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Article ; Online: DNA damage response signaling: A common link between cancer and cardiovascular diseases.

Nikfarjam, Sepideh / Singh, Krishna K

2022 Volume 12, Issue 4, Page(s) 4380–4404

Abstract: DNA damage response (DDR) signaling ensures genomic and proteomic homeostasis to maintain a healthy genome. Dysregulation either in the form of down- or upregulation in the DDR pathways correlates with various pathophysiological states, including cancer ... ...

Abstract	DNA damage response (DDR) signaling ensures genomic and proteomic homeostasis to maintain a healthy genome. Dysregulation either in the form of down- or upregulation in the DDR pathways correlates with various pathophysiological states, including cancer and cardiovascular diseases (CVDs). Impaired DDR is studied as a signature mechanism for cancer; however, it also plays a role in ischemia-reperfusion injury (IRI), inflammation, cardiovascular function, and aging, demonstrating a complex and intriguing relationship between cancer and pathophysiology of CVDs. Accordingly, there are increasing number of reports indicating higher incidences of CVDs in cancer patients. In the present review, we thoroughly discuss (1) different DDR pathways, (2) the functional cross talk among different DDR mechanisms, (3) the role of DDR in cancer, (4) the commonalities and differences of DDR between cancer and CVDs, (5) the role of DDR in pathophysiology of CVDs, (6) interventional strategies for targeting genomic instability in CVDs, and (7) future perspective.
MeSH term(s)	Humans ; DNA Repair ; DNA Damage ; Cardiovascular Diseases/genetics ; Proteomics ; Neoplasms/genetics
Language	English
Publishing date	2022-09-26
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.5274
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Article ; Online: Neurological manifestations of COVID-19: with emphasis on Iranian patients.

Aslan, Cynthia / Nikfarjam, Sepideh / Asadzadeh, Mohammad / Jafari, Reza

Journal of neurovirology

2021 Volume 27, Issue 2, Page(s) 217–227

Abstract: The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has instigated a global pandemic as a formidable and highly contagious infectious disease. Although the respiratory system remains ... ...

Abstract	The novel coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has instigated a global pandemic as a formidable and highly contagious infectious disease. Although the respiratory system remains the most frequently affected organ, several case reports have revealed that the complications are not merely limited to the respiratory system, and neurotropic and neuroinvasive properties have also been observed, leading to neurological diseases. In the present paper, it was intended to review the possible neuroinvasive routes of SARS-CoV-2 and its mechanisms that may cause neurological damage. Additionally, the neurological manifestations of COVID-19 across the globe were discussed with emphasis on Iran, while highlighting the impact of SARS-CoV-2 on the central and peripheral nervous systems.
MeSH term(s)	COVID-19/complications ; Humans ; Iran ; Nervous System Diseases/virology ; SARS-CoV-2
Language	English
Publishing date	2021-03-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-021-00964-2
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Zs.A 4426: Show issues

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Article ; Online: Dexosomes as a cell-free vaccine for cancer immunotherapy.

Nikfarjam, Sepideh / Rezaie, Jafar / Kashanchi, Fatah / Jafari, Reza

Journal of experimental & clinical cancer research : CR

2020 Volume 39, Issue 1, Page(s) 258

Abstract: Dendritic cells (DCs) secrete vast quantities of exosomes termed as dexosomes. Dexosomes are symmetric nanoscale heat-stable vesicles that consist of a lipid bilayer displaying a characteristic series of lipid and protein molecules. They include ... ...

