How Nasal Stem Cells Might Prevent Childhood Deafness

Medical News Today

Sensorineural hearing loss is a type of deafness that generally begins in childhood, a condition that results from hearing cells in the cochlea losing their function. The hearing loss that occurs can often slow the development of the child and possibly cause speech and language problems to develop.

Fortunately, Australian scientists have discovered a possible way to restore or reverse this condition. It has been shown in mice that injecting nasal stem cells into the inner ear can effectively reverse the condition during early onset hearing loss. The stem cells release signaling factors that help preserve the function of the cochlear cells.

“We are exploring the potential of stem cells to prevent or restore hearing loss in people,” said project leader Dr Sharon Oleskevich. “We are encouraged by our initial findings, because all the mice injected with stem cells showed improved hearing in comparison with those given a sham injection. Roughly half of the mice did very well indeed, although it is important to note that hearing was not completely restored to normal hearing levels.”

First Scientist to identify stem cells dies at 84

Thomas Maugh II, Washington Post

Ernest Armstrong McCulloch, 84, passed away January 20 in his hometown of Toronto. Dr. McCulloch, a medical doctor who attended the University of Toronto is best remembered as the first, along with biophysicist James E. Till, to isolate and identify a stem cell.

Their discovery was reached while both were young researchers at the Ontario Cancer Institute at Princess Margaret Hospital. The discovery came as somewhat of an accident while studying the effects of ionizing radiation on mice. The aim of their study was to attempt to learn how exposure to radiation from nuclear weapons killed and also how radiation destroyed tumors. The mice were irradiated to the point that they would die within 30 days without an infusion of undamaged bone marrow cells. Shortly after injecting the cells, Dr. McCulloch discovered nodules in the spleen. His background in bacteriology allowed him to form the hypothesis that these nodules were the source of replenishing blood cells that were keeping the mice alive. These results were published, however received very little attention. Two years later, after hundreds of hours of intensive research, McCulloch and Till published a paper proving that all three types of blood cells – red, white, and platelets were produced by a single stem cell.

This discovery was the precursor for bone marrow transplant therapy, a treatment which has been utilized for 40 years and saved countless lives. “Without their work, we would never have had bone marrow transplants,” Michael Rudnicki, scientific director of the Stem Cell Network, told the Toronto Star. “We might have muddled our way through it . . . but their work provided the theoretical underpinnings for bone marrow transplant as a therapy, which has been in the clinic now for 40 years and has saved countless lives.”

Therapeutic Effects of Intra-Arterial Delivery of Bone Marrow Stromal Cells in Traumatic Brain Injury of Rats—In Vivo Cell Tracking Study by Near-Infrared Fluorescence Imaging

Neurosurgery:
February 2012 – Volume 70 – Issue 2 – p 435–444
doi: 10.1227/NEU.0b013e318230a795
Research-Animal

Osanai, Toshiya MD, PhD*; Kuroda, Satoshi MD, PhD*; Sugiyama, Taku MD, PhD*; Kawabori, Masahito MD*; Ito, Masaki MD*; Shichinohe, Hideo MD, PhD*; Kuge, Yuji PhD‡; Houkin, Kiyohiro MD, PhD*; Tamaki, Nagara MD, PhD‡; Iwasaki, Yoshinobu MD, PhD*

Abstract

BACKGROUND: A noninvasive and effective route of cell delivery should be established to yield maximal therapeutic effects for central nervous system (CNS) disorders.

OBJECTIVE: To elucidate whether intra-arterial delivery of bone marrow stromal cells (BMSCs) significantly promotes functional recovery in traumatic brain injury (TBI) in rats.

METHODS: Rat BMSCs were transplanted through the ipsilateral internal carotid artery 7 days after the onset of cortical freezing injury. The BMSCs were labeled with fluorescent dye, and in vivo optical imaging was employed to monitor the behaviors of cells for 4 weeks after transplantation. Motor function was assessed for 4 weeks, and the transplanted BMSCs were examined using immunohistochemistry.

RESULTS: In vivo optical imaging and histologic analysis clearly demonstrated that the intra-arterially injected BMSCs were engrafted during the first pass without systemic circulation, and the transplanted BMSCs started to migrate from the cerebral capillary bed to the injured CNS tissue within 3 hours. Intra-arterial BMSC transplantation significantly promoted functional recovery after cortical freezing injury. A subgroup of BMSCs expressed the phenotypes of neurons, astrocytes, and endothelial cells around the injured neocortex 4 weeks after transplantation.

