Development, Aging and Regeneration Archives - Page 2 of 3 - Sanford Burnham Prebys
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Unraveling the mystery of muscle regeneration could lead to effective treatment for muscular dystrophies

Authorsgammon
Date

September 22, 2015

By shedding light on the distinct functions of a protein complex that controls the formation of skeletal muscle tissue, SBP researchers could pave the way for the development of novel therapies for neuromuscular diseases.

Continue reading “Unraveling the mystery of muscle regeneration could lead to effective treatment for muscular dystrophies”

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Hearts build new muscle with this simple protein patch

Authorsgammon
Date

September 15, 2015

An international team of researchers has identified a protein that helps heart muscle cells regenerate after a heart attack. Researchers also showed that a patch loaded with the protein and placed inside the heart improved cardiac function and survival rates after a heart attack in mice and pigs. Continue reading “Hearts build new muscle with this simple protein patch”

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Discovery of new role of SOX2 protein sheds light on neurogenesis in the adult brain

Authorsgammon
Date

April 21, 2015

 

Newborn neurons generated from neural progenitor cells in a brain region called the hippocampus play an important role in learning and memory in adults. However, the molecular mechanisms that control this neurogenesis process have not been fully understood. Sanford-Burnham researchers recently shed new light on this question by discovering a key role of a protein called SOX2 in neuronal development. As reported online in Proceedings of the National Academy of Sciences, SOX2 promotes the activation of genes involved in differentiation, enabling neural progenitor cells to turn into mature neurons in the brains of adult mice. Continue reading “Discovery of new role of SOX2 protein sheds light on neurogenesis in the adult brain”

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Discovering a missing link between obesity and heart disease

AuthorGuest Blogger
Date

March 5, 2015

This post was written by Janelle Weaver, PhD, a freelance writer

Heart disease is the number one killer in the United States and a major cause of disability. One major risk factor is obesity, which itself has undergone a dramatic increase in prevalence in the United States over the past 20 years and now affects more than one-third of adults. A major challenge in developing targeted drugs for diet-induced heart disease is to understand how molecular and genetic changes trigger metabolic imbalances that ultimately impair heart function. Continue reading “Discovering a missing link between obesity and heart disease”

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Stem cells grow new hair – Arabic translation

Authorsgammon
Date

January 27, 2015

“دراسة جديدة لنمو الشعر”

في دراسة جديدة، إستخدم الباحثون في معهد سان- برونهام الخلايا الجذعه المحفزة1 في جسم الإنسان لتعمل على توليد ونمو الشعر الجديد. وتمثل هذه الدراسة خطوة أولى نحو تطوير علاج عن طريق الخلايا الجذعية للأشخاص الذين يعانون من مشكلة فغداً الشعر “الصلع” .في الولايات المتحدة وحدها، يعاني أكثر من 40 مليون رجل و 21 مليون إمرأة من مشكلة فقدان الشعر، ولقد تم نشر هذا البحث على الإنترنت في بلوس وان. 

تبرعكم سوف يصنع الفرق الرجاء التبرع للدكتور ألكسي للمضي قدما في هذا الإنجاز.

“لقد قمنا بتطوير طريقة إستخدام الخلايا الجذعية المحفزه لخلق خلية جديدة قادرة على بدء نمو الشعر عند الإنسان”. و قال ألكسي ترسكي و هو دكتور أستاذ مشارك في معهد التنميه، والشيخوخة و برامج التجديد ” طريقة إستعمال الخلايا الجذعية توفر مصدرا غير محدود من الخلايا من المريض لعملية زراعة الشعر وهي ليست محدودة كالطرق المستعملة حالياً عن طريق إستخدام ونزع بصيلات الشعر المتواجدة من الأصل. طور فريق البحث نظام يعمل على تمايز الخلايا الجذعية المحفزة عند الإنسان لتصبح وتتحول إلى خلايا جلدية حليمة. هذه الخلايا الجلدية تعد خلايا فريده من نوعها وتعمل على تنظيم تشكيل بصيلات الشعر و دورة نموه. هذه الخلايا الجلدية لا تعد مناسبة لنمو الشعر من تلقاء نفسها لأنها لا تتوفر بالكميات المطلوبة وتفقد قدرتها بسرعة على حث تشكيل بصيلات الشعر بدون عمله التمايز مع الخلايا الجذعية. 

