en
jalali
1397
5
1
gregorian
2018
8
1
7
3
online
1
fulltext
en
Simulated Microgravity Condition Alters the Gene Expression of some ECM and Adhesive Molecules in Adipose-Derived Stem Cells
Adipose-derived stem cells (ADSCs) are widely used for tissue engineering and regenerative medicine. The beneficial effects of ADSCs on wound healing have already been reported. Remodeling of extracellular matrix (ECM) is the most important physiological event during the wound healing. ECM is sensitive to mechanical stresses and the expression of its components can be therefore influenced. The aim of this study was to investigate the effect of simulated microgravity on the gene expression of some ECM and adhesion molecules in human ADSCs. After isolation and characterization of ADSCs, cells were exposed to simulated microgravity for 1, 3 and 7 days. Real-time PCR, fluorescence immunocytochemistry, and MTT assay were performed to evaluate the alterations of integrin subunit beta 1 (ITGB1), collagen type 3 (ColIII), matrix metalloproteinase-1 (MMP1), CD44, fibrillin (FBN1), vimentin (VIM) genes, and ColIII protein levels as well as cells viability. Microgravity simulation increased the expression of ITGB1, ColIII, MMP1, and CD44 and declined the expression of FBN1 and VIM genes. ColIII protein levels were also increased. There were no significant changes in the viability of cells cultured in microgravity. Since the high expression of ECM components is known as one of the fibroblast markers, our data suggest that pretreatment of ADSCs by simulated microgravity may increase their differentiation capacity towards fibroblastic cells. Microgravity had not adversely affected the viability of ADSCs, and it is likely to be used alone or in combination with biochemical inducers for cell manipulation.
Adipose derived stem cells, simulated microgravity, extracellular matrix, adhesion
146
157
http://ijmcmed.org/browse.php?a_code=A-10-1471-1&slc_lang=en&sid=1
2018/05/30
1397/3/9
2018/09/27
1397/7/5
Farid
Ebnerasuly
Department of Biology, Fars Science and Research Branch, Islamic Azad University, Marvdasht, Iran.
f_ebnerasuly@yahoo.com
00319475328460016161
00319475328460016161
No
Zahra
Hajebrahimi
Aerospace Research Institute, Ministry of Science Research and Technology, Tehran, Iran.
hajebrahimi@ari.ac.ir
00319475328460016162
00319475328460016162
Yes
Seyed Mehdi
Tabaie
Department of Photo Healing and Regeneration, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran.
smtabaie@yahoo.com
00319475328460016163
00319475328460016163
No
Mojtaba
Darbouy
Department of Biology, Fars Science and Research Branch, Islamic Azad University, Marvdasht, Iran.
m.darbouy@lycos.com
00319475328460016164
00319475328460016164
No
en
Stimulatory Effect of Indolic Hormone on As2O3 Cytotoxicity in Breast Cancer Cells: NF-κB-dependent Mechanism of Action of Melatonin
The advent of combination therapy unprecedentedly shifted the paradigm of cancer treatment by reconstructing the conventional protocols. By identifying the anti-tumoral activity for different natural products, recent interest has focused on inventing the combined-modality strategies in order to increase the cure rates of cancer, while reducing the toxic side effects of current intensive regimens. To evaluate whether melatonin, the indolic hormone produced mainly by the pineal gland, could enhance the pro-apoptotic effect of arsenic trioxide (As2O3) in breast cancer, MCF-7 cells were treated with As2O3-plus-melatonin and then the survival, proliferative rate, caspase-3 activity, and mRNA expression level of anti-apoptosis target genes of NF-κB were investigated. Our results delineated that exposure of MCF-7 cells to As2O3 not only reduced the survival of the cells but also induced a caspase-3-dependent apoptotic cell death. Noteworthy, an enhanced induction of apoptosis was found using As2O3 in combination with melatonin. Moreover, RQ-PCR analysis revealed that the enhanced cytotoxic effect of As2O3 in the presence of melatonin is mediated, at least partly, through suppressing the expression of NF-κB anti-apoptotic target genes such as MCL-1, BCL-2, survivin, XIAP, and c-IAP1 in breast cancer cells. The resulting data showed that As2O3, either alone or in combination with melatonin, exerted significant cytotoxic effect against MCF-7 cells. However, further investigations are needed to provide valuable clues for expediting this combination as a therapeutic strategy for breast cancer.