CONCLUSION: Intra-arterial transplantation may be a valuable option for prompt, noninvasive delivery of BMSCs to the injured CNS tissue, enhancing functional recovery after TBI. In vivo optical imaging may provide important information on the intracerebral behaviors of donor cells by noninvasive, serial visualization.

Inhaling Stem Cells for Treating Parkinson’s

Danielyan et al. Rejuvenation Res.

Stem cells have been delivered in a variety of ways: intravenously, into the spinal canal (intrathecally), into the brain (stereotactically), into the joint (intra-articularly), and into the cardiac muscle (endocardially). Scientists from the Department of Clinical Pharmacology, University Hospital of Tübingen , Tübingen, Germany have reported today a new way of delivering stem cells: via the nose.

Previous experiments administering stem cells for the treatment of Parkinson’s were primarily aimed at injection directly into the brain using sterotactic methods. These methods are highly invasive and there is always the potential of causing injury. Additionally some groups have used intravenous administration but the washout and number of cells being stuck in the lung and liver was reported as a potential problem.

The promise of using stem cells for the treatment of Parkinson’s comes not only from the direct regenerative ability of stem cells such as mesenchymal stem cells, but also from the fact that Parkinson’s is associated with inflammatory cytokine production, which has been previously demonstrated to be inhibited by stem cell administration.

Intranasal administration of bone marrow mesenchymal stem cells was performed in rats induced to develop a Parkinson’s like disease in which the dopaminergic cells were killed by administration of the toxin 6-hydroxydopamine (6-OHDA).

In rats that received the stem cells intranasally it was possible to find stem cells in the olfactory bulb, cortex, hippocampus, striatum, cerebellum, brainstem, and spinal cord. Out of 1 × 10(6) MSCs applied intranasally, 24% of the stem cells could be detected for least 4.5 months in the brains of 6-OHDA rats. It appears that the stem cells administered actually could proliferate in vivo as shown by expression of proliferating cell nuclear antigen on the administered mesenchymal stem cells.

Functionally it appeared that the intranasal administration increased the tyrosine hydroxylase level in the lesioned ipsilateral striatum and substantia nigra, and completely eliminated the 6-OHDA-induced increase apoptotic cells as detected by TUNEL. Decreases in dopamine were prevented by cellular administration. A decrease in the inflammatory cytokines TNF, IFN-g, IL-2, 2, 6, and 12 was observed to be associated with the administration of cell therapy.

It will be interesting to see if this easy to apply technique will enter clinical trials. Already clinical trials are using non-conventional means of stem cell administration, for example the topical application of stem cells for burn wounds, which is being performed by Dr. Amit Patel from the University of Utah, who we interviewed for the Cellmedicine news blog above.

Ischemic Stroke Recovery May Be Improved Using Stem Cell Therapy

At the American Heart Association’s International Stroke Conference in New Orleans, two studies suggested that stem cell therapy improves functional recovery following subacute ischemic stroke and may aid in regenerative therapy.

One hundred and twenty subacute ischemic stroke patients were treated with mononuclear bone marrow-derived stem cells. Patients ranged in age from eighteen to seventy five years old. All were treated within seven to thirty days of suffering their strokes. Each patient was assessed using the Barthel index. The results showed that seventy three percent of patients who were treated with stem cells attained a Barthel score of greater than or equal to 60, which is the measure for assisted independence. Only sixty one percent of the patients who were not treated with stem cells achieved similar scores. All patients were tumor free at one year. This study was performed by Kameshwar Prasad, M.B.B.S., M.D., from the All India Institute of Medical Sciences in New Delhi.

In a separate study from the All India Institute of Medical Sciences in New Delhi, Rohit Bhatia, M.D. examined autologous mononuclear mesenchymal stem cell therapy in forty stroke patients who were recruited for the study from three months to one year after their strokes. Patients who were treated with stem cells showed significant improvement based on the Barthel index. No adverse reactions were observed. Dr. Bhatia concluded that intravenous administration of mononuclear and mesenchymal stem cells is safe, feasible and likely facilitates behavioral recovery following stroke.

Autologous mesenchymal stem cells for the treatment of secondary progressive multiple sclerosis: an open-label phase 2a proof-of-concept study

Connick P, Kolappan M, Crawley C, Webber DJ, Patani R, Michell AW, Du MQ, Luan SL, Altmann DR, Thompson AJ, Compston A, Scott MA, Miller DH, Chandran S.

Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

Abstract

BACKGROUND:
More than half of patients with multiple sclerosis have progressive disease characterised by accumulating disability. The absence of treatments for progressive multiple sclerosis represents a major unmet clinical need. On the basis of evidence that mesenchymal stem cells have a beneficial effect in acute and chronic animal models of multiple sclerosis, we aimed to assess the safety and efficacy of these cells as a potential neuroprotective treatment for secondary progressive multiple sclerosis.

METHODS:
Patients with secondary progressive multiple sclerosis involving the visual pathways (expanded disability status score 5·5-6·5) were recruited from the East Anglia and north London regions of the UK. Participants received intravenous infusion of autologous bone-marrow-derived mesenchymal stem cells in this open-label study. Our primary objective was to assess feasibility and safety; we compared adverse events from up to 20 months before treatment until up to 10 months after the infusion. As a secondary objective, we chose efficacy outcomes to assess the anterior visual pathway as a model of wider disease. Masked endpoint analyses was used for electrophysiological and selected imaging outcomes. We used piecewise linear mixed models to assess the change in gradients over time at the point of intervention. This trial is registered with ClinicalTrials.gov, number NCT00395200.

FINDINGS:
We isolated, expanded, characterised, and administered mesenchymal stem cells in ten patients. The mean dose was 1·6×10(6) cells per kg bodyweight (range 1·1-2·0). One patient developed a transient rash shortly after treatment; two patients had self-limiting bacterial infections 3-4 weeks after treatment. We did not identify any serious adverse events. We noted improvement after treatment in visual acuity (difference in monthly rates of change -0·02 logMAR units, 95% CI -0·03 to -0·01; p=0·003) and visual evoked response latency (-1·33 ms, -2·44 to -0·21; p=0·020), with an increase in optic nerve area (difference in monthly rates of change 0·13 mm(2), 0·04 to 0·22; p=0·006). We did not identify any significant effects on colour vision, visual fields, macular volume, retinal nerve fibre layer thickness, or optic nerve magnetisation transfer ratio.

INTERPRETATION:
Autologous mesenchymal stem cells were safely given to patients with secondary progressive multiple sclerosis in our study. The evidence of structural, functional, and physiological improvement after treatment in some visual endpoints is suggestive of neuroprotection.

FUNDING:
Medical Research Council, Multiple Sclerosis Society of Great Britain and Northern Ireland, Evelyn Trust, NHS National Institute for Health Research, Cambridge and UCLH Biomedical Research Centres, Wellcome Trust, Raymond and Beverly Sackler Foundation, and Sir David and Isobel Walker Trust.

Fat Stem Cells Turn to Muscle: A Treatment for Muscular Dystrophy?

New research published in the journal Biomaterials by University of California, San Diego researcher Adam Engler suggests fat-derived stem cells that are developed on a stiff surface transform into mature muscle cells. This remarkable discovery could lead to new treatments for muscular dystrophy in the future.

Fat stem cells and bone marrow stem cells were grown on surfaces with different degrees of hardness ranging from very hard bone-like surfaces to very soft brain tissue-like surfaces.

The researchers found that the fat derived stem cells were much more likely (up to fifty times) to exhibit proteins that are essential to the cells becoming muscle tissue.
Yuk Suk Choi, a post-doc team member, says that the fat-derived stem cells seem to proliferate better than bone marrow cells when introduced to the hard surfaces. “They are actively feeling their environment soon, which allows them to interpret the signals from the interaction of cell and environment that guide development,” explained Choi.

Unlike bone marrow stem cells, stem cells from fat fused together to form myotubes. Although this phenomenon has been observed in the past, it has never been observed at such a high degree by Engler in the lab. Myotubes comprise an essential step in muscle formation.

Next, Engler and his team plan to observe how fused cells from fat perform in lab mice which are afflicted with a particular form of muscular dystrophy.

However, Dr. Engler cautioned, “From the perspective of translating this into a clinically viable therapy, we want to know what components of the environment provide the most important cues for these cells.”

Medistem Begins Phase II Clinical Trial for Heart Failure

Medistem Inc announced today treatment of 3 heart failure patients in the Non-Revascularizable IschEmic Cardiomyopathy treated with Retrograde COronary Sinus Venous DElivery of Cell TheRapy (RECOVER-ERC) trial. The trial is aimed at assessing safety and efficacy of the company’s Endometrial Regenerative Cell (ERC) stem cell product in 60 heart failure patients who have no available treatment options. The cells were discovered by Dr. Neil Riordan and the team at Medistem. The “Universal Donor” adult stem cells will be administered using a novel catheter-based retrograde administration methodology that directly implants cells in a simple, 30 minute, procedure.

