cells and their niches uncovers the initiation of stomach precancerous lesions and origin of gastric cancer, providing options for cancer prevention and intervention. In summary, with the development of stem cell research, gastric stem cells give us more opportunities to prevent and treat stomach diseases.

Retraction Note: Preparation of Decellularized Bovine Tendon Scaffold and Evaluation of Its Interaction with Adipose Tissue-Derived Mesenchymal Stem Cells

Background: Tissue engineering is the science of tissue design and one of the main branches of regenerative medicine that aims to improve and repair tissue injuries. Objectives: This study aimed to decellularize the tissue of bovine Achilles tendon and create a natural 3D scaffold. Then, the interaction of human adipose tissue-derived mesenchymal stem cells (hAd-MSCs) with this 3D scaffold was evaluated for use in tendon injuries. Methods: The bovine Achilles tendon was obtained from a slaughterhouse and decellularized by the combination of ethylenediaminetetraacetic acid (EDTA) and sodium dodecyl sulfate (SDS). Histological and biomechanical tests were used to evaluate the quality of decellularized scaffolds. Adipose-derived mesenchymal stem cells were cultured on scaffolds, and cell viability and cell behavior were evaluated by the MTT test and scanning electron microscopy. Results: The results of histological and biomechanical tests showed the complete removal of cells with the preservation of the extracellular matrix. The results of cell culture on scaffolds also showed that optical absorption in scaffolds containing cells increased over time. Conclusions: In general, the decellularized scaffold in this study did not undergo significant structural changes in the tendon tissue. The interaction between hAd-MSCs and the decellularized scaffold revealed that the scaffold was somehow suitable for cell culture. However, it needs to be more investigated for use in the treatment of tendon injuries of the athletes.

Decellularization optimizes the inhibitory microenvironment of the optic nerve to support neurite growth

Allogeneic or homologous tissue transplantation is an effective strategy to repair tissue injury. However, the central nervous tissues like the brain, spinal cord, and optic nerve are not ideal materials for nervous tissue regeneration due to the excessive axonal inhibitor cues in their microenvironments. In the present study, we found that decellularization optimizes the function of the adult optic nerve in supporting the oriented outgrowth of dorsal root ganglion (DRG) neurites. The neurites growing on the decellularized optic nerve (DON) showed longer extension distances than those growing on the normal optic nerve (ON). Neurite branching was also significantly increased on the DON compared to on the ON. Decellularization selectively removed some axon-inhibitory molecules such as myelin-associated glycoprotein (basically not detected in DON) and chondroitin sulfate proteoglycans (detected in DON at a level less than 0.3 fold that in ON) and preserved some axon-promoted extracellular matrix (ECM) proteins, including collagen IV and laminin (detected at levels 6.0-fold higher in DON than in ON). Furthermore, collagen IV and laminin were shown to be preserved in DON, and their binding activities with integrin α1 were retained to promote the extension of DRG neurites. Together, the findings provide a feasible way to optimize the axon-inhibited microenvironment of central nervous tissues and establish a theoretical basis for the application of DON scaffolds in repairing central nervous injury.

Gli1+ Periodontium Stem Cells Are Regulated by Osteocytes and Occlusal Force.

Teeth are attached to alveolar bone by the periodontal ligament (PDL), which contains stem cells supporting tissue turnover. Here, we identified Gli1+ cells in adult mouse molar PDL as multi-potential stem cells (PDLSCs) giving rise to PDL, alveolar bone, and cementum. They support periodontium tissue turnover and injury repair. Gli1+ PDLSCs are surrounding the neurovascular bundle and more enriched in the apical region. Canonical Wnt signaling is essential for their activation. Alveolar bone osteocytes negatively regulate Gli1+ PDLSCs activity through sclerostin, a Wnt inhibitor. Blockage of sclerostin accelerates the PDLSCs lineage contribution rate invivo. Sclerostin expression is modulated by physiological occlusal force. Removal of occlusal force upregulates sclerostin and inhibits PDLSCs activation. In summary, Gli1+ cells are the multipotential PDLSCs invivo. Osteocytes provide negative feedback to PDLSCs and inhibit their activities through sclerostin. Physiological occlusal force indirectly regulates PDLSCs activities by fine-tuning this feedback loop.

Intermittent Hypoxic Exposure with High Dose of Arginine Impact on Circulating Mediators of Tissue Regeneration.

Intermittent exposure to hypoxia (IHE) increases production of reactive oxygen and nitrogen species which, as signalling molecules, participate in tissue injury–repair–regeneration cascade. The process is also stimulated by arginine whose bioavailability is a limiting factor for NO synthesis. The effects of IHE in combination with arginine (Arg) intake on myogenesis and angiogenesis mediators were examined in a randomized and placebo-controlled trial. Blood samples were collected from 38 elite athletes on the 1st, 7th and 14th days during the training camp. The oral doses of arginine (2 × 6 g/day) and/or IHE using hypoxicator GO2Altitude (IHE and Arg/IHE) were applied. Serum NO and H2O2 concentrations increased significantly and were related to muscle damage (CK activity >900 IU/mL) in IHE and Arg/IHE compared to placebo. The changes in NO and H2O2 elevated the levels of circulating growth factors such as HGF, IHG-1, PDGFBB, BDNF, VEGF and EPO. Modification of the lipid profile, especially reduced non-HDL, was an additional beneficial effect of hypoxic exposure with arginine intake. Intermittent hypoxic exposure combined with high-dose arginine intake was demonstrated to affect circulating mediators of injury–repair–regeneration. Therefore, a combination of IHE and arginine seems to be a potential therapeutic and non-pharmacological method to modulate the myogenesis and angiogenesis in elite athletes.