As2O3, Apoptosis, Combination therapy, Melatonin, NF-κB
158
168
http://ijmcmed.org/browse.php?a_code=A-10-1525-1&slc_lang=en&sid=1
2018/05/302018/07/23
1397/5/1
2018/09/272018/10/18
1397/7/26
AVa
Safaroghli-Azar
Student Research Committee, Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
ava_azari@yahoo.com
00319475328460012636
00319475328460012636
No
Atieh
Pourbagheri-Sigaroodi
Department of Biotechnology, Faculty of Advanced Sciences and Technology, Pharmaceutical Sciences Branch, Islamic Azad University (IAUPS), Tehran, Iran.
atips1991@gmail.com
00319475328460012637
00319475328460012637
No
Davood
Bashash
Department of Hematology and Blood banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
david_5980@yahoo.com
00319475328460012638
00319475328460012638
Yes
Elaheh
Nooshinfar
Cancer Research Center, Shohada Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
e_nooshinfar@yahoo.com
00319475328460012639
00319475328460012639
No
Ali
Anjam-Najmedini
Student Research Committee, Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
alianjam1371@yahoo.com
00319475328460012640
00319475328460012640
No
Soroush
Sadeghi
Student Research Committee, Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
S.sadeghi@yahoo.com
00319475328460012641
00319475328460012641
No
Mostafa
Rezaie-Tavirani
Proteomics Research Center, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
rezaei.tavirani@ibb.ut.ac.ir.
00319475328460012642
00319475328460012642
No
Mohammad Esmaeil
Akbari
Cancer Research Center, Shohada Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
me-akbari@sbmu.ac.ir
00319475328460012643
00319475328460012643
No
en
The Expression of Inflammatory-Related NFκB Genes in Iranian Patients with Pterygium: A Case-Control Study
Pterygium is one of the most common eye conditions without any clear etiology. Some studies have suggested an association between sun exposure and pterygium, but others have proposed the role of genetic variations in its pathogenesis. To date, no study has investigated the association of inflammatory transcription factor, NFκB genes with pterygium in the Middle East. We examined the changes in expression of 3 inflammatory related NFκB1, NFκB2, and RELA genes in patients with pterygium. Thirty patients with pterygium and 30 age and sex-matched controls were enrolled in this case-control study. None of the participants showed any clinical signs of inflammation in their conjunctiva. Demographic information was obtained and the expression levels of three genes including NFκB1, NFκB2, and RELA were measured in their conjunctiva by real-time RT-PCR using gene-specific primers. Mean expression level of NFκB1, NFκB2 and RELA genes in patients were 2.4±0.3, 1.9± 0.5, and 1.8±0.4 times higher than normal subjects, respectively. Higher levels of gene expression were observed in individuals with more outdoor activity and sun exposure. Moreover, a significant correlation was observed between the expression levels of NFκB2 and RELA genes, suggesting a possible NFκB2- RELA heterodimer formation in patients with pterygium. This study has indicated a significant association between expressions of inflammatory-related NFκB1, NFκB2 and RELA genes, and pterygium. Further studies to verify the role of inflammation in the pathogenesis of pterygium, may provide new targets for managing pterygia.
Pterygium, inflammation, gene expression, NF-kappa B, real-time RT-PCR
169
175
http://ijmcmed.org/browse.php?a_code=A-10-1389-2&slc_lang=en&sid=1
2018/05/302018/07/232018/06/15
1397/3/25
2018/09/272018/10/182018/10/18
1397/7/26
Seyed Mohammad Salar
Zaheryani
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
smszaheryany@gmail.com
00319475328460016165
00319475328460016165
No
Mohammad Essmail
Ebrahimi
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
esmaeil.m.ebr@gmail.com
00319475328460016166
00319475328460016166
No
Abdollah
Kasaei
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
kasaei_ali@yahoo.com
00319475328460016167
00319475328460016167
No
Amir
roointan
Department of Medical Biotechnology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical sciences, Shiraz, Iran.
a.roointan@outlook.com
00319475328460016168
00319475328460016168
No
Mahmood
Nejabat
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
nejabatm@sums.ac.ir
00319475328460016169
00319475328460016169
Yes
Mehdi
Dianatpour
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
mdianatpur@gmail.com
00319475328460016170
00319475328460016170
No
Meisam
Ghanbari
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
meisam.ghanbari@gmail.com
00319475328460016171
00319475328460016171
No
Mohammad Reza
Talebnejad
Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
talebnejadmr@yahoo.com
00319475328460016172
00319475328460016172
No
Fakhraddin
Naghibalhossaini
Biochemistry Department, Shiraz University of Medical Sciences, Shiraz, Iran.
