The Evaluation of Nerve Growth Factor Over Expression
on Neural Lineage Specific Genes in Human
Mesenchymal Stem Cells
CELL JOURNAL(Yakhteh)
Vol 18, No 2, Jul-Sep (Summer) 2016
ISI
1.27
Yousef Mortazavi, Ph.D.1, Fatemeh Sheikhsaran, M.Sc.1, Gholamreza Khamisipour, Ph.D.2*, Masoud Soleimani, Ph.D.3, Ali Teimuri, Ph.D.4, Somayeh Shokri, M.Sc.1
kنویسنده مسئول،3 از6
Objective: Treatment and repair of neurodegenerative diseases such as brain tumors,
spinal cord injuries, and functional disorders, including Alzheimer’s disease, are challenging
problems. A common treatment approach for such disorders involves the use of
mesenchymal stem cells (MSCs) as an alternative cell source to replace injured cells.
However, use of these cells in hosts may potentially cause adverse outcomes such as tumorigenesis
and uncontrolled differentiation. In attempt to generate mesenchymal derived
neural cells, we have infected MSCs with recombinant lentiviruses that expressed nerve
growth factor (NGF) and assessed their neural lineage genes.
Materials and Methods: In this experimental study, we cloned the NGF gene sequence
into a helper dependent lentiviral vector that contained the green fluorescent protein (GFP)
gene. The recombinant vector was amplified in DH5 bacterial cells. Recombinant viruses
were generated in the human embryonic kidney 293 (HEK-293) packaging cell line with
the helper vectors and analyzed under fluorescent microscopy. Bone marrow mesenchymal
cells were infected by recombinant viruses for three days followed by assessment of
neural differentiation. We evaluated expression of NGF through measurement of the NGF
protein in culture medium by ELISA; neural specific genes were quantified by real-time
polymerase chain reaction (PCR).
Results: We observed neural morphological changes after three days. Quantitative PCR
showed that expressions of NESTIN, glial derived neurotrophic factor (GDNF), glial fibrillary
acidic protein (GFAP) and Microtubule-associated protein 2 (MAP2) genes increased
following induction of NGF overexpression, whereas expressions of endogenous NGF
and brain derived neural growth factor (BDNF) genes reduced.
Conclusion: Ectopic expression of NGF can induce neurogenesis in MSCs. Direct injection
of MSCs may cause tumorigenesis and an undesirable outcome. Therefore an
alternative choice to overcome this obstacle may be the utilization of differentiated neural
stem cells.
دریافت فایل پیوست
http://celljournal.org/web/journal/article/abstract/4313
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Mechanisms of tumor cell resistance to the current
targeted-therapy agents
Tumor Biology
DOI 10.1007/s13277-016-5059-1 2016
ISI
2.6
Gholamreza Khamisipour1 & Farhad Jadidi-Niaragh2,3,4 & Abdolreza Sotoodeh Jahromi 5 & Keivan zandi 6 & Mohammad Hojjat-Farsangi 7,8
نفراول از 5
Abstract Resistance to chemotherapy agents is a major challenge
infront of cancer patient treatment and researchers. It is
known that several factors, such as multidrug resistance proteins
and ATP-binding cassette families, are cell membrane
transporters that can efflux several substrates such as chemotherapy
agents from the cell cytoplasm. To reduce the adverse
effects of chemotherapy agents, various targeted-based cancer
therapy (TBCT) agents have been developed. TBCT has revolutionized
cancer treatment, and several agents have shown
more specific effects on tumor cells than chemotherapies.
Small molecule inhibitors and monoclonal antibodies are specific
agents that mostly target tumor cells but have low side
effects on normal cells. Although these agents have been very
useful for cancer treatment, however, the presence of natural
and acquired resistance has blunted the advantages of targeted
therapies. Therefore, development of new options might be
necessary. A better understanding of tumor cell resistance
mechanisms to current treatment agents may provide an appropriate
platform for developing and improving new treatment
modalities. Therefore, in this review, different mechanisms
of tumor cell resistance to chemotherapy drugs and
current targeted therapies have been described.
