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Epigenetic Reprogramming Induced Pluripotency Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 2 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i2.139

BACKGROUND: The ability to reprogram mature cells to an embryonic-like state by nuclear transfer or by inducing the expression of key transcription factors has provided us with critical opportunities to linearly map the epigenetic parameters that are essential for attaining pluripotency.CONTENT: Epigenetic reprogramming describes a switch in gene expression of one kind of cell to that of another unrelated cell type. Early studies in frog cloning provided some of the first experimental evidence for reprogramming. Subsequent procedures included mammalian somatic cell nuclear transfer, cell fusion, induction of pluripotency by ectopic gene expression, and direct reprogramming. Through these methods it becomes possible to derive one kind of specialized cell (such as a brain cell) from another, more accessible tissue, such as skin in the same individual. This has potential applications for cell replacement without the immunosuppression treatments commonly required when cells are transferred between genetically different individuals.SUMMARY: Reprogramming with transcription factors offers tremendous promise for the future development of patient-specific pluripotent cells and for studies of human disease. The identification of optimized protocols for the differentiation of iPS cells and ES cells into multiple functional cell types in vitro and their proper engraftment in vivo will be challenged in the coming years. Given that the first small molecule approaches aimed at activating pluripotency genes have already been devised and that murine iPS cells have recently been derived by using non-integrative transient expression strategies of the reprogramming factors, we expect that human iPS cells without permanent genetic alterations will soon be generated.KEYWORDS: epigenetics, reprogramming, pluripotency, stem cells, iPS cells, chromatin, DNA methylation

Inflammation and Atherosclerosis: Current Pathogenesis Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 2 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i2.165

BACKGROUND: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown.CONTENT: Chronic inflammation is recognized as a major driving force in atherogenesis. The sites of atherosclerotic plaque development in the arterial wall are characterized by cholesterol accumulation and infiltration of peripheral blood monocytes, which gradually differentiate into macrophages. Cholesterol crystals, the common constituents of atherosclerotic lesions, include NLRP3 inflammasome activation and IL-1β secretion in human macrophages, promote an inflammatory milieu and thus drive lesion progression. Consequently, the cholesterol crystal-induced inflammasome activation may represent an important link between cholesterol metabolism and inflammation in atherosclerotic lesions. SUMMARY: The crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation. The cholesterol crystal-induced inflammasome activation in macrophages may represent an important link between cholesterol metabolism and inflammation in atherosclerotic lesions. This finding provides new insights into the pathogenesis of atherosclerosis and indicates new potential molecular targets for the therapy of this disease.KEYWORDS: atherosclerosis, inflammation, neutrophil, macrophages, inflammasome, cholesterol crystal

Novel Sources of Fetal Stem Cells for Future Regenerative Medicine Yani Lina; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 1 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i1.155

BACKGROUND: Mesenchymal stromal cells are multipotent cells considered to be of great promise for use in regenerative medicine. However, the cell dose may be a critical factor in many clinical conditions and the yield resulting from the ex vivo expansion of mesenchymal stromal cells derived from bone marrow may be insufficient. Thus, alternative sources of mesenchymal stromal cells need to be explored.CONTENT: There are multiple extra-embryonic tissues emerging during gestation including umbilical cord blood (UCB), amniotic fluid (AF), Wharton’s jelly, the amniotic membrane and the placenta, which are all discarded following birth. Fetal stem cells from these sources actually represent a new class of stem cells developmentally and operationally located between the state of embryonic stem cells and adult stem cells, sharing and exhibiting features of pluripotency and multipotency, without necessarily implying that they can generate every type of tissue.SUMMARY: Fetal stem cells have been recently isolated from several tissues (amniotic fluid, umbilical cord, Wharton’s jelly, amnion and placenta). They are derived either from the fetus proper or from the supportive extra-embryonic structures. They represent ideal sources for regenerative medicine since they are easily accessible, exhibit high proliferation rates, do not form teratomas and present no ethical reservations like embryonic stem cells (ESC). Their functional features indicate that they actually represent intermediates between ESC and adult stem cells.KEYWORDS: mesenchymal stem cells, fetal stem cells, amniotic fluid, umbilical cord, placenta, wharton’s jelly

The Stem Cell Hypothesis of Aging Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 2, No 1 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i1.108