fakhraddin.naghibalhossaini@mail.mcgill.ca
00319475328460016173
00319475328460016173
No
en
Effects of Resveratrol on FOXO1 and FOXO3a Genes Expression in Adipose Tissue, Serum Insulin, Insulin Resistance and Serum SOD Activity in Type 2 Diabetic Rats
Induced oxidative stress in diabetes mellitus (DM) plays a critical role in insulin resistance. Fork head-related transcription factor (FOXO) proteins are important transcriptional factors involved in oxidative stress and insulin resistance. Resveratrol (RSV) is a polyphenol with hypoglycemic and antioxidant properties. The aims of the present study were to examine the effects of RSV on FOXO gene expression, serum superoxide dismutase (SOD) activity, insulin level, and insulin resistance in type 2 diabetic (T2DM) rats. Thirty male Wistar rats were used in this study. DM was induced in rats (n=24) using streptozotocin (STZ) and nicotinamide; then, they were divided into 4 groups of 6 rats each. Six untreated normal rats were used as normal control group; diabetic rats in groups 2 to 5 were treated with 0, 1, 5 and 10 mg /kg body weight of RSV, respectively for 30 days. At the end of the experimental period, the rats were sacrificed, their sera were separated, and adipose tissues were obtained and stored at −80 °C. Serum glucose and SOD activity levels were determined biochemically, and serum insulin level was determined by ELISA method. Gere expression in FOXO1 and FOXO3a in adipose tissue was evaluated using real‐time PCR. Results indicated that RSV significantly reduced blood glucose level, increased insulin level and improved insulin sensitivity. RSV resulted in an increased serum SOD activity and caused decreased FOXO1 and FOXO3a expression in adipose tissue of rats with T2DM. Therefore, by attenuation of FOXO expression in adipose tissue of T2DM rats, RSV showed a hypoglycemic potential and antioxidant properties, and consequently ameliorated insulin resistance.
Oxidative stress, diabetes mellitus, FOXO, insulin resistance, resveratrol, superoxide dismutase
176
184
http://ijmcmed.org/browse.php?a_code=A-10-406-3&slc_lang=en&sid=1
2018/05/302018/07/232018/06/152018/09/2
1397/6/11
2018/09/272018/10/182018/10/182018/11/12
1397/8/21
Soheila
Asadi
Department of Clinical Biochemistry, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
sohila.asadi75@yahoo.com
00319475328460016174
00319475328460016174
No
Zohreh
Rahimi
Department of Clinical Biochemistry, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Rahimizus@yahoo.com
00319475328460016175
00319475328460016175
No
Massoud
Sadijam
Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Sjam110@yahoo.com
00319475328460016176
00319475328460016176
No
Nooshin
Shabab
Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
nnshabab2@gmail.com
00319475328460016177
00319475328460016177
No
Mohammad Taghi
Goodarzi
Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
mtgoodarzi@yahoo.com
00319475328460016178
00319475328460016178
Yes
en
Inhibition of Interleukin-1 Receptor-Associated Kinases 1/4, Increases Gene Expression and Serum Level of Adiponectin in Mouse Model of Insulin Resistance
Insulin resistance is a feature of most patients with type 2 diabetes mellitus. Epidemiological evidence suggests a correlation between inflammation and insulin resistant states such as obesity, but the underlying mechanisms are largely unknown. Interleukin-1 receptor-associated kinases (IRAK) play a central role in inflammatory responses by regulating the expression of various inflammatory genes in immune cells. This study was aimed to investigate the effect of IRAK inhibitor on gene transcription and serum concentration of adiponectin in insulin-resistant mice. Experimental mice were randomly divided into 6 groups: the healthy control group was fed a regular chow diet while other groups were fed with a high-fat diet for 12 weeks. After this period, animals were treated with IRAK inhibitor, pioglitazone, both IRAK and pioglitazone, and DMSO, for two weeks. Adiponectin gene expression level was analyzed by real-time PCR. Additionally, serum adiponectin levels were measured by ELISA. Homeostasis model assessment-adiponectin (HOMA-AD) as an insulin sensitivity index was calculated. IRAK inhibitor and pioglitazone increased significantly the expression of adiponectin gene. Also, adiponectin concentration in the control group (9.67±1.1 μg/ml) increased to 25.34±2.04 μg/ml in pioglitazone treatment group. IRAK inhibitor also increased adiponectin concentration (18.24±1.53 μg/ml) but did not show a synergistic effect with pioglitazone when administered simultaneously (26.66±2.5 μg/ml). HOMA-AD was 0.33±0.04 in the pioglitazone-treated group, 0.6±0.13 in IRAK inhibitor group, and 0.31±0.03 in animals that received IRAKi and pioglitazone. Our findings suggest that increased adiponectin secretion from adipose tissue mediated by IRAK inhibitor may increase the insulin sensitivity in an animal model of insulin resistance.