“We are honored to have had the opportunity to present at the prestigious Cardiovascular Stem Cell Research Symposium, alongside companies such as Athersys, Aastrom, Pluristem, Cardio3, Cytori, and Mesoblast,” stated Thomas Ichim, CEO of Medistem. “The RECOVER-ERC trial is the first trial combining a novel stem cell, with a novel administration procedure. Today cardiac administration of stem cells is relatively invasive and can only be performed at specialized institutions, we feel the retrograde procedure will circumvent this hurdle.”

Medistem has been focusing on the endometrium because this is a unique tissue in that it undergoes approximately 500 cycles of highly vascularized tissue growth and regression within a tightly controlled manner in the lifetime of the average female. One of the first series of data describing stem cells in the endometrium came from Prianishnikov in 1978 who reported that three types of stem cells exist: estradiol-sensitive cells, estradiol- and progesterone-sensitive cells and progesterone-sensitive cells.

Interestingly, a study in 1982 demonstrated that cells in the endometrium destined to generate the decidual portion of the placenta are bone marrow derived, which prompted the speculation of a stem cell like cell in the endometrium. Further hinting at the possibility of stem cells in the endometrium were studies demonstrating expression of telomerase in endometrial tissue collected during the proliferative phase. One of the first reports of cloned stem cells from the endometrium was by Gargett’s group who identified clonogenic cells capable of generating stromal and epithelial cell colonies, however no differentiation into other tissues was reported. The phenotype of these cells was found to be CD90 positive and CD146 positive. The cells isolated by this group appear to be related to maintaining structural aspects of the endometrium but to date have not demonstrated therapeutic potential. In 2007, Meng et al, used the process of cloning rapidly proliferating adherence cells derived from menstrual blood and generated a homogenous cell population expressing CD9, CD29, CD41a, CD44, CD59, CD73, CD90, and CD105 and lacking CD14, CD34, CD45 and STRO-1 expression. Shortly after, Patel’s group reported a population of cells isolated using c-kit selection of menstrual blood mononuclear cells. The cells had a similar phenotype, proliferative capacity, and ability to be expanded for over 68 doublings without induction of karyotypic abnormalities. Interestingly both groups found expression of the pluripotency gene OCT-4 but not NANOG. More recent investigations have confirmed these initial findings. For example, Park et al demonstrated that endometrial cells are significantly more potent originating sources for dedifferentiation into inducible pluripotent cells as compared to other cell populations. Specifically, human endometrial cells displayed accelerated expression of endogenous NANOG and OCT4 during reprogramming compared with neonatal skin fibroblasts. Additionally, the reprogramming resulted in an average colony-forming iPS efficiency of 0.49 ± 0.10%, with a range from 0.31-0.66%, compared with the neonatal skin fibroblasts, resulting in an average efficiency of 0.03 ± 0.00% per transduction, with a range from 0.02-0.03%. Suggesting pluripotency within the endometrium compartment, another study demonstrated that purification of side population (eg rhodamine effluxing) cells from the endometrium results in a population of cells expressing transdifferentiation potential with a genetic signature similar to other types of somatic stem cells.

Given the possibility of ERC playing a key role in angiogenesis, Murphy et al utilized an aggressive hindlimb ischemia model combined with nerve excision in order to generate a model of limb ischemia resulting in limb loss. ERC administration was capable of reducing limb loss in all treated animals, whereas control animals suffered necrosis. In the same study, ERC were demonstrated to inhibit ongoing mixed lymphocyte reaction, stimulate production of the anti-inflammatory cytokine IL-4 and inhibit production of IFN-g and TNF-alpha. It is important to note that the animal model involved administration of human ERC into immunocompetent BALB/c mice. The relationship between angiogenesis and post myocardial infarct healing is well-known. Given previous work by Umezawa’s group demonstrating myocytic differentiation of ERC-like cells, administration of ERC into a model of post infarct cardiac injury was performed. Recovery was compared to bone marrow MSC. A superior rate of post-infarct recovery of ejection fraction, as well as reduction in fibrosis was observed with the ERC-like cells. Furthermore, it was demonstrated that the cells were capable of functionally integrating with existing cardiomyocytes and exerted effects through direct differentiation. The investigators also demonstrated in vitro generation of cardiomyocyte cells that had functional properties.

