The National Institute of Health estimates that nearly 250,000 people in the United States are currently living with a spinal cord injury (SCI). Most often a result of an accident, SCIs typically result in the loss of neurons and axonal damage resulting in the loss of function.
SCIs can be divided into two distinct phases, the initial physical injury and the secondary injury which typically occurs hours to days later. In most cases of SCI, damage to the axonal and tissue damage is caused by compression and/or contusion to the spinal cord. The secondary SCI injury occurs in the hours and days after the initial injury and is characterized by persistent inflammation, glial scar formation, demyelination of surrounding neurons, and death of cells. Over time, research has demonstrated that, in all aspects of secondary injury, the inflammatory response is the major cause and leads to widespread cell damage and lesion expansion.
Recent research has demonstrated that stem cells, including mesenchymal stem cells, neural stem/progenitor, and embryonic stem cells, possess anti-inflammatory properties and promote functional recovery after SCI by inducing macrophages M1/M2 phenotype transformation.
In this review, Cheng and He discuss the general features of macrophages in response to SCI, the phenotype, and function of macrophages in SCI, and the effects of stem cells on macrophage polarization and its role in stem cell-based therapies for SCI.
Macrophages accumulate in and around an SCI and play a very important role in neuroinflammation. Considering that recent research demonstrates the different, but important, contributions M1 and M2 macrophages make toward repairing tissue damage, this process is thought to be a promising therapeutic treatment for controlling the inflammation occurring after initial SCI.
According to this review, there are both positive and negative effects of macrophages on tissue repair and regeneration after an SCI. Interestingly, some studies show that infiltrating macrophages has harmful effects, especially in the early stages of an SCI. On the other hand, studies also indicated that macrophages have beneficial effects on tissue repair. These results included findings indicating that activated macrophages could provide a beneficial microenvironment that is good for the regeneration of sensory axons.
While the exact reason for the opposite effects of macrophages on the pathological process of SCI is not yet known, it’s thought to be because of the different phenotypes of macrophages – M1 (classical activation) and M2 (alternative activation).
Additionally, studies have demonstrated that M2 macrophages are important for efficient remyelination after CNS injury, while M1 macrophages hinder neurogenesis and inhibit neurite outgrowth and induce growth cone collapse of cortical neurons.
Considering these findings, the authors point out that polarization of macrophages to M2 is beneficial – and often preferred to M1- to facilitate the recovery after SCI. These findings have also demonstrated stem cell therapy to hold tremendous potential for therapeutic uses in the treatment/recovery after a spinal cord injury.
There is accumulating evidence indicating that the current preference of M2 macrophages compared to M1 macrophages correlates with remission of SCI in cases receiving SCI interventions including anti-inflammatory therapies and stem cells. The authors of this review conclude that while the exact process by which stem cells regulate macrophage polarization has yet to be determined, stem cells can alter macrophage polarization and promote functional recovery postinjury.
Cigarette smoking continues to be the leading contributor to preventable disease and death in the United States, including cancer, heart disease, stroke, lung diseases, diabetes, and chronic obstructive pulmonary disease (COPD). Smoking cigarettes also increases the risk of tuberculosis, certain eye diseases, chronic pain, and problems of the immune system, including rheumatoid arthritis.
An abundance of clinical research has clearly shown the detrimental effects cigarette smoke has on nearly every area of the body. However, while assumed to be equally dangerous in its effect on stem cells, there is surprisingly little research exploring the negative implications of cigarette smoking on stem cells.
In this review, Nguyen et al. share findings of recent studies on the effects of cigarette smoking and nicotine on mesenchymal stem cells (MSCs), with a specific focus on dental stem cells.
With their ability to self-renew, develop into specialized cell types, and migrate to potential sites of injury, stem cells have demonstrated the potential to build every tissue in the body and have also demonstrated great potential for tissue regeneration and associated therapeutic uses.
As the potential benefits and weaknesses of stem cells continue to be discovered, researchers have found that cigarette smoking negatively impacts the abilities of stem cells while also limiting stem cell viability for transplantation and regeneration.
While there has been a recent decline in the percentage of U.S. adults who smoke, over 34 million U.S. adults continue to be regular cigarette smokers. Interestingly, research has demonstrated the concentration of nicotine to be significantly higher in saliva than in blood plasma following nicotine administration via cigarette, e-cigarette, and nicotine patch – in some cases measuring up to eight times higher concentrations. Considering this research, and considering the established detrimental effects of e-cigarette vapor – and presumably nicotine – on teeth and dental implants, the authors of this review hypothesized that there would be a similar effect when dental stem cells are exposed to cigarette smoke.