Abstract	Dendritic cells (DCs) secrete vast quantities of exosomes termed as dexosomes. Dexosomes are symmetric nanoscale heat-stable vesicles that consist of a lipid bilayer displaying a characteristic series of lipid and protein molecules. They include tetraspanins and all established proteins for presenting antigenic material such as the major histocompatibility complex class I/II (MHC I/II) and CD1a, b, c, d proteins and CD86 costimulatory molecule. Dexosomes contribute to antigen-specific cellular immune responses by incorporating the MHC proteins with antigen molecules and transferring the antigen-MHC complexes and other associated molecules to naïve DCs. A variety of ex vivo and in vivo studies demonstrated that antigen-loaded dexosomes were able to initiate potent antitumor immunity. Human dexosomes can be easily prepared using monocyte-derived DCs isolated by leukapheresis of peripheral blood and treated ex vivo by cytokines and other factors. The feasibility of implementing dexosomes as therapeutic antitumor vaccines has been verified in two phase I and one phase II clinical trials in malignant melanoma and non small cell lung carcinoma patients. These studies proved the safety of dexosome administration and showed that dexosome vaccines have the capacity to trigger both the adaptive (T lymphocytes) and the innate (natural killer cells) immune cell recalls. In the current review, we will focus on the perspective of utilizing dexosome vaccines in the context of cancer immunotherapy.
MeSH term(s)	Cancer Vaccines/pharmacology ; Cancer Vaccines/therapeutic use ; Dendritic Cells/immunology ; Exosomes/immunology ; Humans ; Immunotherapy/methods
Chemical Substances	Cancer Vaccines
Language	English
Publishing date	2020-11-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-020-01781-x
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Article ; Online: Mesenchymal stem cell derived-exosomes: a modern approach in translational medicine.

Nikfarjam, Sepideh / Rezaie, Jafar / Zolbanin, Naime Majidi / Jafari, Reza

Journal of translational medicine

2020 Volume 18, Issue 1, Page(s) 449

Abstract: Mesenchymal stem cells (MSCs) have captured great attention in regenerative medicine for over a few decades by virtue of their differentiation capacity, potent immunomodulatory properties, and their ability to be favorably cultured and manipulated. ... ...

Abstract	Mesenchymal stem cells (MSCs) have captured great attention in regenerative medicine for over a few decades by virtue of their differentiation capacity, potent immunomodulatory properties, and their ability to be favorably cultured and manipulated. Recent investigations implied that the pleiotropic effects of MSCs is not associated to their ability of differentiation, but rather is mediated by the secretion of soluble paracrine factors. Exosomes, nanoscale extracellular vesicles, are one of these paracrine mediators. Exosomes transfer functional cargos like miRNA and mRNA molecules, peptides, proteins, cytokines and lipids from MSCs to the recipient cells. Exosomes participate in intercellular communication events and contribute to the healing of injured or diseased tissues and organs. Studies reported that exosomes alone are responsible for the therapeutic effects of MSCs in numerous experimental models. Therefore, MSC-derived exosomes can be manipulated and applied to establish a novel cell-free therapeutic approach for treatment of a variety of diseases including heart, kidney, liver, immune and neurological diseases, and cutaneous wound healing. In comparison with their donor cells, MSC-derived exosomes offer more stable entities and diminished safety risks regarding the administration of live cells, e.g. microvasculature occlusion risk. This review discusses the exosome isolation methods invented and utilized in the clinical setting thus far and presents a summary of current information on MSC exosomes in translational medicine.
MeSH term(s)	Exosomes ; Extracellular Vesicles ; Mesenchymal Stem Cells ; Regenerative Medicine ; Translational Medical Research
Language	English
Publishing date	2020-11-27
Publishing country	England
Document type	Journal Article ; Review
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-020-02622-3
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Article ; Online: Interleukin-1

Mardi, Amirhossein / Meidaninikjeh, Sepideh / Nikfarjam, Sepideh / Majidi Zolbanin, Naime / Jafari, Reza

Viral immunology

2021 Volume 34, Issue 10, Page(s) 679–688

Abstract: The newfound coronavirus disease 2019 (COVID-19), initiated by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an international public health concern, threatening the lives of millions of people worldwide. The virus seems to have a ... ...

