Idiopathic Pulmonary Fibrosis (IPF) is a disease that consists of the scarring of the lungs. It is the most common type of pulmonary fibrosis. This disease is irreversible and becomes worse over time. In patients with IPF, treatment relies mostly on the clinical application of new drugs. Unfortunately, these drugs do not repair damaged lung tissue; therefore, these medications only have the ability to slow down disease progression. With this dilemma, stem cell treatment has become a popular alternative in the treatment of IPF, specifically mesenchymal stem cells (MSCs). MSC therapy would repair damaged lung tissue, thus not delaying the progression of the disease, but instead repairing the lungs of the patient. In addition, the application of exosomes has also gained popularity because of their functionality in intracellular communication. There is a need for regenerating the damaged lung tissue of patients with IPF, which can be accomplished with stem cell therapy. The clinical application of MSCs has been proven safe in patients with this degenerative disease, thus this finding has justified more research for the application of stem cell therapy in patients with IPF.
{"title":"The Effect of Mesenchymal Stem Cells and Exosomes to Treat Idiopathic Pulmonary Fibrosis","authors":"D. Chase, V. Gallicchio","doi":"10.33425/2639-9512.1035","DOIUrl":"https://doi.org/10.33425/2639-9512.1035","url":null,"abstract":"Idiopathic Pulmonary Fibrosis (IPF) is a disease that consists of the scarring of the lungs. It is the most common type of pulmonary fibrosis. This disease is irreversible and becomes worse over time. In patients with IPF, treatment relies mostly on the clinical application of new drugs. Unfortunately, these drugs do not repair damaged lung tissue; therefore, these medications only have the ability to slow down disease progression. With this dilemma, stem cell treatment has become a popular alternative in the treatment of IPF, specifically mesenchymal stem cells (MSCs). MSC therapy would repair damaged lung tissue, thus not delaying the progression of the disease, but instead repairing the lungs of the patient. In addition, the application of exosomes has also gained popularity because of their functionality in intracellular communication. There is a need for regenerating the damaged lung tissue of patients with IPF, which can be accomplished with stem cell therapy. The clinical application of MSCs has been proven safe in patients with this degenerative disease, thus this finding has justified more research for the application of stem cell therapy in patients with IPF.","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77942475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2017-01-27DOI: 10.16966/2472-6990.113
Stephen E Harris, Michael Rediske, Rebecca Neitzke, Audrey Rakian
The periodontium is a complex tissue with epithelial components and a complex set of mesodermal derived alveolar bone, cellular and a cellular cementum, and tendon like ligaments (PDL). The current evidence demonstrates that the major pool of periodontal stem cells is derived from a population of micro vascular associated aSMA-positive stem/progenitor (PSC) cells that by lineage tracing form all three major mesodermal derived components of the periodontium. With in vitro aSMA+ stem cells, transcriptome and chip- seq experiments, the gene network and enhancer maps were determined at several differentiation states of the PSC. Current work on the role of the Bmp2 gene in the periodontal stem cell differentiation demonstrated that this Wnt regulated gene, Bmp2, is necessary for differentiation to all three major mesodermal derived component of the periodontium. The mechanism and use of Sclerostin antibody as an activator of Wnt signaling and Bmp2 gene as a potential route to treat craniofacial bone loss is discussed. As well, the mechanism and use of Pth in the treatment of periodontal bone loss or other craniofacial bone loss is presented in this review.
