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Journal Molecular and Cellular Biomedical Sciences

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Angliana Chouw, Rina Triana, Nurrani Mustika Dewi, Siska Darmayanti, Miftakh Nur Rahman, Ardian Susanto, Bayu Winata Putera, Cynthia Retna Sartika
Molecular and Cellular Biomedical Sciences, Volume 2, pp 48-54; doi:10.21705/mcbs.v2i2.28

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
Khairina Nasution, Imam Budi Putra, Nelva Karmila Jusuf
Molecular and Cellular Biomedical Sciences, Volume 2, pp 70-2; doi:10.21705/mcbs.v2i2.33

Abstract:Background: Acne vulgaris is a chronic inflammation of pilosebaceous follicle that can spontaneously heal with clinical manifestations such as blackhead, papules, pustules, nodule, and cyst on the face, upper chest, arms, and back. Until now, the effect of lipid metabolism on sebaceous gland secretions in the pathogenesis of acne vulgaris is still under research.Materials and Methods: An analytic observational study with cross sectional design involving 30 acne vulgaris and 30 control subjects was conducted. Blood samples were taken from subjects and lipid profile levels were measured. The data were then statistically analyzed.Results: From this research, there was no significant association between lipid profiles with acne vulgaris. There was not any significant difference between the acne vulgaris and the control subjects for total cholesterol, High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL) and triglyceride levels (p>0.05).Conclusion: There is no significant association between lipid profiles levels and acne vulgaris.Keywords: acne vulgaris, lipid profiles, total cholesterol, HDL, LDL, triglyceride
Ferry Sandra
Molecular and Cellular Biomedical Sciences, Volume 2, pp 55-9; doi:10.21705/mcbs.v2i2.2

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
I Gusti Putu Suka Aryana, Anak Agung Ayu Ratih Hapsari, Raden Ayu Tuty Kuswardhani
Molecular and Cellular Biomedical Sciences, Volume 2, pp 38-47; doi:10.21705/mcbs.v2i2.32

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
Wahyu Widowati, Diana Krisanti Jasaputra, Sutiman Bambang Sumitro, Mochammad Aris Widodo, Ervi Afifah, Rizal Rizal, Dwi Davidson Rihibiha, Hanna Sari Widya Kusuma, Harry Murti, Indra Bachtiar, et al.
Molecular and Cellular Biomedical Sciences, Volume 2, pp 60-9; doi:10.21705/mcbs.v2i2.21

Abstract:Background: Breast cancer (BC) is the leading cause of death cancer in women. Cancer therapies using TNFα and IFNγ have been recently developed by direct effects and activation of immune responses. This study was performed to evaluate the effects of TNFα and IFNγ directly, and TNFα and IFNγ secreted by Conditioned Medium-human Wharton’s Jelly Mesenchymal Stem Cells (CM-hWJMSCs) toward apoptosis of BC cells (MCF7).Materials and Methods: BC cells were induced by TNFα and IFNγ in 175 and 350ng/mL, respectively. CM-hWJMSCs were produced by co-culture hWJMSCs and NK cells that secreted TNFα, IFNγ, perforin (Prf1), granzyme B (GzmB) for treating BC cells. The BC cells were treated with CM-hWJMSCs in 50%. The expression of apoptotic genes Bax, p53, and the antiapoptotic gene Bcl-2 were determined using RT-PCR.Results: TNFα and IFNγ at concentration of 350 ng/mL induced higher Bax expression compared to 175 ng/mL. TNFα and IFNγ 350 ng/mL, 175 ng/mL induced p53 expression, whilst TNFα and IFNγ at 350 ng/mL decreased Bcl-2 expression. Perf1, GzmB, TNFα and IFNγ-containing CM-hWJMSCs induced significantly apoptosis percentage, induced Bax expression, but did not effect p53, Bcl-2 expression.Conclusion: TNFα and IFNγ directly induce Bax, p53, decrease Bcl-2 gene expression. The Prf1, GzmB, TNFα, IFNγ-containing CM-hWJMSCs induce apoptosis and Bax expression.Keywords: breast cancer, Wharton’s Jelly mesenchymal stem cells, TNFα, IFNγ
Daniel Gonzalez, Szeifoul Afadlal, Kristin Lizal, Yulius Hermanto, Takanori Miki, Yoshiki Takeuchi, Irawan Satriotomo
Molecular and Cellular Biomedical Sciences, Volume 2; doi:10.21705/mcbs.v2i1.11