The RECOVER-ERC TRIAL that has begun will recruit 60 patients with congestive heart failure, which will be randomized into 3 groups of 20 patients each. Group 1 will receive 50 million ERC, Group 2 will receive 100 million and Group 3 will receive 200 million. Cells will be administered via catheter-based retrograde administration into the coronary sinus, a 30 minute procedure developed by Dr. Amit Patel’s Team. Each group will comprise of 15 patients receiving cells and 5 patients receiving placebo. Efficacy endpoints include ECHO and MRI analysis, which will be conducted at 6 months after treatment. The trial design is similar to the recent Mesoblast Phase II cardiac study, in order to enable comparison of efficacy.

Mechanism by Which Injured Tissue “Tells” Stem Cells to Leave Bone Marrow

Urao et al. Stem Cells. 2012 Jan 30.

In addition to the established role of bone marrow derived stem cells in producing blood cells, an interesting aspect of these stem cells is to assist/accelerate tissue healing after injury. Perhaps the most studied example of this is in the situation of myocardial infarction (heart attack), in which damaged heart muscle sends out signals to the bone marrow, which cause selective homing of bone marrow stem cells into the damaged heart tissue. This is believed to occur via activation of the transcription factor HIF-1 alpha due to lack of oxygen in the tissue. HIF-1 alpha binds to DNA and induces activation of a variety of genes that are involved in angiogenesis such as VEGF, FGF-2, and IL-20. Additionally, HIF-1 alpha stimulates production of the chemokine stromal derived factor (SDF)-1, which attracts bone marrow stem cells by binding to the CXCR4 receptor. The importance of SDF-1 in terms of bone marrow stem cell migration is exemplified in the situation of bone marrow transplantation. When a transplant is performed the bone marrow recipient is administered the donor stem cells intravenously and not intraosteolly (inside the bone). The reason for this is because the bone marrow itself constantly produces SDF-1 which attracts injected stem cells that express CXCR4.

During infarction, the concentration of SDF-1 produced by the damaged heart muscle is higher than the concentration of SDF-1 in the bone marrow, and as a result, stem cells from the bone marrow leave the bones, enter circulation, and home to the heart. Similar examples are found in the situation of stroke. In stroke patients, not only do bone marrow stem cells enter circulation after the stroke, but it has been reported that patients with higher number of stem cells in circulation actually have better outcomes.

The possibility of chemically “mobilizing” bone marrow stem cells into circulation is very attractive. On the one hand, it would be conceptually possible to augment the extent of regeneration by increasing the number of circulating stem cells, and on the other hand, it may be possible to perform “bone marrow transplantation” without the painful procedure of drilling holes through the bones of the donor. In fact, the second possibility is actually part of clinical practice. Doctors use the drug G-CSF, otherwise known as Neupogen, to cause donor migration of bone marrow stem cells into circulation, which are then harvested by leukopheresis, so that bone marrow puncture is not needed. The first possibility, the therapeutic use of bone marrow mobilization has resulted in mixed data. Some groups have demonstrated significant improvement in heart attack patients treated with G-CSF, whereas others have reported no benefit. Recently a new way of mobilizing stem cells has been approved by the FDA: a small molecule drug called Mozobil which blocks the interaction between SDF-1 and CXCR4. This drug was developed by the company Anormed and sold to Genzyme, a major Biopharmaceutical company.

In a recent paper, the role of oxidative stress was investigated in the animal model of critical limb ischemia. Critical limb ischemia is a condition in which patients experience poor circulation in the lower extremities, usually as a result of advanced peripheral artery disease. To replicate this condition in animals, the femoral artery which feeds the leg is ligated, and perfusion of the leg is measured, usually with Doppler ultrasound. In the mouse model there is a gradual recovery of blood flow as a result of spontaneous angiogenesis (new blood vessel formation). It is believed that bone marrow stem cells are involved in the formation of these new blood vessels.

While it is known that ischemia in the leg muscle is associated with recruitment of stem cells by production of SDF-1, little is known involving the changes that occur in the bone marrow as a result of ischemia in the leg.