{"title":"Periodontal Biology: Stem Cells, Bmp2 Gene, Transcriptional Enhancers, and Use of Sclerostin Antibody and Pth for Treatment of Periodontal Disease and Bone Loss.","authors":"Stephen E Harris, Michael Rediske, Rebecca Neitzke, Audrey Rakian","doi":"10.16966/2472-6990.113","DOIUrl":"10.16966/2472-6990.113","url":null,"abstract":"<p><p>The periodontium is a complex tissue with epithelial components and a complex set of mesodermal derived alveolar bone, cellular and a cellular cementum, and tendon like ligaments (PDL). The current evidence demonstrates that the major pool of periodontal stem cells is derived from a population of micro vascular associated aSMA-positive stem/progenitor (PSC) cells that by lineage tracing form all three major mesodermal derived components of the periodontium. With <i>in vitro</i> aSMA+ stem cells, transcriptome and chip- seq experiments, the gene network and enhancer maps were determined at several differentiation states of the PSC. Current work on the role of the Bmp2 gene in the periodontal stem cell differentiation demonstrated that this Wnt regulated gene, Bmp2, is necessary for differentiation to all three major mesodermal derived component of the periodontium. The mechanism and use of Sclerostin antibody as an activator of Wnt signaling and Bmp2 gene as a potential route to treat craniofacial bone loss is discussed. As well, the mechanism and use of Pth in the treatment of periodontal bone loss or other craniofacial bone loss is presented in this review.</p>","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35843239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-01Epub Date: 2016-05-12DOI: 10.16966/2472-6990.110
Joshuah Gagan, Carolyn Fraze, David A Stout
Stem cells have become a revived biotechnology that is beginning to expand the field of regenerative medicine. Although stem cells are capable of regenerating tissues, current research trends tend to side on developing fully functional organs and other clinical uses including in situ stem cell repair through three-dimensional printing methods. Through several tests and techniques, it can be shown that most stem cell printing methods are possible and that most tests come out with high cell viability. Furthermore, the importance of bioprinting is to benefit the field of regenerative medicine, which looks into artificial organ transplants for the thousands of patients without donors. Although the field is not brand new, understanding the integration and use of additive manufacturing with biomaterials is essential in developing fully functional organs. There is a heavy emphasis on the biomaterials themselves since they have a crucial role in creating an organ that is mechanically robust and adaptable in vivo. Covered in this review article are many featured tests, which also touch on the importance of including a biomaterial that is capable of maintaining a viable microenvironment. These include biomaterials such as hydrogels, biopolymers, and synthetic extra cellular matrices (ECM) built for stem cells to proliferate, differentiate, and give freedom to cell communication after printing.
{"title":"Three-Dimensional Stem Cell Bioprinting.","authors":"Joshuah Gagan, Carolyn Fraze, David A Stout","doi":"10.16966/2472-6990.110","DOIUrl":"https://doi.org/10.16966/2472-6990.110","url":null,"abstract":"<p><p>Stem cells have become a revived biotechnology that is beginning to expand the field of regenerative medicine. Although stem cells are capable of regenerating tissues, current research trends tend to side on developing fully functional organs and other clinical uses including <i>in situ</i> stem cell repair through three-dimensional printing methods. Through several tests and techniques, it can be shown that most stem cell printing methods are possible and that most tests come out with high cell viability. Furthermore, the importance of bioprinting is to benefit the field of regenerative medicine, which looks into artificial organ transplants for the thousands of patients without donors. Although the field is not brand new, understanding the integration and use of additive manufacturing with biomaterials is essential in developing fully functional organs. There is a heavy emphasis on the biomaterials themselves since they have a crucial role in creating an organ that is mechanically robust and adaptable <i>in vivo</i>. Covered in this review article are many featured tests, which also touch on the importance of including a biomaterial that is capable of maintaining a viable microenvironment. These include biomaterials such as hydrogels, biopolymers, and synthetic extra cellular matrices (ECM) built for stem cells to proliferate, differentiate, and give freedom to cell communication after printing.</p>","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8320738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39274375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dikshya Bastakoty, Sarika Saraswati, P. Joshi, James B. Atkinson, I. Feoktistov, Jun Liu, Jennifer L. Harris, P. Young
AIMS The WNT/β-catenin pathway is temporarily activated in the heart following myocardial infarction (MI). Despite data from genetic models indicating both positive and negative roles for the WNT pathway depending on the model used, the effect of therapeutic inhibition of WNT pathway on post-injury outcome and the cellular mediators involved are not completely understood. Using a newly available, small molecule, GNF-6231, which averts WNT pathway activation by blocking secretion of all WNT ligands, we sought to investigate whether therapeutic inhibition of the WNT pathway temporarily after infarct can mitigate post injury cardiac dysfunction and fibrosis and the cellular mechanisms responsible for the effects. METHODS AND RESULTS Pharmacologic inhibition of the WNT pathway by post-MI intravenous injection of GNF-6231 in C57Bl/6 mice significantly reduced the decline in cardiac function (Fractional Shortening at day 30: 38.71 ± 4.13% in GNF-6231 treated vs. 34.89 ± 4.86% in vehicle-treated), prevented adverse cardiac remodeling, and reduced infarct size (9.07 ± 3.98% vs. 17.18 ± 4.97%). WNT inhibition augmented proliferation of interstitial cells, particularly in the distal myocardium, inhibited apoptosis of cardiomyocytes, and reduced myofibroblast proliferation in the peri-infarct region. In vitro studies showed that WNT inhibition increased proliferation of Sca1+ cardiac progenitors, improved survival of cardiomyocytes, and inhibited collagen I synthesis by cardiac myofibroblasts. CONCLUSION Systemic, temporary pharmacologic inhibition of the WNT pathway using an orally bioavailable drug immediately following MI resulted in improved function, reduced adverse remodeling and reduced infarct size in mice. Therapeutic WNT inhibition affected multiple aspects of infarct repair: it promoted proliferation of cardiac progenitors and other interstitial cells, inhibited myofibroblast proliferation, improved cardiomyocyte survival, and reduced collagen I gene expression by myofibroblasts. Our data point to a promising role for WNT inhibitory therapeutics as a new class of drugs to drive post-MI repair and prevent heart failure.
