Publications by authors named "S Hirin Azizidoost"

13 Publications

  • Page 1 of 1

Impact of Methyl-β-Cyclodextrin and Apolipoprotein A-I on The Expression of ATP-Binding Cassette Transporter A1 and Cholesterol Depletion in C57BL/6 Mice Astrocytes.

Cell J 2021 Apr 1;23(1):93-98. Epub 2021 Mar 1.

Cellular and Molecular Research Center, Department of Biochemistry, Medical School, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Email:

Objective: Dysregulation of cholesterol metabolism in the brain is responsible for many lipid storage disorders, including Niemann-Pick disease type C (NPC). Here, we have investigated whether cyclodextrin (CD) and apolipoprotein A-I (apoA-I) induce the same signal to inhibit cell cholesterol accumulation by focusing on the main proteins involved in cholesterol homeostasis in response to CD and apoA-I treatment.

Materials And Methods: In this experimental study, astrocytes were treated with apoA-I or CD and then lysed in RIPA buffer. We used Western blot to detect protein levels of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR) and ATP-binding cassette transporter A1 (ABCA1). Cell cholesterol content and cholesterol release in the medium were also measured.

Results: ApoA-I induced a significant increase in ABCA1 and a mild increase in HMGCR protein level, whereas CD caused a significant increase in HMGCR with a significant decrease in ABCA1. Both apoA-I and CD increased cholesterol release in the medium. A mild, but not significant increase, in cell cholesterol content was seen by apoA-I; however, a significant increase in cell cholesterol was detected when the astrocytes were treated with CD.

Conclusion: CD, like apoA-I, depletes cellular cholesterol. This depletion occurs in a different way from apoA-I that is through cholesterol efflux. Depletion of cell cholesterol with CDs led to reduced protein levels of ABCA1 along with increased HMGCR and accumulation of cell cholesterol. This suggested that CDs, unlike apoA-I, could impair the balance between cholesterol synthesis and release, and interfere with cellular function that depends on ABCA1.
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http://dx.doi.org/10.22074/cellj.2021.7061DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7944131PMC
April 2021

T-Cell Molecular Modulation Responses in Atherosclerosis Anergy.

Lab Med 2020 Nov;51(6):557-565

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Atherosclerosis continues to be a major cause of death in patients with cardiovascular diseases. The cooperative role of immunity has been recently considered in atherosclerotic plaque inflammation, especially adaptive immune response by T cells. In this review, we examine the possible role of T cells in atherosclerosis-mediated inflammation and conceivable therapeutic strategies that can ameliorate complications of atherosclerosis. The cytokines secreted by T-lymphocyte subsets, different pathophysiological profiles of microRNAs (miRs), and the growth factor/receptor axis have diverse effects on the inflammatory cycle of atherosclerosis. Manipulation of miRNA expression and prominent growth factor receptors involved in inflammatory cytokine secretion in atherosclerosis can be considered diagnostic biomarkers in the induction of anergy and blockade of atherosclerotic development. This manuscript reviews immunomodulation of T cells responses in atherosclerosis anergy.
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http://dx.doi.org/10.1093/labmed/lmaa003DOI Listing
November 2020

Effect of Hydroalcoholic Ginger Extract on Brain HMG-CoA Reductase and CYP46A1 Levels in Streptozotocin-induced Diabetic Rats.

Avicenna J Med Biotechnol 2019 Jul-Sep;11(3):234-238

Department of Biochemistry, Cellular and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Patients with diabetes present with lipid disorders, including hypercholesterolemia, which can be a high-risk factor for atherosclerosis. Recently, increasing interest has been focused on anti-lipidemic function of herbal medicines, especially (known as ginger), in diabetes. However, the mechanism underlying the effect of ginger on some players involved in cholesterol homeostasis of Central Nervous System (CNS) among diabetic patients remains unclear. To our knowledge, this is the first study to investigate the effect of ginger on brain regulation of Hydroxymethylglutaryl-CoA Reductase (HMG-CoA reductase) and Cholesterol 24-hydroxylase (CYP46A1), which provides a rational model for understanding brain dyslipidemia mechanisms associated with diabetes.

Methods: Brains of rats were isolated from four groups: control, non-treated diabetic, and treated diabetic groups receiving 200 or 400 of hydroalcoholic extracts of ginger for eight weeks. HMG-CoA reductase and CYP46A1 levels in brain homogenates were determined by western-blot technique.