Reviewing the effect that cigarette smoke has on MSCs, the authors found that exposing MSCs to cigarette smoke extract (CSE) and nicotine impaired cell migration, increased early and late osteogenic differentiation markers, decreased cell proliferation, and significantly inhibited the ability of MSCs to differentiate to other types of cells.
Nguyen et al. reviewed research that determined cigarette smoke produced a negative impact on the proliferation and differentiation of dental pulp stem cells (DPSCs). Specifically, this research demonstrated a significantly higher depression of alkaline phosphatase (ALP) and osteocalcin (OC) genes in smokers when compared to nonsmokers. Additional studies found that smokers demonstrated reduced calcium deposition levels and production of ALP when compared to nonsmokers.
Cigarette smoke and nicotine were also found to negatively affect the migration capability of dental stem cells, slowing the migration rate by up to 12% in smokers while also producing a smaller reduction of scratch wound areas when compared to nonsmokers.
While there are not many studies directly comparing the effects of cigarette smoke and nicotine on MSCs and dental stem cells, the authors conclude that dental stem cells exhibit similar characteristics to bone marrow MSCs and that both of these types of stem cells demonstrate similar negative responses upon their exposure to nicotine.
While the authors call for further research to better understand the specific effects of cigarette smoke on dental stem cells, the authors conclude that the findings demonstrating similar responses to cigarette smoke and nicotine between dental stem cells and MSCs can be used to inform future dental stem cell studies. These findings will help dentists better identify which patients might be at an increased risk of poor healing in the oral cavity and if smoking cessation should be considered before undergoing any invasive or traumatic dental procedure, such as tooth extraction.
The National Institute of Health estimates that nearly 250,000 people in the United States are currently living with a spinal cord injury (SCI). Most often a result of an accident, SCIs typically result in the loss of neurons and axonal damage resulting in the loss of function.
SCIs can be divided into two distinct phases, the initial physical injury and the secondary injury which typically occurs hours to days later. In most cases of SCI, damage to the axonal and tissue damage is caused by compression and/or contusion to the spinal cord. The secondary SCI injury occurs in the hours and days after the initial injury and is characterized by persistent inflammation, glial scar formation, demyelination of surrounding neurons, and death of cells. Over time, research has demonstrated that, in all aspects of secondary injury, the inflammatory response is the major cause and leads to widespread cell damage and lesion expansion.
Recent research has demonstrated that stem cells, including mesenchymal stem cells (MSCs), neural stem/progenitor, and embryonic stem cells, possess anti-inflammatory properties and promote functional recovery after SCI by inducing macrophages M1/M2 phenotype transformation.
In this review, Cheng and He discuss the general feature of macrophages in response to SCI, the phenotype, and function of macrophages in SCI, and the effects of stem cells on macrophage polarization and its role in stem cell-based therapies for SCI.
Macrophages accumulate in and around an SCI and play a very important role in neuroinflammation. Considering that recent research demonstrates the different, but important, contributions M1 and M2 macrophages make toward repairing tissue damage, this process is thought to be a promising therapeutic treatment for controlling the inflammation occurring after initial SCI.
According to this review, there are both positive and negative effects of macrophages on tissue repair and regeneration after an SCI. Interestingly, some studies show that infiltrating macrophages has harmful effects, especially in the early stages of an SCI. On the other hand, studies also indicated that macrophages have beneficial effects on tissue repair. These results included findings indicating that activated macrophages could provide a beneficial microenvironment that is good for the regeneration of sensory axons.
While the exact reason for the opposite effects of macrophages on the pathological process of SCI is not yet known, it’s thought to be because of the different phenotypes of macrophages – M1 (classical activation) and M2 (alternative activation).
Additionally, studies have demonstrated that M2 macrophages are important for efficient remyelination after CNS injury, while M1 macrophages hinder neurogenesis and inhibit neurite outgrowth and induce growth cone collapse of cortical neurons.
Considering these findings, the authors point out that polarization of macrophages to M2 is beneficial – and often preferred to M1- to facilitate the recovery after SCI. These findings have also demonstrated stem cell transplantation to hold tremendous potential for therapeutic uses in the treatment/recovery after SCI.