BACKGROUND: There is probably no single way to age. Indeed, so far there is no single accepted explanation or mechanisms of aging (although more than 300 theories have been proposed). There is an overall decline in tissue regenerative potential with age, and the question arises as to whether this is due to the intrinsic aging of stem cells or rather to the impairment of stem cell function in the aged tissue environment.CONTENT: Recent data suggest that we age, in part, because our self-renewing stem cells grow old as a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such as changes in their supporting niches. Mechanisms that suppress the development of cancer, such as senescence and apoptosis, which rely on telomere shortening and the activities of p53 and p16INK4a may also induce an unwanted consequence: a decline in the replicative function of certain stem cells types with advancing age. This decrease regenerative capacity appears to pointing to the stem cell hypothesis of aging.SUMMARY: Recent evidence suggested that we grow old partly because of our stem cells grow old as a result of mechanisms that suppress the development of cancer over a lifetime. We believe that a further, more precise mechanistic understanding of this process will be required before this knowledge can be translated into human anti-aging therapies.KEYWORDS: stem cells, senescence, telomere, DNA damage, epigenetic, aging

Adipose Tissue Biology: An Update Review Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.98

BACKGROUND: Obesity is a major health problem in most countries in the world today. It increases the risk of diabetes, heart disease, fatty liver and some form of cancer. Adipose tissue biology is currently one of the “hot” areas of biomedical science, as fundamental for the development of novel therapeutics for obesity and its related disorders.CONTENT: Adipose tissue consist predominantly of adipocytes, adipose-derived stromal cells (ASCs), vascular endothelial cells, pericytes, fibroblast, macrophages, and extracellular matrix. Adipose tissue metabolism is extremely dynamic, and the supply of and removal of substrates in the blood is acutely regulated according to the nutritional state. Adipose tissue possesses the ability to a very large extent to modulate its own metabolic activities including differentiation of new adipocytes and production of blood vessels as necessary to accommodate increasing fat stores. At the same time, adipocytes signal to other tissue to regulate their energy metabolism in accordance with the body's nutritional state. Ultimately adipocyte fat stores have to match the body's overall surplus or deficit of energy. Obesity causes adipose tissue dysfunction and results in obesity-related disorders.SUMMARY: It is now clear that adipose tissue is a complex and highly active metabolic and endocrine organ. Undestanding the molecular mechanisms underlying obesity and its associated disease cluster is also of great significance as the need for new and more effective therapeutic strategies is more urgent than ever. KEYWORDS: Obesity, Adipocyte, Adipose, Tissue, Adipogenesis, Angiogenesis, Lipid Droplet, Lipolysis, Plasticity, Dysfunction

GFAP and S100B Protein are Associated with Discharged NIHSS of Anterior Circulation Ischemic Stroke Yenny Surjawan; Suryani As'ad; Teguh A S Ranakusuma; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 2 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i2.170

BACKGROUND: Patient with larger ischemic lesion will suffer more severe neurogical deficit. The utility of MRI for lesion size measurement is still limited, therefore additional approach was pursued through examination of markers released by damaged brain cell, GFAP and S100B protein. The aim of this study is to know whether both markers are associated with the neurological deficit of anterior circulation ischemic stroke. METHODS: This observational prospective study enrolled 74 patients with anterior circulation ischemic stroke diagnosis. GFAP and S100B protein were measured with ELISA using blood collected at 48 to 72 hours after onset. The neurological deficit was assessed with NIHSS ad discharged.RESULTS: There was a significant association between GFAP level and discharged NIHSS (p=0.008) with 100% sensitivity and 100% negative predictive value. S100B protein also showed a significant correlation with discharged NIHSS (r=0.488; p=0.000) and this correlation could be described with an equation (OR=1.009; 95% CI=1.0003-1.0188; p=0.044). S100B protein at 78.3215 ng/L would give true prediction as 73.9% (95% CI=62.7%-85.2%, p=0.001). CONCLUSIONS: GFAP and S100B protein that were measured at 48 to 72 hours after onset were significantly associated with NIHSS at discharge. KEYWORDS: GFAP, S100B protein, discharged NIHSS, ischemic stroke

25(OH)D was Correlated with Increased Risk of Insulin Resistance, but Not Mediated by Adiponectin and hsCRP Anggi Kartikawati; Yani Lina; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 2 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i2.166

BACKGROUND: Studies have shown that change of calcium and vitamin D homeostasis is associated with insulin resistance, decreased beta cell function, metabolic syndrome, glucose intolerance and diabetes. Evidence suggests that vitamin D insufficiency is inversely related to risk of metabolic disorders including type-2 Diabetes Mellitus (T2DM), although the underlying mechanisms are not yet understood. Hence, current study was conducted to investigate correlation between 25(OH)D and insulin resistance through adiponectin or High Sensitivity C-Reactive Protein (hsCRP) in centrally obese men.METHODS: This was a cross-sectional study involving 80 centrally obese men with waist circumference (WC) >90 cm and age 30-60 years. Total 25(OH)D concentration was measured by Enzyme-Linked Immunosorbent Assay (ELISA) method. Insulin resistance was calculated by HOMA model.RESULTS: This study showed there was no correlation of 25(OH)D-WC (r=0.006 and p=0.957), 25(OH)D-adiponectin (r=0.179 and p=0.111) abd 25(OH)D-hsCRP (r=-0.223 and p=0.334), but we observed statistically significant negative correlation between 25(OH)D and insulin resistance index (HOMA-IR) (r=0.461 and p=0.041).CONCLUSIONS: We conclude that low 25(OH)D concentration was significantly associated with increased risk of insulin resistance. Since the adiponectin or hsCRP was not correlated, the possible pathways need to be futher investigated.KEYWORDS: central obesity, 25(OH)D, adiponectin, hsCRP, insulin resistance (HOMA-IR)