Results: Ginger root extract caused a significant decrease in HMG-CoA reductase and an increase in CYP46A1 levels in treated diabetic groups compared to diabetic control. In comparison to diabetic group, these effects were more remarkable with 400 concentration of ginger extract.

Conclusion: The findings showed that ginger extract has a regulatory effect on proteins involved in cholesterol homeostasis in CNS by a significant down- and up-regulation of HMG-CoA reductase and CYP46A1 levels, respectively. It can be suggested that adding ginger to daily diet of diabetic patients has useful effects and may ameliorate diabetes complications.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6626506PMC
August 2019

Complex karyotype in myelodysplastic syndromes: Diagnostic procedure and prognostic susceptibility.

Oncol Rev 2019 Jan 4;13(1):389. Epub 2019 Feb 4.

Thalassemia & Hemoglobinopathy Research center, research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Complex karyotype (CK) is a poor prognosis factor in hematological malignancies. Studies have shown that the presence of CK in myelodysplastic syndrome (MDS) can be associated with MDS progression to acute myeloid leukemia. The goal of this review was to examine the relationship between different types of CK with MDS, as well as its possible role in the deterioration and progression of MDS to leukemia. The content used in this paper has been obtained by a PubMed and Google Scholar search of English language papers (1975-2018) using the terms and . A single independent abnormality can be associated with a good prognosis. However, the coexistence of a series of abnormalities can lead to CK, which is associated with the deterioration of MDS and its progression to leukemia. Therefore, CK may be referred to as a prognostic factor in MDS. The detection of independent cytogenetic disorders that altogether can result in CK could be used as a prognostic model for laboratory and clinical use.
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http://dx.doi.org/10.4081/oncol.2019.389DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379782PMC
January 2019

Role of bone marrow adipocytes in leukemia and chemotherapy challenges.

Cell Mol Life Sci 2019 Jul 4;76(13):2489-2497. Epub 2019 Feb 4.

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Adipose tissue (AT) is an extramedullary reservoir of normal hematopoietic stem cells (HSCs). Adipocytes prevent the production of normal HSCs via secretion of inflammatory factors, and adipocyte-derived free fatty acids may contribute to the development and progression of leukemia via providing energy for leukemic cells. In addition, adipocytes are able to metabolize and inactivate therapeutic agents, reducing the concentrations of active drugs in adipocyte-rich microenvironments. The aim of this study was to detect the role of adipocytes in the progression and treatment of leukemia. Relevant literature was identified through a PubMed search (2000-2018) of English-language papers using the following terms: leukemia, adipocyte, leukemic stem cell, chemotherapy, and bone marrow. Findings suggest the striking interplay between leukemic cells and adipocytes to create a unique microenvironment supporting the metabolic demands and survival of leukemic cells. Based on these findings, targeting lipid metabolism of leukemic cells and adipocytes in combination with standard therapeutic agents might present novel treatment options.
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http://dx.doi.org/10.1007/s00018-019-03031-6DOI Listing
July 2019

Vitamin D and its receptor polymorphisms: New possible prognostic biomarkers in leukemias.

Oncol Rev 2018 Jul 8;12(2):366. Epub 2018 Oct 8.

Department of Biochemistry and Hematology, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.

Several factors such as chromosomal translocations, gene mutations, and polymorphisms are involved in the pathogenesis of leukemia/lymphoma. Recently, the role of vitamin D (VD) and vitamin D receptor (VDR) polymorphisms in hematologic malignancies has been considered. In this review, we examine the possible role of VD levels, as well as VDR polymorphisms as prognostic biomarkers in leukemia/lymphoma. Relevant English language literature were searched and retrieved from Google Scholar search engine (1985-2017). The following keywords were used: , , , , and . Increased serum levels of VD in patients with leukemia are associated with a better prognosis. However, low VD levels are associated with a poor prognosis, and VDR polymorphisms in various leukemias can have prognostic value. VD biomarker can be regarded as a potential prognostic factor for a number of leukemias, including acute myeloblastic leukemia (AML), chronic lymphoblastic leukemia (CLL), and diffuse large B-cell lymphoma (DLBCL). There is a significant relationship between different polymorphisms of VDR (including Taq I and Fok I) with several leukemia types such as ALL and AML, which may have prognostic value.
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http://dx.doi.org/10.4081/oncol.2018.366DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199555PMC
July 2018

Signaling-chemokine axis network in brain as a sanctuary site for metastasis.