Immunoregulatory Property of C-Type Lectin-Like Receptors in Fibrosing Interstitial Lung Diseases.

The innate immune system identifies exogenous threats or endogenous stress through germline-encoded receptors called pattern recognition receptors (PRRs) that initiate consecutive downstream signaling pathways to control immune responses. However, the contribution of the immune system and inflammation to fibrosing interstitial lung diseases (ILD) remains poorly understood. Immunoreceptor tyrosine-based motif-bearing C-type lectin-like receptors (CTLRs) may interact with various immune cells during tissue injury and wound repair processes. Dectin-1 is a CTLR with dominant mechanisms manifested through its intracellular signaling cascades, which regulate fibrosis-promoting properties through gene transcription and cytokine activation. Additionally, immune impairment in ILD facilitates microbiome colonization; hence, Dectin-1 is the master protector in host pulmonary defense against fungal invasion. Recent progress in determining the signaling pathways that control the balance of fibrosis has implicated immunoreceptor tyrosine-based motif-bearing CTLRs as being involved, either directly or indirectly, in the pathogenesis of fibrosing ILD.

Advances in the research of effects of epithelial-mesenchymal interaction on wound healing and scar formation

Wound healing is a dynamic process which involves interaction of various types of cells, cytokines, and extracellular matrix. Among them, epithelial cells and mesenchymal cells are the key components which involve in wound healing and scar formation. Related scholars had done a great number of studies about the functions of epithelial cells and fibroblasts(Fbs) in wound healing and scar formation. The results showed that under the stimulation of complex microenvironment, epithelial cells would lose their epithelial characteristics and acquire the typical characteristics and migration ability of mesenchymal cells. At the same time, with the complex changes of cell structure and cell behavior, they would participate in the process of tissue wound repair, including normal or fibrotic repair, by covering the wound with migration. Fbs are the key cells for the wound fibrotic repair, and play important roles in the process of wound healing, including excessive wound healing or delayed wound healing. In the recent years, the researchers realized that the cross-talk between epithelial cells and Fbs in wound healing, which is referred to as epithelial-mesenchymal interaction, significantly changes the biological behaviors of these two cell types, which affects the dermal remodeling and re-epithelialization quality of wound. Epithelial-mesenchymal interaction plays an important role in skin morphogenesis during embryonic development and maintaining the structural integrity of adult skin. In the process of re-epithelialization, Fbs could promote the proliferation and migration of keratinocytes, meanwhile keratinocytes would receive the signals from Fbs to reconstruct functional epithelium, which has become a hot topic in the field of wound healing at present. In this paper, a comprehensive analysis of the literature on the role of epithelial-mesenchymal interaction in wound healing and scar formation at home and abroad in recent years is presented for the reference of relevant scholars.

Exosomes derived from umbilical cord mesenchymal stem cells alleviate viral myocarditis through activating AMPK/mTOR-mediated autophagy flux pathway.

Human umbilical cord mesenchymal stem cell‐derived exosomes (hucMSC‐exosomes) have been implicated as a novel therapeutic approach for tissue injury repair and regeneration, but the effects of hucMSC‐exosomes on coxsackievirus B3 (CVB3)‐induced myocarditis remain unknown. The object of the present study is to investigate whether hucMSC‐exosomes have therapeutic effects on CVB3‐induced myocarditis (VMC). HucMSC‐exosomes were identified using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM) and Western blot. The purified hucMSC‐exosomes tagged with PKH26 were tail intravenously injected into VMC model mice in vivo and used to administrate CVB3‐infected human cardiomyocytes (HCMs) in vitro, respectively. The effects of hucMSC‐exosomes on myocardial pathology injury, proinflammatory cytokines and cardiac function were evaluated through haematoxylin and eosin (H&E) staining, quantitative polymerase chain reaction (qPCR) and Doppler echocardiography. The anti‐apoptosis role and potential mechanism of hucMSC‐exosomes were explored using TUNEL staining, flow cytometry, immunohistochemistry, Ad‐mRFP‐GFP‐LC3 transduction and Western blot. In vivo results showed that hucMSC‐exosomes (50 μg iv) significantly alleviated myocardium injury, shrank the production of proinflammatory cytokines and improved cardiac function. Moreover, in vitro data showed that hucMSC‐exosomes (50 μg/mL) inhibited the apoptosis of CVB3‐infected HCM through increasing pAMPK/AMPK ratio and up‐regulating autophagy proteins LC3II/I, BECLIN‐1 and anti‐apoptosis protein BCL‐2 as well as decreasing pmTOR/mTOR ratio, promoting the degradation of autophagy flux protein P62 and down‐regulating apoptosis protein BAX. In conclusion, hucMSC‐exosomes could alleviate CVB3‐induced myocarditis via activating AMPK/mTOR‐mediated autophagy flux pathway to attenuate cardiomyocyte apoptosis, which will be benefit for MSC‐exosome therapy of myocarditis in the future.