MicroRNAs in Obesity, Metabolic Syndrome and Diabetes Mellitus Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 1 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i1.130

BACKGROUND: MicroRNAs (miRNAs) are small regulatory RNAs that play important roles in development of diseases. Several studies have provided evidences showing that miRNAs affect pathways that are fundamental for metabolic control in adipocyte and skeletal muscle differentiations. Some miRNAs have been implicated in lipid, amino acid, and glucose homeostasis. This leads to the possibility that miRNAs may contribute to common metabolic diseases and point to novel therapeutic opportunities based on targeting of miRNAs.CONTENT: miRNAs have been recognized as a class of epigenetic regulators of metabolism and energy homeostasis, primarily because the simultaneous regulation of a large number of target genes can be accomplished by a single miRNA. Emerging evidences suggest that miRNAs play a key role in the pathological development of obesity by affecting adipocyte differentiation. miRNAs have been implicated as novel protagonists in the pathogenesis of Diabetes Mellitus (DM), regulation of insulin production, secretion and action. They also appear to play a role in the development of diabetic complications such as nephropathy and cardiac hypertrophy.SUMMARY: Involvement of miRNAs in glucose and lipid metabolism has provided strong evidences to confirm their roles as key players in regulation of complex metabolic pathways. Additionally, it indicates potential outlook for novel therapeutic strategies in the management of obesity, metabolic syndrome and DM. Further research in this field is needed to ascertain the full potential of miRNAs as novel metabolic biomarkers and potent therapeutic agents against obesity and its metabolic disorders.KEYWORDS: obesity, metabolic syndrome, diabetes, miRNAs, adipogenesis, insulin, pancreatic cells

Mitochondrial Dysfunction in Metabolic Disease Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 3 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i3.172

BACKGROUND: Mitochondrial function and behavior are central to the physiology of humans and, consequently, "mitochondrial dysfunction" has been implicated in a wide range of disease.CONTENT: Mitochondrial ROS might attack various mitochondrial constituents, causing mitochondrial DNA mutations and oxidative damage to respiratory enzymes. A defect in mitochondrial respiratory enzymes would increase mitochondrial production of ROS, causing further mitochondrial damage and dysfunction. Mitochondrial dysfunction is associated with diseases, such as neurodegenerative disorders, cardiomyopathies, metabolic syndrome, obesity, and cancer. Pathways that improve mitochondrial function, attenuate mitochondrial oxidative stress, and regulate mitochondrial biogenesis have recently emerged as potential therapeutic targets.SUMMARY: Mitochondria perform diverse yet interconnected functions, produce ATP and many biosynthetic intermediates while also contribute to cellular stress responses such as autophagy and apoptosis. Mitochondria form a dynamic, interconnected network that is intimately integrated with other cellular compartments. It is therefore not suprising that mitochondrial dysfunction has emerged as a key factor in a myriad of diseases, including neurodegenerative, cancer, and metabolic disorders. Interventions that modulate processes involved in regulation of mitochondrial turnover, with calorie restriction and induction of mitochondrial biogenesis, are of particular interest.KEYWORDS: mitochondrial biogenesis, mitochondrial dysfunction, reactive oxygen species (ROS), metabolic diseases

Gut Hormones and Energy Balance, The Future for Obesity Therapy? Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.99

BACKGROUND: The prevalence of obesity is increasing in both developed and developing countries along with associated diseases such as type 2 diabetes and coronary heart disease. The recent discovery of a number of gut hormones that play a role in appetite regulation and are released or suppressed in response to a meal may offer new targets for the treatments of obesity.CONTENT: In addition to the obvious role of the gut in the digestion and absorption of nutrient, the intestine and associated visceral organs, including the pancreas, liver, and visceral adipose depots, have important sensing and signaling roles in the regulation of energy homeostatis. Signals reflecting energy stores, recent nutritional state, and other parameters are integrated in the central nervous system, particularly in the hypotalamus, to coordinate energy intake and expenditure.SUMMARY: Our understanding of the role of the gut in energy balance and insights into gut-derived signals will stimulate previously unexplored therapeutics for obesity and other disorders of energy balance.KEYWORDS: obesity, energy, balance, gut hormones, satiation, satiety

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