Abstract	The newfound coronavirus disease 2019 (COVID-19), initiated by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an international public health concern, threatening the lives of millions of people worldwide. The virus seems to have a propensity to infect older males, especially those with underlying diseases. The cytokine storm following hyperactivated immune responses due to SARS-CoV-2 infection is probably the crucial source of severe pneumonia that leads to acute lung injury, systemic inflammatory response syndrome, or acute respiratory distress syndrome, and finally multiple organ dysfunction syndromes, as well as death in many cases. Several studies revealed that interleukin (IL)-1
MeSH term(s)	Acute Lung Injury/drug therapy ; Acute Lung Injury/immunology ; Acute Lung Injury/pathology ; COVID-19/drug therapy ; COVID-19/immunology ; COVID-19/mortality ; COVID-19/pathology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/pathology ; Humans ; Interleukin-1/antagonists & inhibitors ; Interleukin-1/immunology ; Multiple Organ Failure/drug therapy ; Multiple Organ Failure/immunology ; Multiple Organ Failure/pathology ; Respiratory Distress Syndrome/drug therapy ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/pathology ; SARS-CoV-2/immunology ; SARS-CoV-2/pathogenicity
Chemical Substances	Interleukin-1
Language	English
Publishing date	2021-12-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639075-4
ISSN	1557-8976 ; 0882-8245
ISSN (online)	1557-8976
ISSN	0882-8245
DOI	10.1089/vim.2021.0071
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Zs.A 2227: Show issues

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Article ; Online: Immunopharmacological perspective on zinc in SARS-CoV-2 infection.

Asl, Sima Heydarzadeh / Nikfarjam, Sepideh / Majidi Zolbanin, Naime / Nassiri, Reza / Jafari, Reza

International immunopharmacology

2021 Volume 96, Page(s) 107630

Abstract: The novel SARS-CoV-2 which was first reported in China is the cause of infection known as COVID-19. In comparison with other coronaviruses such as SARS-CoV and MERS, the mortality rate of SARS-CoV-2 is lower but the transmissibility is higher. Immune ... ...

Abstract	The novel SARS-CoV-2 which was first reported in China is the cause of infection known as COVID-19. In comparison with other coronaviruses such as SARS-CoV and MERS, the mortality rate of SARS-CoV-2 is lower but the transmissibility is higher. Immune dysregulation is the most common feature of the immunopathogenesis of COVID-19 that leads to hyperinflammation. Micronutrients such as zinc are essential for normal immune function. According to the assessment of WHO, approximately one-third of the world's society suffer from zinc deficiency. Low plasma levels of zinc are associated with abnormal immune system functions such as impaired chemotaxis of polymorphonuclear cells (PMNs) and phagocytosis, dysregulated intracellular killing, overexpression of the inflammatory cytokines, lymphopenia, decreased antibody production, and sensitivity to microbes especially viral respiratory infections. Zinc exerts numerous direct and indirect effects against a wide variety of viral species particularly RNA viruses. The use of zinc and a combination of zinc-pyrithione at low concentrations impede SARS-CoV replication in vitro. Accordingly, zinc can inhibit the elongation step of RNA transcription. Furthermore, zinc might improve antiviral immunity by up-regulation of IFNα through JAK/STAT1 signaling pathway in leukocytes. On the other hand, zinc supplementation might ameliorate tissue damage caused by mechanical ventilation in critical COVID-19 patients. Finally, zinc might be used in combination with antiviral medications for the management of COVID-19 patients. In the current review article, we review and discuss the immunobiological roles and antiviral properties as well as the therapeutic application of zinc in SARS-CoV-2 and related coronaviruses infections.
MeSH term(s)	COVID-19/pathology ; Humans ; SARS-CoV-2/drug effects ; Virus Replication/drug effects ; Zinc/metabolism ; Zinc/pharmacology
Chemical Substances	Zinc (J41CSQ7QDS)
Language	English
Publishing date	2021-04-01
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2021.107630
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Zs.A 5408: Show issues

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Article ; Online: Endothelial cell-specific loss of eNOS differentially affects endothelial function.

Bu, Shuhan / Nguyen, Hien C / Nikfarjam, Sepideh / Michels, David C R / Rasheed, Berk / Maheshkumar, Sauraish / Singh, Shweta / Singh, Krishna K

PloS one

2022 Volume 17, Issue 9, Page(s) e0274487

Abstract: The endothelium maintains and regulates vascular homeostasis mainly by balancing interplay between vasorelaxation and vasoconstriction via regulating Nitric Oxide (NO) availability. Endothelial nitric oxide synthase (eNOS) is one of three NOS isoforms ... ...