{"title":"Temporary, Systemic Inhibition of the WNT/β-Catenin Pathway promotes Regenerative Cardiac Repair following Myocardial Infarct.","authors":"Dikshya Bastakoty, Sarika Saraswati, P. Joshi, James B. Atkinson, I. Feoktistov, Jun Liu, Jennifer L. Harris, P. Young","doi":"10.16966/2472-6990.111","DOIUrl":"https://doi.org/10.16966/2472-6990.111","url":null,"abstract":"AIMS\u0000The WNT/β-catenin pathway is temporarily activated in the heart following myocardial infarction (MI). Despite data from genetic models indicating both positive and negative roles for the WNT pathway depending on the model used, the effect of therapeutic inhibition of WNT pathway on post-injury outcome and the cellular mediators involved are not completely understood. Using a newly available, small molecule, GNF-6231, which averts WNT pathway activation by blocking secretion of all WNT ligands, we sought to investigate whether therapeutic inhibition of the WNT pathway temporarily after infarct can mitigate post injury cardiac dysfunction and fibrosis and the cellular mechanisms responsible for the effects.\u0000\u0000\u0000METHODS AND RESULTS\u0000Pharmacologic inhibition of the WNT pathway by post-MI intravenous injection of GNF-6231 in C57Bl/6 mice significantly reduced the decline in cardiac function (Fractional Shortening at day 30: 38.71 ± 4.13% in GNF-6231 treated vs. 34.89 ± 4.86% in vehicle-treated), prevented adverse cardiac remodeling, and reduced infarct size (9.07 ± 3.98% vs. 17.18 ± 4.97%). WNT inhibition augmented proliferation of interstitial cells, particularly in the distal myocardium, inhibited apoptosis of cardiomyocytes, and reduced myofibroblast proliferation in the peri-infarct region. In vitro studies showed that WNT inhibition increased proliferation of Sca1+ cardiac progenitors, improved survival of cardiomyocytes, and inhibited collagen I synthesis by cardiac myofibroblasts.\u0000\u0000\u0000CONCLUSION\u0000Systemic, temporary pharmacologic inhibition of the WNT pathway using an orally bioavailable drug immediately following MI resulted in improved function, reduced adverse remodeling and reduced infarct size in mice. Therapeutic WNT inhibition affected multiple aspects of infarct repair: it promoted proliferation of cardiac progenitors and other interstitial cells, inhibited myofibroblast proliferation, improved cardiomyocyte survival, and reduced collagen I gene expression by myofibroblasts. Our data point to a promising role for WNT inhibitory therapeutics as a new class of drugs to drive post-MI repair and prevent heart failure.","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"109 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79497761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem-cell niche is composed of a group of cells within the specific anatomic location that function to maintain stem cells. The niche referring to a microenvironment is capable of generating extrinsic factors that modulate stem cell proliferation and fate determination [1]. During development, various niche factors act on stem cells to alter gene expression, and induce their proliferation or differentiation for the development of the fetus. The highly plastic state of the stem/progenitor cells during developmental and tissue maintenance permits the required flexibility for proper tissue formation and repair. Unfortunately, this plasticity also provides an opportunity for aberrant cellular reprogramming via epigenetic mechanisms due to inappropriate exposures to toxins [2]. The developmental adverse exposure can lead to persistent, life-long effects and resulting in a variety of diseases [3].