Scientists demonstrated that after mice are subjected to hindlimb ischemia, there is a major increase in the production of free radicals in the bone marrow, specifically in the endosteal and central region of the bone marrow. Interestingly, these free radicals appear to be made by the enzyme Nox2 because mice lacking this enzyme do not have free radicals produced in the bone marrow as a result of leg ischemia. The enzyme appears to be expressed mainly in the Gr-1(+) myeloid suppressor cells that are found in the bone marrow. Free radicals were found to be associated with expression of HIF-1 alpha, implying occurrence of localized hypoxia. As can be expected, HIF-1 alpha expression was also found to associate with production of the angiogenic cytokine VEGF. It appeared that bone marrow VEGF expression was associated with expansion of bone marrow Lin(-) progenitor cell survival and expansion, leading to their mobilization into systemic circulation. It was furthermore demonstrated that ischemia of the leg increased expression of the proteolytic enzymes MT1-MMP and MMP-9 activity in the bone marrow, which did not occur in mice lacking Nox2.

The identification of NOX2 as being critical in the mobilization of bone marrow stem cells in response to ischemia suggests that antioxidants may actually modulate the extent of bone marrow stem cell mobilization. Conversely, if one believes the concept proposed, then oxidative stress (at least in a short term setting) would be beneficial towards mobilization. This is supported by studies showing that hyperbaric oxygen induces transient mobilization of bone marrow stem cells. For example Dhar et al. published (Equine peripheral blood-derived mesenchymal stem cells: Isolation, identification, trilineage differentiation and effect of hyperbaric oxygen treatment. Equine Vet J. 2012 Feb 15) that hyperbaric oxygen treatment in horses increased yield of mesenchymal stem cells collected from peripheral blood. Thom et al (Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. Wound Repair Regen. 2011 Mar-Apr;19(2):149-61) reported 2-fold increases in hematopoietic stem cells (identified by CD34 expression) in diabetic patients who received hyperbaric oxygen. This study also demonstrated that the CD34 cells that were found in circulation contained high expression of HIF-1 alpha, implying that they may possess angiogenic activity. An interesting experiment would have been if they removed the cells and assessed in vitro angiogenic activity. Indeed it is known that in patients with diabetes the CD34 cells possess a reduced angiogenic activity. If hyperbaric oxygen stimulates this angiogenic activity, it may be a relatively non-invasive method of augmenting the “rejuvenation” potential of the patient’s own stem cells. Another interesting finding of the study was that hyperbaric oxygen was associated with an increase in nitric oxide production by platelets. Since nitric oxide can act as an anticoagulant, this may be another benefit of using hyperbaric oxygen.

One important question is the potency of the stem cell mobilization induced by hyperbaric oxygen. Specifically, while it is nice that an increase in CD34 cells is observed, what activity do these cells actually have ? An earlier study by Thom et al (Stem Cell Mobilization by Hyperbaric Oxygen. Am J Physiol Heart Circ Physiol. 2006 Apr;290(4):H1378-86) demonstrated that the colony-forming ability of the mobilized cells was actually 16-20 fold higher compared to controls. Colony-forming ability is an assessment of the stem cells to generate new cells in vitro.

Thus the paper we discussed sheds some interesting light on the connection between “oxidative medicine” and stem cell biology. Obviously more studies are needed before specific medical recommendations can be made, however, given the large number of patients being treated with alternative medicine techniques such as hyperbaric oxygen, one must ask whether other treatments of this nature also affect stem cells. For example, what about ozone therapy? Or intravenous ascorbic acid?

Bone Marrow Stem Cells Significantly Improve Cardiac Mortality Rate in Heart Disease Patients

Texas Heart Institute researcher, Emerson Perin MD, PhD revealed that heart patients who were treated with bone marrow-derived adult stem cells died at a significantly lower rate that those who did not receive stem cells. Dr. Perin’s scientific findings represent yet another positive step in the ongoing fight against heart disease.

Dr. Perin is the Director of Clinical Research for Cardiovascular Medicine and Medical Director for the Stem Cell Institute at the Texas Heart Institute in Houston, Texas. Dr. Perin’s study showed that patients treated with stem cells were 90% less likes to die from an adverse cardiac event than patients who were not treated with stem cells.

“We obtained remarkable results from our study in which we injected stem cells derived from the bone marrow of a healthy donor into patients with heart failure. Heart function and exercise capacity improved in some cell-treated patients. Most importantly, cell therapy significantly reduced cardiac adverse events, including death. Three of 15 (20%) control patients died of cardiac causes, whereas only 1 of 45 (2%) cell-treated patients had a cardiac-related death. Despite the small numbers, our findings showed that cell therapy significantly improved cardiac mortality,” said Dr. Perin.