Abstract	The endothelium maintains and regulates vascular homeostasis mainly by balancing interplay between vasorelaxation and vasoconstriction via regulating Nitric Oxide (NO) availability. Endothelial nitric oxide synthase (eNOS) is one of three NOS isoforms that catalyses the synthesis of NO to regulate endothelial function. However, eNOS's role in the regulation of endothelial function, such as cell proliferation and migration remain unclear. To gain a better understanding, we genetically knocked down eNOS in cultured endothelial cells using sieNOS and evaluated cell proliferation, migration and also tube forming potential in vitro. To our surprise, loss of eNOS significantly induced endothelial cell proliferation, which was associated with significant downregulation of both cell cycle inhibitor p21 and cell proliferation antigen Ki-67. Knockdown of eNOS induced cell migration but inhibited formation of tube-like structures in vitro. Mechanistically, loss of eNOS was associated with activation of MAPK/ERK and inhibition of PI3-K/AKT signaling pathway. On the contrary, pharmacologic inhibition of eNOS by inhibitors L-NAME or L-NMMA, inhibited cell proliferation. Genetic and pharmacologic inhibition of eNOS, both promoted endothelial cell migration but inhibited tube-forming potential. Our findings confirm that eNOS regulate endothelial function by inversely controlling endothelial cell proliferation and migration, and by directly regulating its tube-forming potential. Differential results obtained following pharmacologic versus genetic inhibition of eNOS indicates a more complex mechanism behind eNOS regulation and activity in endothelial cells, warranting further investigation.
MeSH term(s)	Cells, Cultured ; Endothelial Cells/metabolism ; Endothelium/metabolism ; Ki-67 Antigen/metabolism ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; omega-N-Methylarginine/metabolism
Chemical Substances	Ki-67 Antigen ; Protein Isoforms ; omega-N-Methylarginine (27JT06E6GR) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2022-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0274487
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Article ; Online: Loss of fatty acid binding protein 3 ameliorates lipopolysaccharide-induced inflammation and endothelial dysfunction.

Nguyen, Hien C / Bu, Shuhan / Nikfarjam, Sepideh / Rasheed, Berk / Michels, David C R / Singh, Aman / Singh, Shweta / Marszal, Caroline / McGuire, John J / Feng, Qingping / Frisbee, Jefferson C / Qadura, Mohammad / Singh, Krishna K

The Journal of biological chemistry

2023 Volume 299, Issue 3, Page(s) 102921

Abstract: Circulating fatty acid-binding protein 3 (FABP3) is an effective biomarker of myocardial injury and peripheral artery disease (PAD). The endothelium, which forms the inner most layer of every blood vessel, is exposed to higher levels of FABP3 in PAD or ... ...

Abstract	Circulating fatty acid-binding protein 3 (FABP3) is an effective biomarker of myocardial injury and peripheral artery disease (PAD). The endothelium, which forms the inner most layer of every blood vessel, is exposed to higher levels of FABP3 in PAD or following myocardial injury, but the pathophysiological role of endothelial FABP3, the effect of FABP3 exposure on endothelial cells, and related mechanisms are unknown. Here, we aimed to evaluate the pathophysiological role of endothelial FABP3 and related mechanisms in vitro. Our molecular and functional in vitro analyses show that (1) FABP3 is basally expressed in endothelial cells; (2) inflammatory stress in the form of lipopolysaccharide (LPS) upregulated endothelial FABP3 expression; (3) loss of endogenous FABP3 protected endothelial cells against LPS-induced endothelial dysfunction; however, exogenous FABP3 exposure exacerbated LPS-induced inflammation; (4) loss of endogenous FABP3 protected against LPS-induced endothelial dysfunction by promoting cell survival and anti-inflammatory and pro-angiogenic signaling pathways. Together, these findings suggest that gain-of endothelial FABP3 exacerbates, whereas loss-of endothelial FABP3 inhibits LPS-induced endothelial dysfunction by promoting cell survival and anti-inflammatory and pro-angiogenic signaling. We propose that an increased circulating FABP3 in myocardial injury or PAD patients may be detrimental to endothelial function, and therefore, therapies aimed at inhibiting FABP3 may improve endothelial function in diseased states.
MeSH term(s)	Humans ; Endothelial Cells/pathology ; Fatty Acid Binding Protein 3/genetics ; Inflammation/chemically induced ; Lipopolysaccharides ; Signal Transduction/genetics ; Cell Survival/genetics
Chemical Substances	Fatty Acid Binding Protein 3 ; Lipopolysaccharides
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.102921
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Article: ---Successful Application of Whole Cell Panning for Isolation of Phage Antibody Fragments Specific to Differentiated Gastric Cancer Cells.