دریافت فایل پیوست
http://link.springer.com/article/10.1007/s13277-016-5059-1
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Knockdown of microRNA-29a Changes the Expression of Heat Shock
Proteins in Breast Carcinoma MCF-7 Cells
Oncology Research
Vol. 23, pp. 69–78
ISI
3.927
Encieh Choghaei,* Gholamreza Khamisipour,† Mojtaba Falahati,* Behrooz Naeimi,† Majid Mossahebi-Mohammadi,‡ Rahim Tahmasebi,† Mojtaba Hasanpour,† Shakib Shamsian,† and Zahra Sadat Hashemi§
نویسنده مسئول نفر دوم از 9
Breast cancer is the most commonly occurring cancer among women. MicroRNAs as noncoding small RNA
molecules play pivotal roles in cancer-related biological processes. Increased levels of microRNA-29a in the
serum of breast cancer patients have been reported. Since heat shock proteins (HSPs) play important roles in cell
events, the quantitative fluctuations in their cellular levels could be deemed as key indicators of how the exerted
treatment alters cell behavior. In this regard, using an antisense small RNA, we attempted to investigate the effects
of miR-29a knockdown on the expression of HSPs genes in the MCF-7 breast cancer cell line. MCF-7 cells were
cultured in high-glucose Dulbecco’s modified Eagle’s medium with 10% FBS. Studied cells were subdivided
into five groups: treated with scramble, anti-miR-29a, anti-miR-29a + Taxol, Taxol, and control. Taxol was added
24 h post-anti-miR transfection and RNA extraction, and cDNA synthesis was done 48 h later. The changes in
expression of HSP27, HSP40, HSP60, HSP70, and HSP90 were evaluated by real-time PCR. Our results revealed
that inhibitors of microRNA-29a promote apoptosis through upregulation of HSP60 level and downregulation
of HSP27, HSP40, HSP70, and HSP90 levels and could be contemplated as a compelling alternative for Taxol
employment with similar effects and/or to sensitize cancer cells to chemotherapy with fewer side effects.
دریافت فایل پیوست
https://www.cognizantcommunication.com/journal-titles/oncology-research
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Clinical manifestations of β-Thalassemia major in two different altitudes; Bushehr and Shahrekord
International Journal of Hematology- Oncology and Stem Cell Research
April, 1, 2016 IJHOSCR 10(2)
Pubmed
Mohammad Reza Ravanbod1, Ali Movahed2, Afshin Ostovar3, Ali Hajigholami4, Gholamreza Khamisipour5, Shokrollah Farrokhi6, Hossein Darabi7, Yasaman Khosravi7, Mohammad Kazzem Gheybi7
5 از 9
Background: Patients with β-thalassemia major (TM) develop iron overload through increased iron absorption and transfusional therapy and it’s the most important complication of TM. Thalassemia is common in coastal regions and lands with low altitudes. The aim of this study is to determine the effect of high and low altitude on serum ferritin and treatment requirement in two groups of β-thalassemia major (TM) patients. Subjects and Methods: Patients were divided into two groups, the first group (No: 50) living at sea level (in the port of Bushehr, Iran) and the second group (No: 40) living at the altitude of 2061 m (in the city of Shahrekord, Iran). All patient’s clinical history, blood transfusion and laboratory tests including complete blood count and hemoglobin electrophoresis were reviewed. Results: There were no significant difference in ferritin levels, transfusion period and diabetes incidence of the two cities patients (P> 0.05). Patient’s cardiac function and liver condition were significantly better in patients of Bushehr (P<0.05). Patients under 20 years in Bushehr were less splenectomized in comparison with Shahrekord (P<0.05). Conclusion: Our result showed that some of clinical manifestations of patients in low altitude such as cardiac and liver condition were better. But it did not affect ferritin level probably due to transfusion and chelating therapy. Totally patients of Bushehr had better conditions and had longer survivals.
دریافت فایل پیوست
http://ijhoscr.tums.ac.ir/index.php/ijhoscr
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