3D printing of chemical-empowered tendon stem/progenitor cells for functional tissue repair

Biomaterials ◽  
2021 ◽  
pp. 120722
Author(s):  
Yanjie Zhang ◽  
Tingyun Lei ◽  
Chenqi Tang ◽  
Yangwu Chen ◽  
Youguo Liao ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Naosuke Kamei ◽  
Kivanc Atesok ◽  
Mitsuo Ochi

Endothelial progenitor cells (EPCs) derived from bone marrow and blood can differentiate into endothelial cells and promote neovascularization. In addition, EPCs are a promising cell source for the repair of various types of vascularized tissues and have been used in animal experiments and clinical trials for tissue repair. In this review, we focused on the kinetics of endogenous EPCs during tissue repair and the application of EPCs or stem cell populations containing EPCs for tissue regeneration in musculoskeletal and neural tissues including the bone, skeletal muscle, ligaments, spinal cord, and peripheral nerves. EPCs can be mobilized from bone marrow and recruited to injured tissue to contribute to neovascularization and tissue repair. In addition, EPCs or stem cell populations containing EPCs promote neovascularization and tissue repair through their differentiation to endothelial cells or tissue-specific cells, the upregulation of growth factors, and the induction and activation of endogenous stem cells. Human peripheral blood CD34(+) cells containing EPCs have been used in clinical trials of bone repair. Thus, EPCs are a promising cell source for the treatment of musculoskeletal and neural tissue injury.


2020 ◽  
Vol 46 (6) ◽  
pp. 7609-7614 ◽  
Author(s):  
Tianyuan Zhou ◽  
Le Zhang ◽  
Qing Yao ◽  
Yuelong Ma ◽  
Chen Hou ◽  
...  

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3902-3902
Author(s):  
Ioannis Papassotiriou ◽  
Antonia Spiropoulos ◽  
Maria Tsironi ◽  
Katerina Skenderi ◽  
Alexandra Margeli ◽  
...  

Abstract The “Spartathlon” ultradistance foot race (246 Km continuous, prolonged, brisk exercise for up to 36 hours) provides a unique model of prolonged duration exercise that reveals dramatic systemic inflammatory changes. Endothelial progenitor cells (EPCs) have been shown to participate in vascular repair and angiogenesis, while circulating bone marrow originated fibrocytes represent multipotent cells mediating tissue repair and remodeling after injury. In this study we investigated the effect of this type of exercise on the number of circulating EPCs and fibrocytes along with molecules of endothelium dysfunction and chemotactic proteins in 10 “Spartathlon” athletes before, at the end and at 48 h post race. The EPCs were obtained by culturing peripheral blood mononuclear cells (PBMC) under endothelial cell conditions (EndoCult) and were measured as colony-forming units (CFUs). Circulating fibrocytes were cultured from PBMCs in IMDM medium supplemented with IL-3 and M-CSF and identified as CD45+CD14+CD34lowCollagen-I+ fibroblastic cells. We also determined the plasma levels of E-, L- and P-selectins, sICAM-1, sVCAM-1, thrombomodulin, lipocalin-2, IL-8 and MCP-1 with appropriate methodology. Circulating EPCs increased by nearly ten-fold in peripheral blood at the end of the “Spartathlon” race (from 48±15 cells/ml to 464±36 cells/ml) and they remained increased (420±28 cells/ml) even at 48h post race. The percentage of the CD45+CD14+CD34lowCollagen-I+ fibrocytes cultured from PBMCs before, at the end, and 48 h post race did not reveal any significant difference (64.5±6.2% vs 70.8±8.5% vs 68±4.8% respectively). Plasma levels of lipocalin-2, IL-8, MCP-1, E-selectin, sICAM, sVCAM and thrombomodulin were increased significantly at the end of the race and returned at the pre race levels 48 h post race, while L- and P-selectins remained unaffected before and at the end of the race, presenting a similar decline at 48 h post race. Our study demonstrates that acute inflammatory tissue damage induced by exhausting exercise increases EPCs but not fibrocytes. Given the ability of EPCs to promote angiogenesis and vascular regeneration and the association of fibrocytes with tissue fibrosis after persistent inflammation, we conclude that this kind of repair cell mobilization may serve as a physiologic repair mechanism in acute inflammatory tissue injury.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Yuliya Plutino ◽  
Federica Barchiesi ◽  
Nikiana Simigdala ◽  
Bruno Imthurn ◽  
Raghvendra Dubey

