A. Chouw, R. Triana, Nurrani Mustika Dewi, S. Darmayanti, Miftakh Nur Rahman, Ardian Susanto, Bayu Winata Putera, C. R. Sartika
Stroke is a leading cause of death and long-term disability. This due to the ischemic event that cause by embolism of blockage blood flow. Thrombolytic agent plasminogen activator (tPA) is the only treatment approved by FDA. However, the used of tPA is limited to the short time window period. Neural stem cells (NSCs) show the potential to repair neuronal damage naturally after stroke. However, isolating NSCs is a challenging process due to the limitations of the method and its invasiveness. Some studies that had used mesenchymal stem cell (MSCs) as the main source of stem cell for therapy show that MSCs have the potency to differentiate into NSCs. in vitro, a differentiation process from MSC to NSC has been developed by combining the supplement or growth factor needed in the culture media.Keywords: stem cells, neuron stem cell, mesenchymal stem cell, stroke, trans-differentiation
{"title":"Ischemic Stroke: New Neuron Recovery Approach with Mesenchymal and Neural Stem Cells","authors":"A. Chouw, R. Triana, Nurrani Mustika Dewi, S. Darmayanti, Miftakh Nur Rahman, Ardian Susanto, Bayu Winata Putera, C. R. Sartika","doi":"10.21705/MCBS.V2I2.28","DOIUrl":"https://doi.org/10.21705/MCBS.V2I2.28","url":null,"abstract":"Stroke is a leading cause of death and long-term disability. This due to the ischemic event that cause by embolism of blockage blood flow. Thrombolytic agent plasminogen activator (tPA) is the only treatment approved by FDA. However, the used of tPA is limited to the short time window period. Neural stem cells (NSCs) show the potential to repair neuronal damage naturally after stroke. However, isolating NSCs is a challenging process due to the limitations of the method and its invasiveness. Some studies that had used mesenchymal stem cell (MSCs) as the main source of stem cell for therapy show that MSCs have the potency to differentiate into NSCs. in vitro, a differentiation process from MSC to NSC has been developed by combining the supplement or growth factor needed in the culture media.Keywords: stem cells, neuron stem cell, mesenchymal stem cell, stroke, trans-differentiation","PeriodicalId":53387,"journal":{"name":"MCBS Molecular and Cellular Biomedical Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82047024","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}
Background: Survivin, a member of the inhibitor of apoptosis protein family, has been associated with protection from cell apoptosis and regulation of mitosis. Phosphorylated-Survivin at Ser81 was reported to provide cytoprotection against tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in L929 cells by inducing a backloop activation of phosphatidylinositol 3-kinase (PI3K). Therefore Akt as a possible substrate of PI3K was investigated.Methods: L929 cells were pretreated with/without 50 μM LY294002 or 10 μM Perifosine, and infected with viral particle of Survivin, anti sense of Survivin, Ser81Ala mutated Survivin or vector only. Cells were then harvested, lysed and subjected to immunoblot assay to detect Akt, phosphorylated Akt (Ser473), mammalian target of rapamycin (mTOR), phosphorylated-mTOR (Ser2448).Results: Survivin induced Akt and mTOR phosphorylations in a viral particle concentration dependent manner. Pretreatment of LY294002 or Perifosine prior to Survivin infection, attenuated Akt or mTOR phosphorylations, respectively. Low Akt or mTOR phosphorylations were observed when L929 cells were infected with Ser81Ala mutated Survivin.Conclusion: Ser81 phosphorylation site of Survivin played an important role in activating Survivin/PKA/PI3K/Akt/mTOR signaling pathway.Keywords: survivin, Ser81, Akt, mTOR, LY294002, perifosine
{"title":"Survivin Ser81 Plays An Important Role in PI3K/Akt/mTOR Signaling Pathway","authors":"F. Sandra","doi":"10.21705/MCBS.V2I2.2","DOIUrl":"https://doi.org/10.21705/MCBS.V2I2.2","url":null,"abstract":"Background: Survivin, a member of the inhibitor of apoptosis protein family, has been associated with protection from cell apoptosis and regulation of mitosis. Phosphorylated-Survivin at Ser81 was reported to provide cytoprotection against tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in L929 cells by inducing a backloop activation of phosphatidylinositol 3-kinase (PI3K). Therefore Akt as a possible substrate of PI3K was investigated.Methods: L929 cells were pretreated with/without 50 μM LY294002 or 10 μM Perifosine, and infected with viral particle of Survivin, anti sense of Survivin, Ser81Ala mutated Survivin or vector only. Cells were then harvested, lysed and subjected to immunoblot assay to detect Akt, phosphorylated Akt (Ser473), mammalian target of rapamycin (mTOR), phosphorylated-mTOR (Ser2448).Results: Survivin induced Akt and mTOR phosphorylations in a viral particle concentration dependent manner. Pretreatment of LY294002 or Perifosine prior to Survivin infection, attenuated Akt or mTOR phosphorylations, respectively. Low Akt or mTOR phosphorylations were observed when L929 cells were infected with Ser81Ala mutated Survivin.Conclusion: Ser81 phosphorylation site of Survivin played an important role in activating Survivin/PKA/PI3K/Akt/mTOR signaling pathway.Keywords: survivin, Ser81, Akt, mTOR, LY294002, perifosine","PeriodicalId":53387,"journal":{"name":"MCBS Molecular and Cellular Biomedical Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85007405","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}