Abstract:Background: It is known that eye enucleation causes various morphological and functional alterations in the central nervous system (CNS). The purpose of this study was to examine the sub-chronic effects of monocular enucleation on the distribution of the calcium binding proteins calbindin D28k (CB) and parvalbumin (PV) as well as the glial fibrillary acidic protein (GFAP) immunoreactivity in the superior colliculus (SC) of Wistar rats.Materials and Methods: Thirty young adult (8 weeks) male Wistar rats from SLC (Shizuoka, Japan), weighing 200-250 grams, were housed in separate cages under controlled conditions with a constant temperature kept in 12:12 light/dark cycle and ad libitum water and food. In this study the rats were divided into two groups, a control and an enucleated groups. The experimental group received unilateral eye enucleation and was allowed 1, 4 or 12 weeks recovery before sacrificed.Results: Unilateral enucleation over a period of 1 week or more caused a decrease in the number CB-immunoreactive (CBIR) neurons. This loss was associated with an increase in GFAP-IR astrocytes in the superficial gray layer and the optic layer of the SC with contralateral side predominance. In addition, the CB-IR neurons illustrated a smaller soma and poor dendritic arborization. Conversely, the GFAP-IR astrocytes were hypertrophied with longer foot processes on the contralateral side of enucleation. Interestingly, the number of PV-IR neurons was elevated for up to 4 weeks in enucleated rats versus shamoperated rats.Conclusion: This study demonstrates the importance of calcium-binding protein homeostasis and reversible glial response for maintaining variability of neuronal function in sub-cortical visual centers following optic nerve deafferentation.Keywords: enucleation, superior colliculus, calbindin D28k, parvalbumin, glial fibrillary acidic protein
Janti Sudiono, Sofia Thalib
Molecular and Cellular Biomedical Sciences, Volume 2; doi:10.21705/mcbs.v2i1.18

Abstract:Background: Angiogenesis is an important and fundamental process for new blood vessels to provide nutrients and oxygen needed by tumor cells to grow, develop, and in case of cancer also to metastasize into other organs. This study aims to evaluate the intensity of angiogenesis within benign (papillomas) and malignant (squamous cell carcinoma) epithelial tumors.Materials and methods: This analytic observational study with cross-sectional design using histopathology slide sample that were clinically diagnosed as squamous cell carcinoma (n=3) and papilloma (n=3). Microscopically, the angiogenesis characterized with lumen lined by endothelial cells with or without red blood cells inside within sub epithelial connective tissue of papilloma and squamous cell carcinoma by Hematoxylin Eosin stain. Angiogenesis intensity was counted from four areas under magnification of (10x10), each area was scored under (10x40) magnification.Results: Angiogenesis intensity of papilloma and squamous cell carcinoma are (45.17±14.573) and (55.18±6.26041) respectively. T-test analysis showed there was no significant difference (p=0.336>0.05).Conclusions: Angiogenesis intensity of papilloma is less than those of squamous cell carcinoma.Keywords: angiogenesis, oral epithelial tumor, benign, malignant
Kent Wijaya Setiawan, Ferry Sandra
Molecular and Cellular Biomedical Sciences, Volume 2; doi:10.21705/mcbs.v2i1.13