J Cell Physiol 2019 04 6;234(4):3376-3382. Epub 2018 Sep 6.

Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Background: Brain metastasis remains a major cause of death in patients with solid cancers. The co-operation between several molecular factors such as chemokines, chemokine receptors, and signaling pathways is involved in the pathogenesis of brain metastasis mostly from solid tumors. In this review, we examine the possible role of chemokine/receptor axis, as well as signaling pathways as prognostic biomarkers in brain metastasis.

Methods: Relevant English language literature were searched and retrieved from Google Scholar search engine (1993-2017). The following keywords were used: "chemokine," "signaling pathway," "brain," "metastasis," and "niche."

Results: Increased expression of chemokines like CXCL12 and dysregulated signaling intermediates such as Notch in patients with solid tumors (e.g., breast cancer) is associated with brain metastasis.

Conclusions: As biomarkers for brain metastasis, chemokine, and signaling intermediates are potential prognostic factors in a number of solid tumor, including breast cancer, melanoma, and lung cancer.
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http://dx.doi.org/10.1002/jcp.27305DOI Listing
April 2019

The role and clinical implications of the endosteal niche and osteoblasts in regulating leukemia.

Clin Transl Oncol 2017 Sep 9;19(9):1059-1066. Epub 2017 Mar 9.

Health Research Institute, Research Center of Thalassemia and Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, 61357-15794, Iran.

Osteoblasts are one among the critical components of the endosteal bone marrow (BM) niche. In addition to hematopoietic stem cell fate, their role in leukemogenesis as well as metastasis of a variety of cancers has been demonstrated in various studies. In this regard, endosteal niche can have a dual role as an initiator and protective role against leukemia. Knowledge of growth factors, chemokines and cytokines secreted by osteoblasts as well as their interaction with signaling pathways inform our understanding of the development, prognosis, recurrence and treatment of malignant BM diseases. Clinical progress in targeting the endosteal niche is also discussed.
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http://dx.doi.org/10.1007/s12094-017-1642-1DOI Listing
September 2017

Hepatic metastatic niche: from normal to pre-metastatic and metastatic niche.

Tumour Biol 2016 Feb 11;37(2):1493-503. Epub 2015 Dec 11.

Health research institute, Research Center of Thalassemia &Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Liver is the organ responsible for hematopoiesis during fetal life, which is also a target organ of metastasis for several cancers. In order to recognize the hepatic metastatic changes, obtain a better grasp of cancer prevention, treatment, and inhibition mode of hepatic metastasis progression, we investigate the changes and transformation of normal hepatic niche cells to metastatic niche ones in this review. On the other hand, since metastatic diseases alter the liver function, the changes in a number of cancers that metastasize to the liver have also been reviewed. Relevant English-language literature was searched and retrieved from PubMed (1994-2014) using the following keywords: hepatic stem cell niche, hepatic metastatic niche, chemokine, and microRNAs (miRNAs). Also, over 86 published studies were investigated, and bioinformatics analysis of differentially expressed miRNAs in hepatic cancer and metastasis was performed. Metastasis is developed in several stages with specific changes and mechanisms in each stage. Recognition of these changes would lead to detection of new biomarkers and clinical targets involved in specific stages of liver metastasis. Investigation of the hepatic stem cell niche, development of metastasis in liver tissue, as well as changes in chemokines and miRNAs in metastatic hepatic niche can significantly contribute to faster detection of liver metastasis progression.
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http://dx.doi.org/10.1007/s13277-015-4557-xDOI Listing
February 2016

Bone marrow niche in the myelodysplastic syndromes.

Leuk Res 2015 Oct 14;39(10):1020-7. Epub 2015 Jul 14.