Therapeutic use of Endothelial Progenitor Cells (EPCs) is known to repair and protect against cardiovascular damage. Since androgens are associated with cardiovascular protection in men, we investigated the mechanism(s) by which androgens (dihydrotestosterone; DHT) can modulate androgen receptor (AR) dependent EPC activity. Tube/capillary formation and androgen receptor expression by cultured EPCs was assessed using 2D-cultures/co-cultures, western blotting and RT-PCR. Treatment with DHT (100nM) induced capillary/tube formation by EPCs (≈179±3%; p<.05 vs control) and these effects were attenuated by AR antagonist flutamide and AR siRNA. DHT (10-100nM) up-regulated AR protein expression and this effect was abrogated by AR antagonist flutamide (1μM), AR silencing siRNA and cycloheximide (protein synthesis inhibitor). Compared to AR protein, DHT did not induce AR mRNA expression and DHT-induced AR expression was not blocked by the transcription inhibitor actinomycin-D (10ng/ml). Treatment with proteasome inhibitor MG132 (100nM) mimicked the effects of DHT on AR protein expression, moreover, when combined with DHT, the stimulatory effects on AR expression were additive. To ascertain the role of protein stabilization in mediating AR up-regulation in EPCs, the effects of MG132 and DHT on Raf-1, which is known to undergo proteasomal degradation, were assessed. Treatment with MG132, but not DHT, increased Raf-1 expression in EPCs. Moreover, the stimulatory effects of DHT on capillary formation were enhanced in presence of MG132. These findings suggest that DHT up-regulates AR expression and function in EPCs via protein stabilization, however, participation of other pathways cannot be ruled out. In EPCs, DHT induces capillary formation via AR and regulates AR expression in an autologous fashion. Since, androgens induce endothelial growth, and most patients receiving EPCs for cardiovascular repair are older, the low endogenous levels of androgens would decrease the potential of stem cell mediated tissue repair. More importantly, pretreatment of patients or priming of EPCs with androgens/DHT, as well as co-administration of DHT with EPCs may potentiate ARs and EPC mediate cardiovascular tissue repair in men.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Aleksandra Klimczak ◽  
Urszula Kozlowska

Multipotent mesenchymal stromal/stem cells (MSCs) reside in many human organs and comprise heterogeneous population of cells with self-renewal ability. These cells can be isolated from different tissues, and their morphology, immunophenotype, and differentiation potential are dependent on their tissue of origin. Each organ contains specific population of stromal cells which maintain regeneration process of the tissue where they reside, but some of them have much more wide plasticity and differentiate into multiple cells lineage. MSCs isolated from adult human tissues are ideal candidates for tissue regeneration and tissue engineering. However, MSCs do not only contribute to structurally tissue repair but also MSC possess strong immunomodulatory and anti-inflammatory properties and may influence in tissue repair by modulation of local environment. This paper is presenting an overview of the current knowledge of biology of tissue-resident mesenchymal stromal and progenitor cells (originated from bone marrow, liver, skeletal muscle, skin, heart, and lung) associated with tissue regeneration and tissue homeostasis.


BioResources ◽  
2018 ◽  
Vol 13 (3) ◽  
pp. 5909-5924
Author(s):  
Yani Jiang ◽  
Xiaodong Xv ◽  
Dongfang Liu ◽  
Zhe Yang ◽  
Qi Zhang ◽  
...  