عند البالغين، هذه الخلايا الجلدية يمكن تضخيمها خارج الجسم، وأنها سرعان ما تفقد خصائصها في عملية تحفيز الشعر”.يقول الدكتور ألكسي “لقد قمنا بإبتكار نظام يعمل لدفع الخليا الجذعية المحفزه عند الإنسان لتتمايز أو تتحول إلى خلايا جلدية حليمة، وقد أكد نجاح التجربة حيث أكد على قدرة هذه الخلايا على حث نمو الشعر عند زرعها عند الفئران”. خطوتنا التاليه هي زراعة الخلايا الجذعية المحفزة عند الإنسان مرة أخرى إلى جسم الإنسان، و نحن حالياً نسعى إلى شركات لتنفيذ الخطوة الأخيرة”. 

شاهد المزيد على الرابط 
 

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Stem cells grow new hair – Chinese translation

Authorsgammon
Date

January 27, 2015

用干细胞促生毛发

在一项新的研究中,桑福德 – 伯纳姆的研究人员利用人类多能干细胞促生出新的头发。该研究代表了以细胞为基础的治疗人类脱发的第一步。仅在美国,就有超过4000万男性和21万女性有着脱发困扰。这项研究在PLOS ONE在线发表。 

您的资助很重要。请帮助捷列克博士继续这项研究!

“我们已开发出一种使用人类多能干细胞的方法,来创造能够引发人体毛发生长的新的细胞。该方法相对于目前那种依赖于将毛囊从头的一个部位移植到另一个部位的方法有显着的改善,”阿列克谢-捷列克博士说。身为桑福德 – 伯纳姆的研究院发展、老化、再生项目副教授的捷列克博士还指出:“我们的干细胞的方法为移植提供了无限多的来自病人的细胞源,而不受现有的毛囊的限制。” 

该研究小组开发了促使多能干细胞成为真皮毛乳头细胞的程序。真皮毛乳头细胞是一种调节毛囊形成和生长周期的独特细胞。如果只靠本身的话,毛乳头细胞并不适合于头发移植,原因是:它们的采集量不够,而且在采集后便很快失去其诱导毛囊形成的能力。 

“对成人来说,真皮毛乳头细胞不易在体外扩增,而且会很快失去它们的生发功能,”捷列克博士说。他还说:“我们开发了一个驱动人类多能干细胞分化为毛乳头细胞的程序,并通过移植到小鼠身上的实验证实了它们的生发能力。” 

“我们的下一个步骤是将那些由人类多能干细胞衍生出的人类真皮毛乳头细胞移植回人体。目前,我们正在寻求合作伙伴来实现这最后一步。” 

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Using stem cells to grow new hair

Authorsgammon
Date

January 27, 2015

In a new study, Sanford-Burnham researchers have used human pluripotent stem cells to generate new hair. The study represents the first step toward the development of a cell-based treatment for people with hair loss. In the United States alone, more than 40 million men and 21 million women are affected by hair loss. The research was published online in PLOS ONE.

“We have developed a method using human pluripotent stem cells to create new cells capable of initiating human hair growth. The method is a marked improvement over current methods that rely on transplanting existing hair follicles from one part of the head to another,” said Alexey Terskikh, PhD, associate professor in the Development, Aging, and Regeneration Program. “Our stem cell method provides an unlimited source of cells from the patient for transplantation and isn’t limited by the availability of existing hair follicles.”

The research team developed a protocol that coaxed human pluripotent stem cells to become dermal papilla cells. They are a unique population of cells that regulate hair-follicle formation and growth cycle. Human dermal papilla cells on their own are not suitable for hair transplants because they cannot be obtained in necessary amounts and rapidly lose their ability to induce hair-follicle formation in culture.

“In adults, dermal papilla cells cannot be readily amplified outside of the body and they quickly lose their hair-inducing properties,” said Terskikh. “We developed a protocol to drive human pluripotent stem cells to differentiate into dermal papilla cells and confirmed their ability to induce hair growth when transplanted into mice.”

“Our next step is to transplant human dermal papilla cells derived from human pluripotent stem cells back into human subjects,” said Terskikh. “We are currently seeking partnerships to implement this final step.”

View translations of this story

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Newly discovered cell stress pathway could hold therapeutic promise for diverse diseases

AuthorGuest Blogger
Date

January 5, 2015

This post was written by Janelle Weaver, PhD, a freelance writer.

When cells are faced with unfavorable environmental conditions, such as limited nutrient availability, the activation of adaptive stress responses can help protect them against damage or death. For example, stressed cells can maintain sufficient energy levels for survival by degrading and recycling unnecessary or dysfunctional cellular components. This survival mechanism, known as autophagy (literally, ‘self-digestion’), also plays key roles in a variety of biological processes such as development and aging, and is often perturbed in various diseases. Even though tight control of autophagy is key to survival, relatively little is known about the signaling molecules that regulate this essential process.