Insulin resistance, Inflammation, Adiponectin, IRAK inhibitor
185
192
http://ijmcmed.org/browse.php?a_code=A-10-1561-1&slc_lang=en&sid=1
2018/05/302018/07/232018/06/152018/09/22018/08/17
1397/5/26
2018/09/272018/10/182018/10/182018/11/122018/10/8
1397/7/16
Athena
Rajaie
Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
a.rajaienejad@gmail.com
00319475328460016179
00319475328460016179
No
Mostafa
Allahyari
Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
mostafa.allah1993@gmail.com
00319475328460016180
00319475328460016180
No
Mahdieh
Nazari-Robati
Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
mn_robati@yahoo.com
00319475328460016181
00319475328460016181
No
Hossein
Fallah
Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
hf59ma@gmail.com
00319475328460016182
00319475328460016182
Yes
en
Metformin Protects Against Radiation-Induced Heart Injury and Attenuates the Up-regulation of Dual Oxidase Genes Following Rat’s Chest Irradiation
Radiation-induced heart toxicity is one of the serious side effects after a radiation disaster or radiotherapy for patients with chest cancers, leading to a reduction in the quality of life of the patients. Evidence has shown that infiltration of inflammatory cells plays a key role in the development of functional damages to the heart via chronic up-regulation of some pro-fibrotic and pro-inflammatory cytokines. These changes are associated with continuous free radical production and increased stiffness of heart muscle. IL-4 and IL-13 are two important pro-fibrotic cytokines which contribute to the side effects of exposure to ionizing radiation. Recent studies have proposed that IL-4 through upregulation of DUOX2, and IL-13 via stimulation of DUOX1 gene expression, are involved in the development of late effects of radiation. In the present study, we aimed to detect changes in the expression of these pathways following irradiation of rat’s heart. Furthermore, we evaluated the possible protective effect of metformin on the development of these abnormal changes. 20 male rats were divided into 4 groups (control, radiation, metformin-treated, metformin + radiation). These rats were irradiated with 15 Gy 60Co gamma rays and sacrificed after 10 weeks for evaluation of the changes in the expression of IL4R1, IL-13R2a, DUOX1, and DUOX2. In addition, the levels of IL-4 and IL-13 cytokines, as well as infiltration of macrophages and lymphocytes were detected. Results showed an upregulation of both DUOX1 and DUOX2 pathways in the presence of metformin, while the level of IL-13 did not show any significant change. This was associated with infiltration of macrophages and lymphocytes. Also, treatment with metformin could significantly attenuate the accumulation of inflammatory cells, and upregulate these pathways. Therefore, suppression of dual oxidase genes by metformin may be a contributory factor to its protective effect.
Radiation, metformin, heart Injury, IL-4, IL-13, DUOX1, DUOX2
193
202
http://ijmcmed.org/browse.php?a_code=A-10-1547-1&slc_lang=en&sid=1
2018/05/302018/07/232018/06/152018/09/22018/08/172018/08/12
1397/5/21
2018/09/272018/10/182018/10/182018/11/122018/10/82018/10/5
1397/7/13
Rasoul
Yahyapour
School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.
00319475328460016183
00319475328460016183
No
Peyman
Amini
Department of Radiology, Faculty of Paramedical, Tehran University of Medical Sciences, Tehran, Iran.
00319475328460016184
00319475328460016184
No
Hana
Saffar
Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran.
00319475328460016185
00319475328460016185
No
Saeed
Rezapoor
Department of Radiology, Faculty of Paramedical, Tehran University of Medical Sciences, Tehran, Iran.
00319475328460016186
00319475328460016186
No
Elahe
Motevaseli
Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
00319475328460016187
00319475328460016187
No
Mohsen
Cheki
Department of Radiologic Technology, Faculty of Paramedicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
00319475328460016188
00319475328460016188
No
Bagher
Farhood
Departments of Medical Physics and Radiology, Faculty of Paramedical Sciences, Kashan University of Medical Sciences, Kashan, Iran.
00319475328460016189
00319475328460016189
No
Farzad
Nouruzi
Department of Medical Radiation Engineering, Science and Research Branch, Islamic Azad University, Tehran, Iran.
00319475328460016190
00319475328460016190
No
Dheyauldeen
Shabeeb
Department of Medical Physics and Biomedical Engineering, Faculty of Medicine, Tehran University of Medical Sciences (International Campus), Tehran, Iran; Department of Physiology, College of Medicine, University of Misan, Misan, Iraq.
00319475328460016191
00319475328460016191
No
Ahmed Eleojo
Musa
Department of Medical Physics and Biomedical Engineering, Faculty of Medicine, Tehran University of Medical Sciences (International Campus), Tehran, Iran; Research center for molecular and cellular imaging, Tehran University of Medical Sciences (International Campus), Tehran, Iran.
00319475328460016192
00319475328460016192
No
Masoud
Najafi
Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran.
najafi_ma@yahoo.com
00319475328460016193
00319475328460016193
Yes