There is accumulating evidence indicating that the current preference of M2 macrophages compared to M1 macrophages correlates with remission of SCI in cases receiving SCI interventions including anti-inflammatory therapies and stem cells. The authors of this review conclude that while the exact process by which stem cells regulate macrophage polarization has yet to be determined, stem cells can alter macrophage polarization and promote functional recovery postinjury.
Currently, it’s estimated that over 1.3 million people in the U.S., and 10 million people around the world, are living with inflammatory bowel disease (IBD). IBD is a chronic and recurrent disease characterized by inflammation of the tissues of the digestive tract[1]. Two specific diseases included under the term IBD include Crohn’s disease (CD) and ulcerative colitis (UC).
While the exact cause of IBD has yet to be determined, research seems to suggest abnormal activation of the immune system, genetic susceptibility, and altered intestinal flora resulting from mucus barrier defects play some type of role in the pathogenesis of this disease. Currently, a complete IBD treatment or cure exists. Recent research has also demonstrated that adults with IBD are more likely to suffer from other chronic conditions, including diabetes, arthritis, lung cancer, and heart disease[2].
Clinical trials using stem cell therapy have demonstrated promising results for the potential treatment of IBD, including long-term remission in some patients.
In this review, Zhang et al. review the upcoming stem cell transplantation methods for clinical application and the results of ongoing clinical trials exploring the use of stem cell transplantation as a potential treatment for IBD.
Specific stem cells, known as hematopoietic stem cells (HSC), have been shown to be particularly effective when used as a therapeutic treatment. HSCs are isolated from blood, bone marrow, and cord blood that migrate directly to damaged mucosal tissues. Initially used in patients with IBD because of other hematologic indications, including leukemia and non-Hodgkin’s lymphoma, the use of HSC therapy (HSCT) demonstrated improvement in intestinal lesions. Further study using HSCT showed that some patients with UC and CD demonstrated sustained clinical and endoscopic improvement. The authors point out that while these limited clinical trials have demonstrated promising results, the observed risk of relapse currently prevents HSCT from being classified as an effective treatment and calls for larger samples and longer-term efficacy observations.
Another stem cell treatment currently being evaluated for the treatment of IBD is the use of mesenchymal stem cells (MSCs). When injected intravenously, MSCs demonstrate the ability to reach the injured area of the intestine, colonize mucosa to control inflammation, improve microcirculation, and repair damaged tissues. A systematic review conducted by Lalu et al. found that the use of MSCs did not show significant side effects and was a relatively safe therapeutic treatment option.
Zhang et al. conclude that the significant advance in stem cell research made over the past twenty years has made them a promising therapeutic option for the treatment of IBD. Although a limited number of clinical trials have confirmed the efficacy of specific stem cells, specifically HSC and MSCs in IBD, the authors point out that the current treatments need to be improved and further research must be conducted in order to fully understand the complexity associated with the condition.
While this review focuses primarily on the use of HSC and MSC, Zhang et al. call for continued preclinical exploration of other cell therapy methods with the goal of improving the quality of life of IBD patients.
An estimated 100 million people in the U.S. have some form of acute or chronic liver disease. Many factors, including viral and bacterial infections, substance abuse, diabetes, and fat deposition, contribute to conditions that harm the liver.
Left untreated, these liver conditions often progress to more serious diseases that often require a liver transplant. Historically, a host of issues – including a low number of tissue donors, a high rate of tissue rejection, medicine-induced immunosuppression, and high associated medical costs – has limited access to, and the effectiveness of, liver transplantation as a viable solution.
Considering the limited options available for the successful treatment of liver disease, identifying alternative treatment options has become very important. Recently, the potential treatment of acute and chronic liver disease using regenerative medicine, also known as stem cell therapy, has garnered an increased amount of attention.
While a number of different types of stem cells have been used to treat liver disease, mesenchymal stem cells (MSCs) have been the most studied and successful in reducing the need for liver transplantation.
MSCs have been used to repair liver tissue through a number of different methods, including co-culturing with HSCs to reduce and prevent the progression of fibrosis and the proliferation of disease-causing cells through the production and secretion of specific inflammatory factors.
Treatment of liver disease with MSCs has also been shown to increase endothelial precursor cell proliferation while suppressing apoptosis in LSECs and hepatocytes, and by lowering serum transaminase enzyme levels. MSCs have also been shown to compensate for hepatocyte reduction resulting through liver-disease induced apoptosis by differentiating into hepatocyte-like cells.