Sanford-Burnham researchers have made important progress in addressing this gap in knowledge by discovering that proteins called STK3 and STK4 regulate autophagy across diverse species. As reported recently in Molecular Cell, the newly identified mode of autophagy regulation could potentially have important clinical implications for the treatment of a broad range of diseases, including cancer, diabetes, Alzheimer’s disease, cardiac dysfunction, and immune-related diseases.

“Our discovery is fundamental to our molecular understanding of how autophagy is regulated,” said senior study author Malene Hansen, PhD, associate professor of the Development, Aging, and Regeneration Program at Sanford-Burnham. “Because impairment in the autophagy process has been linked to many disorders in humans, we believe that pharmacological agents targeting this novel regulatory circuit may hold great therapeutic potential.”

Critical kinases

Autophagy is a cellular recycling process involving a highly intricate and complex series of events. Cellular components such as abnormal molecules or damaged organelles are first sequestered within vesicles known as autophagosomes. These vesicles then fuse with organelles called lysosomes, which contain enzymes that break down various molecules. This fusion process results in the formation of hybrid organelles called autolysosomes, where the defective cellular components are enzymatically degraded and recycled. A protein called LC3 plays crucial roles in the formation of autophagosomes and the recruitment of dysfunctional cellular components to these vesicles. The signaling events that coordinate LC3’s various functions in autophagy have not been clear, but new research from the Hansen lab now proposes a novel and essential role for the mammalian Hippo kinases STK3 and STK4 in regulating autophagy by targeting LC3 for phosphorylation.

In their study, Hansen and her team describe that deficiency in both STK3 and STK4 impairs autophagy not just in mammalian cells, but also in nematodes and yeast. When exploring how the kinases regulate autophagy in mammalian cells, the researchers discovered that phosphorylation of LC3 by STK3 and STK4, specifically on the amino acid threonine 50, is critical for fusion between autophagosomes and lysosomes—an essential step in the autophagy process. “Collectively, the results of this study strongly support a critical and evolutionarily conserved role for STK3 and STK4 in regulating autophagy, by phosphorylating the key autophagy protein LC3, at least in mammalian cells,” Hansen said.

Killing bacteria

Previous studies have shown that STK4 also plays a role in regulating antibacterial and antiviral immunity in mammals, including humans. Moreover, autophagy is known to play a role in the clearance of intracellular pathogens. “These findings, taken together with our discovery that deficiency in STK3 and STK4 severely compromises autophagy, led us to test whether STK4 also plays a role in antimicrobial immunity through its function in autophagy,” said lead study author Deepti Wilkinson, Ph.D., a postdoctoral fellow in Hansen’s lab.

To test this notion, the researchers collaborated with Victor Nizet MD, professor of Pediatrics and Pharmacy  at UC San Diego and found that indeed mouse embryonic cells deficient in both STK3 and STK4 were unable to efficiently kill intracellular group A streptococci—bacteria known to be cleared by autophagy. However, an LC3 mutation that resulted in constant phosphorylation at threonine 50 restored the ability of the STK3/STK4-deficient cells to kill the bacteria. “This finding suggests that the same STK4-LC3 signaling pathway involved in autophagy also contributes to the response of mammalian cells to infection with intracellular pathogens and could play a role in human immune-related disease,” Wilkinson said.

Correcting defects

Moving forward, the researchers plan to further probe the molecular mechanisms by which STK3 and STK4 regulate autophagy. They will also investigate the therapeutic implications of the STK3/STK4 signaling pathway for tumor suppression as well as immune-related disorders such as bacterial and viral infections. “Understanding how autophagy works and why it sometimes stops to function optimally is essential for fighting diseases such as cancer, diabetes and neurodegeneration,” Hansen said.

“We have made a major contribution towards this endeavor by showing that STK3 and STK4 play an essential role in keeping the process of autophagy running smoothly by directly phosphorylating the key autophagy protein LC3. We hope our discoveries will lead to the development of effective drugs that can help correct autophagy defects that commonly occur in these diseases,” added Hansen.

A copy of the paper can be found at: http://www.ncbi.nlm.nih.gov/pubmed/25544559

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Sanford-Burnham researcher awarded American Federation for Aging Research award

Authorsgammon
Date

December 23, 2014

Malene Hansen, PhD, associate professor in our Development, Aging, and Regeneration Program has been awarded the Julie Martin Mid-Career Award in Aging Research. The award includes a new grant to continue her research in the field of aging. Hansen is a three-time American Federation for Aging Research (AFAR) grant recipient. AFAR’s grants are given to scientists at institutions nationwide based on hard work, ingenuity, and leadership that advance cutting-edge research to help us live healthier, longer lives. Continue reading “Sanford-Burnham researcher awarded American Federation for Aging Research award”