Abstract:Dynamic changes of naïve T cells determine mature T cells activity in cell-mediated immune response. It is important to understand the mechanism of homeostasis maintenance affect response to novel antigen toward T cell receptor-major histocompatibility complex interaction. Most of the analysis of naïve T cells relies on flow cytometric immunophenotyping to observe surface antigen alteration within maturation stage. The combination of different surface molecules, such as the cluster of differentiation 62L (CD62L), C-C chemokine receptor type 7 (CCR7), CD27, CD28, and CD45, can give satisfied discrimination between naïve T cells and other subsets. This parameter can be used to monitor the dynamic change of naïve T cells in some chronic diseases, like human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Most of the patient experience loss of naive T cells due to a chronic immune response, which related to apoptotic induction in proliferating cells by viral activity. Some pathogens trigger the migration of naive T cells into lymph nodes to facilitate direct contact with the host cells. The virus infects the cells, use cells proliferation to multiply, and induce apoptosis of host cells after the virions released. Alteration of naive T cells in chronic disease becomes a parameter to oversee the treatment and to determine the future prognosis of the disease. In highly active antiretroviral therapy for HIV infection, observation of naïve T cells and combination of surface molecules, CD45RO− and CD27+ is used to show the improvement and proliferation rate of total naïve T cells. On the other hand, the transformation of naïve T cells into CMV-specific T cells become really important in CMV prognosis. These conditions suggest that dynamic change of naïve T cells affect to the clinical condition of chronic disease patients.Keywords: naïve T cells, immunophenotyping, HIV, CMV
Ferry Sandra
Molecular and Cellular Biomedical Sciences, Volume 2; doi:10.21705/mcbs.v2i1.19

Abstract:Stem cell research has been developed and today we can witness some stem cell clinical trials are on going in Indonesia. To meet a successful stem cell treatment, several factors need to be considered, such as cell number. Cell number has been reported to be crucial, and therefore optimal cell number should be achieved. Meanwhile, in some circumstances, cell number is not enough, therefore, cell number should be enriched in an in vitro stem cell culture setting. In an in vitro stem cell culture, besides suitable and sterile equipment, reagents such as culture medium, serum and antibiotics are all important. Although all those criteria are fulfilled, somehow stem cell enrichment cannot be achieved, cell number is still below the target. Modification of stem cell microenvironment should then be an alternative. The addition of growth factors is a part of the strategies to reach a better enrichment. So that, stem cells could later be induced to proliferate at a higher rate. This strategy was then pursued by the scientist involved in herbal medicine. Herbal extracts were now highly investigated due to its potential to induce cell proliferation. Some herbal extracts inducing proliferation and differentiation of stem cell will be shown and described.Keywords: herbal extract, stem cell, progenitor cell, proliferation, differentiation
Ketherin Ketherin, Ferry Sandra
Molecular and Cellular Biomedical Sciences, Volume 2; doi:10.21705/mcbs.v2i1.16

Abstract:Osteoclast activities are responsible for the resorption of bone cells found in several bone diseases, one of which is periodontitis and arthritis. The downregulating signals of Receptor Activator of Nuclear Factor kB (RANK)-RANK Ligand and Tumor Necrosis Factor (TNF)-a are the major cause of the bone destruction. Studies and experiments have been performed to overcome this matter. Various medications are now available to treat bone-related diseases, targeting the specific aspect of the signaling. Synthetic drugs such as denosumab and bisphosphonates have complex pharmacological action and have been the leading choice in treatment. Evidence in studies proved that natural resources including herbal products have potential application to therapy for bone loss, with caffeic acid and Caffeic Acid Phenethyl Ester (CAPE) showing significant inhibitory results and Chinese herbs such as Herba epimedii (Yín Yáng Huò) and Fructus psoraleae(Bǔ Gǔ Zhī) proved to contain components that give similar effects to estrogen. The purpose of this review is to discuss the therapy value of available synthetic and natural therapeutic agents. Understanding the mechanisms of both agents will not only clarify their function as therapeutic agents, but can also be the key to the treatment of diseases caused by bone resorption by targeting specific aspects of osteoclastogenesis.Keywords: osteoclastogenesis, TNF, RANKL, bone resorption, natural resource, signaling, treatment
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