Health Research Institute, Research Center of Thalassemia & Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

The myelodysplastic syndromes (MDS) are a diverse group of clonal hematopoietic malignancies characterized by ineffective hematopoiesis, progressive bone marrow (BM) failure, cytogenetic and molecular abnormalities, and variable risk of progression to acute myeloid leukemia (AML). The BM microenvironment in MDS plays an important role in the development of this disorder. The BM stromal cells of MDS patients often harbor distinct chromosomal aberrations than the hematopoietic elements, suggesting different genetic origins. Perturbed cytokine secretions from BM stromal cells such as multipotent mesenchymal stem cells (MSCs) and endothelial cells are associated with increased proliferation and survival of malignant hematopoietic cells. Within the MDS BM there are also alterations in stromal cell composition, signaling and angiogenesis between Low- and High-risk MDS patients. Several open lines of investigation into the MDS niche remain, including the timing of stromal defects in context to dysplastic hematopoiesis. Another important, unanswered question is the impact of age on BM stroma function and regulation (or dysregulation) or hematopoietic stem/progenitor cells. With a better understanding of the MDS niche, new therapeutic strategies will emerge.
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http://dx.doi.org/10.1016/j.leukres.2015.06.017DOI Listing
October 2015

New insights in cellular and molecular aspects of BM niche in chronic myelogenous leukemia.

Tumour Biol 2014 Nov 19;35(11):10627-33. Epub 2014 Sep 19.

Department of Biochemistry and Hematology, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran.

Hematoproliferative neoplasias like chronic myelogenous leukemia (CML) progressively affect bone marrow niche; however, there are only few specific clinical markers for prediction of disease progression. Here, we review the myeloproliferative niche and molecular changes including signaling pathways as well as microRNA (miRNA) in CML in order to better understand the therapeutic approaches. CML is a three-stage myeloproliferative disorder caused by reciprocal translocation between chromosome 9 and 22. There has been a new interest on treatment of this disorder. Therefore, in order to develop the appropriate therapy, an analysis of the molecular changes involved in malignant cells can be effective. A review of the signaling pathways, miRNA, and related targets can be helpful for better understanding of molecular pathogenesis of CML. Characterizing malignant cells and molecular changes with a focus on their targets may help researchers use molecular targets as effective therapeutic means for CML. On the other hand, interactions between leukemic stem cells and CML niche will help researchers investigate the causes of drug resistance in this disease.
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http://dx.doi.org/10.1007/s13277-014-2610-9DOI Listing
November 2014

The role of notch signaling in bone marrow niche.

Hematology 2015 Mar 12;20(2):93-103. Epub 2014 Apr 12.

Objective: Bone marrow (BM) niche is a three-dimensional structure composed of a series of cells and it is one of the most controversial topics in hematological malignancies, leukemia, and even metastasis. Here, we review the relationship between Notch signaling and different fates of stem cells and other BM niche cells.

Methods: Relevant English-language literature were searched and retrieved from PubMed (2000-2013) using the terms Notch signaling, BM niche, and microRNAs (miRNAs).

Discussion: Notch signaling pathway is a signaling system involved in cellular processes such as proliferation, differentiation, and apoptosis. The notch signaling pathway components are associated with interaction between leukemic, metastatic, and normal cells and their microenvironment. miRNAs play an important role in expression and regulation of signaling molecules. It is necessary to evaluate the relationship between aberrant miRNA expression and notch signaling such as miR-128 and miR-30 in glioma and angiogenesis with notch signaling, respectively.

Conclusions: Characterizing malignant cells and future studies focus on better understanding the variety of cancers and apoptosis with activated Notch signaling pathway, may remain promising this signaling system as a safe and effective therapeutic target.
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http://dx.doi.org/10.1179/1607845414Y.0000000167DOI Listing
March 2015

Bone marrow neoplastic niche in leukemia.

Hematology 2014 Jun 25;19(4):232-8. Epub 2013 Nov 25.

Objectives: Neoplastic niche is a specific microenvironment for growth and proliferation of malignant cells. Here we review the leukemic niche and its constituent stem cells, signaling pathways and essential chemokines.

Methods: Relevant literature was identified by a PubMed search (2000-2013) of English-language literature using the terms neoplastic niche, chemokines, and leukemia.

Discussion: Leukemia is caused by malignant hematopoietic stem cells and precursors. Important molecules and signals are involved in interactions between leukemic cells and their microenvironment. MicroRNAs (miRNAs) play an important role in expression regulation of oncogenes, transcription factors, signaling molecules and in eventual fate of the cell. It seems necessary to evaluate the relationship between aberrant miRNA expression and malignant transformation of bone marrow niche.

Conclusions: Characterizing malignant leukemic cells, activated signaling pathways, and molecules involved in disease progression will result in understanding the causes of drug resistance, relapse factors, and effective treatments.
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http://dx.doi.org/10.1179/1607845413Y.0000000111DOI Listing
June 2014