Considering the observed role of MSCs in liver tissue repair and regeneration, Hazrati et al concluded that the use of MSCs induces the repair and regeneration of liver tissue through immune response modulation, differentiation into HLCs, increased proliferation and decreased apoptosis in hepatocytes, increased apoptosis and reduced function of HSCs and improve the function of LSECs.
The authors also point out that, as of publication, there were 61 active clinical trials using MSCs to treat a variety of liver-related diseases, including cirrhosis, fibrosis, and liver failure. The associated advantages of MSCs in the treatment of acute and chronic inflammatory liver disease include ease of isolation and culture, pluripotency, immunomodulatory and anti-inflammatory properties, extracellular signaling, and their ability to differentiate.
The authors conclude this review by summarizing the observed benefits of using MSCs, and specifically MSC-EVs to improve liver function and support the repair of damaged liver tissue. The authors also point out that while there have been numerous clinical trials using MSCs to treat liver disease, there have been no clinical trials performed on the use of MSC-EVs and call for additional research to investigate the long-term effects of treating liver disease with MSC-EVs.
Osteoporosis is a common bone disease that occurs as a result of the body’s inability to create new bone as fast as the body is losing bone. Characterized by progressively weakened bones and decreased bone density over time, osteoporosis often results in fractures of the wrist, hip, or spine.
Currently, it is estimated that 10 million Americans have osteoporosis and an additional 44 million have low bone density considered significant enough to increase the risk of developing osteoporosis. Recent studies indicate that roughly 50% of women and 25% of men over the age of 50 will break a bone as a result of osteoporosis[1].
While traditional methods of managing osteoporosis include medication, regular participation in weight-bearing exercises, and eating a healthy diet, the condition cannot be cured through these current approaches. Recently, regenerative medicine, also known as stem cell therapy, has drawn attention as a potential new approach to regenerate bone tissue and as a way to treat osteoporosis.
Specific stem cells, known as mesenchymal stem cells (MSCs), are widely considered to be the most promising of all stem cells for regenerative applications – primarily because of their anti-inflammatory, immune-privileged potential and less ethical concerns than other forms of stem cells.
In this review, Arjmand et al. consider all the currently known effects of stem cell-based therapies, including MSC-based therapy, in the treatment of osteoporosis. Several studies have confirmed the relationship between osteoporosis and a clear reduction in endogenous MSCs’ ability to proliferate, differentiate, and ultimately form new bone. Considering this, MSCs have been the most common type of stem cell investigated for the treatment of osteoporosis in both animal models and humans.
The authors point out several advantages of using MSCs in clinical models, including their accessibility and ease of harvesting, immunosuppressive outcomes, and ability to differentiate. Arjmand et al also highlight evidence that indicates MSCs to be effective in this application most likely as a result of their paracrine effects and their supporting regenerative microenvironment ability and not solely a result of their ability to differentiate. Considering these observed paracrine effects, the authors believe MSC transplantation could open a host of new opportunities for the treatment of osteoporosis.
This review concludes by calling for further studies into stem cell therapy as a potential treatment for osteoporosis specifically to understand the outcome and biodistribution of MSCs after transplantation and to further identify important bone loss signaling pathways and genes specific to each individual.
This website and its contents are not intended to treat, cure, diagnose, or prevent any disease. Stemedix, Inc. shall not be held liable for the medical claims made by patient testimonials or videos. They are not to be viewed as a guarantee for each individual. The efficacy for some products presented have not been confirmed by the Food and Drug Administration (FDA).
This website uses cookies to improve your experience while you navigate through the website. Out of these cookies, the cookies that are categorized as necessary are stored on your browser as they are essential for the working of basic functionalities of the website. We also use third-party cookies that help us analyze and understand how you use this website. These cookies will be stored in your browser only with your consent. You also have the option to opt-out of these cookies. But opting out of some of these cookies may have an effect on your browsing experience.
Necessary cookies are absolutely essential for the website to function properly. This category only includes cookies that ensures basic functionalities and security features of the website. These cookies do not store any personal information.
Any cookies that may not be particularly necessary for the website to function and is used specifically to collect user personal data via analytics, ads, other embedded contents are termed as non-necessary cookies. It is mandatory to procure user consent prior to running these cookies on your website.
Subscribe To Our Newsletter
Join our mailing list to receive the latest news and updates from our team.
You have Successfully Subscribed!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
Thanks for your interest!
Request Information Packet
We'll send your FREE information packet that outlines our entire personalized, stress-free stem cell treatment process!
St. Petersburg, Florida