Gelatin (GEL) obtained from animals is famous for its biocompatibility and biodegradability. However, its poor mechanical properties limits possible applications as bio-inks to fabricate tissue scaffolds through three-dimensional (3D) printing. In this work, a high strength hydrogel based on cellulose nanofibers and GEL (CNF/GEL) was designed for 3D printing. Scanning electron microscopy and breaking strength results indicated that a CNF filling content of 10% was the best content in the CNF/GEL hydrogels. The rheological properties of the samples with different solid contents were investigated, and the 10%-CNF/GEL-5 hydrogel was proposed for 3D printing. Then, a printing strategy with optimal conditions, including a crosslinking procedure for obtaining a 3D scaffold, was proposed. The biocompatibility of G-10%-CNF/GEL-5 was also investigated using CCK-8 and Hoechst 33342/PI double-staining assays. These results confirmed that the 10%-CNF/GEL-5 composite hydrogel has potential to be used as a 3D bio-ink for application in tissue repair.


2021 ◽  
pp. 1-14
Author(s):  
Veronika Sedlakova ◽  
Christopher McTiernan ◽  
David Cortes ◽  
Erik J. Suuronen ◽  
Emilio I. Alarcon

Cardiovascular diseases are the leading cause of mortality worldwide. Given the limited endogenous regenerative capabilities of cardiac tissue, patient-specific anatomy, challenges in treatment options, and shortage of donor tissues for transplantation, there is an urgent need for novel approaches in cardiac tissue repair. 3D bioprinting is a technology based on additive manufacturing which allows for the design of precisely controlled and spatially organized structures, which could possibly lead to solutions in cardiac tissue repair. In this review, we describe the basic morphological and physiological specifics of the heart and cardiac tissues and introduce the readers to the fundamental principles underlying 3D printing technology and some of the materials/approaches which have been used to date for cardiac repair. By summarizing recent progress in 3D printing of cardiac tissue and valves with respect to the key features of cardiovascular tissue (such as contractility, conductivity, and vascularization), we highlight how 3D printing can facilitate surgical planning and provide custom-fit implants and properties that match those from the native heart. Finally, we also discuss the suitability of this technology in the design and fabrication of custom-made devices intended for the maturation of the cardiac tissue, a process that has been shown to increase the viability of implants. Altogether this review shows that 3D printing and bioprinting are versatile and highly modulative technologies with wide applications in cardiac regeneration and beyond.


2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Lisa J. Hill ◽  
Hannah F. Botfield ◽  
Ghazala Begum ◽  
Omar Qureshi ◽  
Vasanthy Vigneswara ◽  
...  

AbstractFibrotic disease is a major cause of mortality worldwide, with fibrosis arising from prolonged inflammation and aberrant extracellular matrix dynamics. Compromised cellular and tissue repair processes following injury, infection, metabolic dysfunction, autoimmune conditions and vascular diseases leave tissues susceptible to unresolved inflammation, fibrogenesis, loss of function and scarring. There has been limited clinical success with therapies for inflammatory and fibrotic diseases such that there remains a large unmet therapeutic need to restore normal tissue homoeostasis without detrimental side effects. We investigated the effects of a newly formulated low molecular weight dextran sulfate (LMW-DS), termed ILB®, to resolve inflammation and activate matrix remodelling in rodent and human disease models. We demonstrated modulation of the expression of multiple pro-inflammatory cytokines and chemokines in vitro together with scar resolution and improved matrix remodelling in vivo. Of particular relevance, we demonstrated that ILB® acts, in part, by downregulating transforming growth factor (TGF)β signalling genes and by altering gene expression relating to extracellular matrix dynamics, leading to tissue remodelling, reduced fibrosis and functional tissue regeneration. These observations indicate the potential of ILB® to alleviate fibrotic diseases.


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