I. Aryana, Anak Agung Ayu Ratih Hapsari, R. Kuswardhani
The elderly population will increase as well as increasing life expectancy. Health problems in elderly will be more complex and need a comprehensive management. One of the problems that arise from the aging process is sarcopenia. Sarcopenia is a decreasing in muscle mass and muscle strength or muscle function caused by multifactorial not only due to aging process, but also nutrition, immobilization, genetics and others risk factors. Muscle is an endogen organ that produces various proteins that can affect the health system. This protein is referred to as myokine. Myokine is anti-inflammation cytokine and peptide produced by striated muscles. Physical activity results in myokine secretion that can reduce inflammation due to a sedentary lifestyle. Inflammation can lead to worsening sarcopenia and fat accumulation in striated muscles, thus reducing muscle mass, muscle strength and causing physical inactivity. The most of this type myokine have antiinflammation effect have work as autocrine, paracrine and endocrine. Chronic inflammation is a contributor that plays a role in the pathophysiology of various diseases including sarcopenia, it will protected by myokine. Myokine can affect the metabolism of glucose, fatty acids, angiogenesis, myogenesis, neurogenesis, and can explain the relationship between muscle, liver, fat, tissue and brain. Some knewn myokines include interleukin (IL)-6, IL-8, IL-5, brain-derived neurotrophic factor (BDNF), fibroblast growth factor 21 (FGF-21), leukemia Inhibitory factor (LIF), irisin and secreted protein acidic and rich in cysteine (SPARC). Physical exercise can induce myokine secretion from striated muscle to circulation. Through these mechanisms, myokine is expected to improve metabolism of glucose, fat and protein muscle, liver, fat, tissue, brain and reduce the incidence some comorbidity especially sarcopenia. Finally, it's will be decreasing of disability, morbidity and mortality rate in elderly.Keywords: myokine, sarcopenia, elderly
{"title":"Myokine Regulation as Marker of Sarcopenia in Elderly","authors":"I. Aryana, Anak Agung Ayu Ratih Hapsari, R. Kuswardhani","doi":"10.21705/MCBS.V2I2.32","DOIUrl":"https://doi.org/10.21705/MCBS.V2I2.32","url":null,"abstract":"The elderly population will increase as well as increasing life expectancy. Health problems in elderly will be more complex and need a comprehensive management. One of the problems that arise from the aging process is sarcopenia. Sarcopenia is a decreasing in muscle mass and muscle strength or muscle function caused by multifactorial not only due to aging process, but also nutrition, immobilization, genetics and others risk factors. Muscle is an endogen organ that produces various proteins that can affect the health system. This protein is referred to as myokine. Myokine is anti-inflammation cytokine and peptide produced by striated muscles. Physical activity results in myokine secretion that can reduce inflammation due to a sedentary lifestyle. Inflammation can lead to worsening sarcopenia and fat accumulation in striated muscles, thus reducing muscle mass, muscle strength and causing physical inactivity. The most of this type myokine have antiinflammation effect have work as autocrine, paracrine and endocrine. Chronic inflammation is a contributor that plays a role in the pathophysiology of various diseases including sarcopenia, it will protected by myokine. Myokine can affect the metabolism of glucose, fatty acids, angiogenesis, myogenesis, neurogenesis, and can explain the relationship between muscle, liver, fat, tissue and brain. Some knewn myokines include interleukin (IL)-6, IL-8, IL-5, brain-derived neurotrophic factor (BDNF), fibroblast growth factor 21 (FGF-21), leukemia Inhibitory factor (LIF), irisin and secreted protein acidic and rich in cysteine (SPARC). Physical exercise can induce myokine secretion from striated muscle to circulation. Through these mechanisms, myokine is expected to improve metabolism of glucose, fat and protein muscle, liver, fat, tissue, brain and reduce the incidence some comorbidity especially sarcopenia. Finally, it's will be decreasing of disability, morbidity and mortality rate in elderly.Keywords: myokine, sarcopenia, elderly","PeriodicalId":53387,"journal":{"name":"MCBS Molecular and Cellular Biomedical Sciences","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83518578","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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