Preparation of Decellularized Bovine Tendon Scaffold and Evaluation of Its Interaction with Adipose Tissue-Derived Mesenchymal Stem Cells

Background: Tissue engineering is the science of tissue design and one of the main branches of regenerative medicine that aims to improve and repair tissue injuries. Objectives: This study aimed to decellularize the tissue of bovine Achilles tendon and create a natural 3D scaffold. Then, the interaction of human adipose tissue-derived mesenchymal stem cells (hAd-MSCs) with this 3D scaffold was evaluated for use in tendon injuries. Methods: The bovine Achilles tendon was obtained from a slaughterhouse and decellularized by the combination of ethylenediaminetetraacetic acid (EDTA) and sodium dodecyl sulfate (SDS). Histological and biomechanical tests were used to evaluate the quality of decellularized scaffolds. Adipose-derived mesenchymal stem cells were cultured on scaffolds, and cell viability and cell behavior were evaluated by the MTT test and scanning electron microscopy. Results: The results of histological and biomechanical tests showed the complete removal of cells with the preservation of the extracellular matrix. The results of cell culture on scaffolds also showed that optical absorption in scaffolds containing cells increased over time. Conclusions: In general, the decellularized scaffold in this study did not undergo significant structural changes in the tendon tissue. The interaction between hAd-MSCs and the decellularized scaffold revealed that the scaffold was somehow suitable for cell culture. However, it needs to be more investigated for use in the treatment of tendon injuries of the athletes.

Mechanical on-off gates for regulation of drug release in cutaneous or musculoskeletal tissue repairs.

Drug release synchronized with tissue motion is attractive to cutaneous or musculoskeletal tissue injury repair. Here, we have developed a method of regulating drug release by mechanical on-off gates for potential treatment of repeated injury in these tissues. The mechanical gates consisted of a multilayer structure: A brittle outmost layer adhered to an elastic middle layer, which wrapped an inmost drug carrier to form the composite multilayer structure. When it was stretched, cracks appeared as mechanical gates due to mechanical performance difference between the outmost layer and the middle layer, leading to the drug release. When the external force disappeared, it recovered to stop the drug release. The controlled drug release would therefore be achieved by changing the status (opening or closure) of mechanical gates through applying this on-off mechanical stretching. A prototype based on the composite multilayer structure of adhesive coating and electrospinning technique realized the controlled release of drug and effectively repaired the incision. More types of composite multilayer structures for mechanical drug release were expected to meet curing requirement in cutaneous or musculoskeletal tissues.

MSCs transplantation may be a potential therapeutic strategy for COVID-19 treatment.

At present, SARS-Cov-2 is spread all over the world, becoming a serious threat to people's health. SARS-Cov-2 has a strong infection, and the mortality rate of severe patients after infection is high, but there is no effective treatment. Mesenchymal stem cells (MSCs) have anti-inflammatory and immunomodulatory functions, which can reduce the occurrence of cytokine storm syndrome and acute respiratory distress syndrome. At the same time, MSCs can reduce the level of pulmonary fibrosis and enhance tissue injury repair. In this short report, combined with the progress of preclinical and clinical research, we comment the efficacy of MSCs in the treatment of COVID-19.

Adipose‑derived mesenchymal stem cells ameliorate dibutyltin dichloride‑induced chronic pancreatitis by inhibiting the PI3K/AKT/mTOR signaling pathway.

Adipose-derived mesenchymal stem cells (ASCs) play a positive role in tissue injury repair and regeneration. The aim of this study was to determine whether ASCs could ameliorate chronic pancreatitis (CP) induced by the injection of dibutyltin dichloride (DBTC) and to elucidate its potential mechanisms. Furthermore, this study also explored whether there was a significant difference if the ASCs were injected via the inferior vena cava or the left gastric artery. CP was induced in rats by a single intravenous administration of DBTC, and the accumulation of collagen and apoptotic rates of pancreatic acinar cells were analyzed. According to the results, ASCs markedly reduced DBTC-induced pancreatic damage and collagen deposition in the rat model of CP. Moreover, ASCs significantly decreased pancreatic cell apoptosis by regulating the expression levels of caspase-3, BAX and Bcl-2. These effects were observed regardless of whether the injection was in the inferior vena cava or the left gastric artery. It was also found that the expression levels of phosphorylated PI3K, AKT and mTOR in pancreatic tissues of the DBTC-induced CP model group were significantly increased, while the expression levels of phosphorylated PI3K, AKT and mTOR in the two treatment groups were markedly decreased. ASCs noticeably suppressed the PI3K/AKT/mTOR pathway in the pancreatic tissue of DBTC-induced CP. This study indicated that ASCs protect against pancreatic fibrosis by modulating the PI3K/AKT/mTOR pathway, and have the potential to be a new strategy for the treatment of CP in the future.