{"title":"Converting of Myometrial Stem Cells to Tumor-Initiating Cells: Mechanism of Uterine Fibroid Development","authors":"Qiwei Yang, M. Diamond, A. Al-Hendy","doi":"10.16966/2472-6990.e103","DOIUrl":"https://doi.org/10.16966/2472-6990.e103","url":null,"abstract":"Stem-cell niche is composed of a group of cells within the specific anatomic location that function to maintain stem cells. The niche referring to a microenvironment is capable of generating extrinsic factors that modulate stem cell proliferation and fate determination [1]. During development, various niche factors act on stem cells to alter gene expression, and induce their proliferation or differentiation for the development of the fetus. The highly plastic state of the stem/progenitor cells during developmental and tissue maintenance permits the required flexibility for proper tissue formation and repair. Unfortunately, this plasticity also provides an opportunity for aberrant cellular reprogramming via epigenetic mechanisms due to inappropriate exposures to toxins [2]. The developmental adverse exposure can lead to persistent, life-long effects and resulting in a variety of diseases [3].","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82258269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01Epub Date: 2016-04-27DOI: 10.16966/2472-6990.109
Stephen J Peterson, Luca Vanella, Angelica Bialczak, Joseph Schragenheim, Ming Li, Lars Bellner, Joseph I Shapiro, Nader G Abraham
The development of adipocytes in mice and humans follows a well-defined pathway that commences with a common pluripotent mesenchymal stem cell (MSC), ie., adipogenesis [1]. The early steps of the pathway leading to the generation and the commitment of MSCs to an adipocyte lineage are unknown. Hypothetically, the determination of the fate of MSCs occurs early in cell differentiation (“commitment”) and involves the interplay of intrinsic (genetic) and environmental (local and systemic) conditions that ultimately define the fate of the cell. Factors that determine MSC proliferation and differentiation also govern early adipocyte development and function. Currently, little is known about this process; from MSC-to-preadipocyte differentiation. However, the steps governing the transition from preadipocyte to adipocyte differentiation are not well defined (Figure 1). During adipogenesis MSCs or preadipocytes differentiate into lipid-laden adipocytes [2]. Ox-HDL increases adipogenic properties with a marked effect on the last step of adipocyte-terminal differentiation and release of adipokines including 20-HETE and Ang II.
{"title":"Oxidized HDL and Isoprostane Exert a Potent Adipogenic Effect on Stem Cells: Where in the Lineage?","authors":"Stephen J Peterson, Luca Vanella, Angelica Bialczak, Joseph Schragenheim, Ming Li, Lars Bellner, Joseph I Shapiro, Nader G Abraham","doi":"10.16966/2472-6990.109","DOIUrl":"https://doi.org/10.16966/2472-6990.109","url":null,"abstract":"The development of adipocytes in mice and humans follows a well-defined pathway that commences with a common pluripotent mesenchymal stem cell (MSC), ie., adipogenesis [1]. The early steps of the pathway leading to the generation and the commitment of MSCs to an adipocyte lineage are unknown. Hypothetically, the determination of the fate of MSCs occurs early in cell differentiation (“commitment”) and involves the interplay of intrinsic (genetic) and environmental (local and systemic) conditions that ultimately define the fate of the cell. Factors that determine MSC proliferation and differentiation also govern early adipocyte development and function. Currently, little is known about this process; from MSC-to-preadipocyte differentiation. However, the steps governing the transition from preadipocyte to adipocyte differentiation are not well defined (Figure 1). During adipogenesis MSCs or preadipocytes differentiate into lipid-laden adipocytes [2]. Ox-HDL increases adipogenic properties with a marked effect on the last step of adipocyte-terminal differentiation and release of adipokines including 20-HETE and Ang II.","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5807016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35819842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Allocution de Monsieur Jun LING, Consul Général de Chine à Strasbourg, à l’occasion de la cérémonie d’ouverture du 9ème symposium franco-chinois","authors":"","doi":"10.3233/bhr210004","DOIUrl":"https://doi.org/10.3233/bhr210004","url":null,"abstract":"","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"116 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87781487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Concluding Remarks","authors":"D. George, J. Magdalou, J. Stoltz","doi":"10.3233/bhr210037","DOIUrl":"https://doi.org/10.3233/bhr210037","url":null,"abstract":"","PeriodicalId":91668,"journal":{"name":"Cell, stem cells and regenerative medicine","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85380605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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