Nikfarjam, Sepideh / Tohidkia, Mohammad Reza / Mehdipour, Tayebeh / Soleimani, Ramin / Rahimi, Ali Akbar Rahim / Nouri, Mohammad

Advanced pharmaceutical bulletin

2019 Volume 9, Issue 4, Page(s) 624–631

Abstract: Purpose: ...

Abstract	Purpose:
Language	English
Publishing date	2019-10-24
Publishing country	Iran
Document type	Journal Article
ZDB-ID	3018440-X
ISSN	2251-7308 ; 2228-5881
ISSN (online)	2251-7308
ISSN	2228-5881
DOI	10.15171/apb.2019.072
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Article ; Online: Transcriptomics of angiotensin II-induced long noncoding and coding RNAs in endothelial cells.

Bu, Shuhan / Nguyen, Hien C / Michels, David C R / Rasheed, Berk / Nikfarjam, Sepideh / Singh, Rohan / Wang, Lynn / Patel, Darshil A / Singh, Shweta / Qadura, Mohammad / Singh, Krishna K

Journal of hypertension

2022 Volume 40, Issue 7, Page(s) 1303–1313

Abstract: Objective: Angiotensin II (Ang II)-induced endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases such as systemic hypertension, cardiac hypertrophy and atherosclerosis. Recently, long noncoding RNAs (lncRNAs) ... ...

Abstract	Objective: Angiotensin II (Ang II)-induced endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases such as systemic hypertension, cardiac hypertrophy and atherosclerosis. Recently, long noncoding RNAs (lncRNAs) have been shown to play an essential role in the pathobiology of cardiovascular diseases; however, the effect of Ang II on lncRNAs and coding RNAs expression in endothelial cells has not been evaluated. Accordingly, we sought to evaluate the expression profiles of lncRNAs and coding RNAs in endothelial cells following treatment with Ang II. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured and treated with Ang II (10-6 mol/l) for 24 h. The cells were then profiled for the expression of lncRNAs and mRNAs using the Arraystar Human lncRNA Expression Microarray V3.0. Results: In HUVECs following Ang II treatment, from a total of 30 584 lncRNA targets screened, 25 targets were significantly upregulated, while 69 were downregulated. In the same HUVECs samples, from 26 106 mRNA targets screened, 28 targets were significantly upregulated and 67 were downregulated. Of the differentially expressed lncRNAs, RP11-354P11.2 and RP11-360F5.1 were the most upregulated (11-fold) and downregulated (three-fold) lncRNAs, respectively. Assigning the differentially regulated genes into functional groups using bioinformatics reveals numerous genes involved in the nucleotide excision repair and ECM-receptor interaction. Conclusion: This is the first study to profile the Ang II-induced differentially expressed lncRNAs and mRNAs in human endothelial cells. Our results reveal novel targets and substantially extend the list of potential candidate genes involved in Ang II-induced endothelial dysfunction and cardiovascular diseases.
MeSH term(s)	Angiotensin II/metabolism ; Angiotensin II/pharmacology ; Cardiovascular Diseases/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcriptome
Chemical Substances	RNA, Long Noncoding ; RNA, Messenger ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2022-07-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000003140
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