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Article ; Online: Mesenchymal stem cell treatment for hyperactive immune response in patients with COVID-19.

Manoharan, Ragul / Kore, Rajshekhar A / Mehta, Jawahar L

2022 Volume 14, Issue 13, Page(s) 1055–1065

Abstract: The human immune system protects the body against invasive organisms and kicks into a hyperactive mode in COVID-19 patients, particularly in those who are critically sick. Therapeutic regimens directed at the hyperactive immune system have been found to ... ...

Abstract	The human immune system protects the body against invasive organisms and kicks into a hyperactive mode in COVID-19 patients, particularly in those who are critically sick. Therapeutic regimens directed at the hyperactive immune system have been found to be effective in the treatment of patients with COVID-19. An evolving potential treatment option is therapy with mesenchymal stem cells (MSCs) due to their regenerative and reparative ability in epithelial cells. Clinical trials have reported the safe usage of MSC therapy. Systemic effects of MSC treatment have included a reduction in pro-inflammatory cytokines and a decrease in the levels of CRP, IL-6, and lactase dehydrogenase, which function as independent biomarkers for COVID-19 mortality and respiratory failure.
MeSH term(s)	COVID-19/therapy ; Humans ; Immunity ; Mesenchymal Stem Cell Transplantation/adverse effects ; Mesenchymal Stem Cells ; SARS-CoV-2
Language	English
Publishing date	2022-07-20
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2495964-9
ISSN	1750-7448 ; 1750-743X
ISSN (online)	1750-7448
ISSN	1750-743X
DOI	10.2217/imt-2021-0245
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Article ; Online: The structural basis of effective LOX-1 inhibition.

Kore, Rajshekhar A / Bagchi, Ashim K / Varughese, Kottayil I / Mehta, Jawahar L

Future medicinal chemistry

2022 Volume 14, Issue 10, Page(s) 731–743

Abstract: Along with other scavenger receptors, splice variants of LOX-1 play an important role in modulating numerous subcellular mechanisms such as normal cell development, differentiation and growth in response to physiological stimuli. Thus, LOX-1 activity is ... ...

Abstract	Along with other scavenger receptors, splice variants of LOX-1 play an important role in modulating numerous subcellular mechanisms such as normal cell development, differentiation and growth in response to physiological stimuli. Thus, LOX-1 activity is a key regulator in determining the severity of many genetic, metabolic, cardiovascular, renal, and neurodegenerative diseases and/or cancer. Increased expression of LOX-1 precipitates pathological disorders during the aging process. Therefore, it becomes important to develop novel LOX-1 inhibitors based on its ligand binding polarity and/or affinity and disrupt the uptake of its ligand: oxidized low-density lipoproteins (ox-LDL). In this review, we shed light on the presently studied and developed novel LOX-1 inhibitors that may have potential for treatment of diseases characterized by LOX-1 activation.
MeSH term(s)	Ligands ; Scavenger Receptors, Class E/genetics ; Scavenger Receptors, Class E/metabolism
Chemical Substances	Ligands ; Scavenger Receptors, Class E
Language	English
Publishing date	2022-04-25
Publishing country	England
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc-2022-0011
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Article ; Online: Erratum: NLRP3 inflammasome

Ding, Zufeng / Wang, Xianwei / Liu, Shijie / Zhou, Sichang / Kore, Rajshekhar A / Mu, Shengyu / Deng, Xiaoyan / Fan, Yubo / Mehta, Jawahar L

Theranostics

2022 Volume 12, Issue 1, Page(s) 418

Abstract: This corrects the article DOI: 10.7150/thno.45939.]. ...

Abstract	[This corrects the article DOI: 10.7150/thno.45939.].
Language	English
Publishing date	2022-01-01
Publishing country	Australia
Document type	Published Erratum
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.68759
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Article ; Online: Author Correction: Molecular events in MSC exosome mediated cytoprotection in cardiomyocytes.

Kore, Rajshekhar A / Henson, Jeffrey C / Hamzah, Rabab N / Griffin, Robert J / Tackett, Alan J / Ding, Zufeng / Mehta, Jawahar L

Scientific reports

2022 Volume 12, Issue 1, Page(s) 7874

Language	English
Publishing date	2022-05-12
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-11690-y
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Article ; Online: Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes.

Kore, Rajshekhar A / Jenkins, Samir V / Jamshidi-Parsian, Azemat / Tackett, Alan J / Griffin, Robert J / Ayyadevara, Srinivas / Mehta, Jawahar L

Biochemistry and biophysics reports

2023 Volume 34, Page(s) 101463

Abstract: Mesenchymal stem cell (MSC) exosomes have been found to attenuate cardiac systolic and diastolic dysfunction in animal models of ischemia. Exosomes carry a plethora of active and inactive proteins as their cargo, which are readily available to the ... ...

Abstract	Mesenchymal stem cell (MSC) exosomes have been found to attenuate cardiac systolic and diastolic dysfunction in animal models of ischemia. Exosomes carry a plethora of active and inactive proteins as their cargo, which are readily available to the recipient cell for use in intracellular signaling pathways-depending on the stresses, such as ischemia or hypoxia. Among the exosomal proteins are the often-overlooked cargo of transcriptional regulators. These transcriptional regulators influence the transcriptome and subsequently the proteome of recipient cell. Here, we report the transcriptional factors and regulators differentially modulated and their potential role in modulating cardiac function in MSC exosome treated ischemic mice hearts. Our analysis shows ischemic stress modulating transcriptional regulators and factors such as HSF1 and HIF1A in the infarct and peri-infarct areas of ischemic hearts which is mitigated by MSC exosomes. Similarly, STAT3 and SMAD3 are also modulated by MSC exosomes. Interestingly, NOTCH1 and β-catenin were detected in the ischemic hearts. The differential expression of these regulators and factors drives changes in various biological process governed in the ischemic cardiac cells. We believe these studies will advance our understanding of cardiac dysfunction occurring in the ischemic hearts and lay the groundwork for further studies on the modulation of cardiac function during ischemia by MSC exosomes.
Language	English
Publishing date	2023-04-14
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2831046-9
ISSN	2405-5808 ; 2405-5808
ISSN (online)	2405-5808
ISSN	2405-5808
DOI	10.1016/j.bbrep.2023.101463
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Article ; Online: Proteomic analysis of transcription factors involved in the alteration of ischemic mouse heart as modulated by MSC exosomes

Rajshekhar A. Kore / Samir V. Jenkins / Azemat Jamshidi-Parsian / Alan J. Tackett / Robert J. Griffin / Srinivas Ayyadevara / Jawahar L. Mehta

Biochemistry and Biophysics Reports, Vol 34, Iss , Pp 101463- (2023)

2023

Abstract	Mesenchymal stem cell (MSC) exosomes have been found to attenuate cardiac systolic and diastolic dysfunction in animal models of ischemia. Exosomes carry a plethora of active and inactive proteins as their cargo, which are readily available to the recipient cell for use in intracellular signaling pathways-depending on the stresses, such as ischemia or hypoxia. Among the exosomal proteins are the often-overlooked cargo of transcriptional regulators. These transcriptional regulators influence the transcriptome and subsequently the proteome of recipient cell. Here, we report the transcriptional factors and regulators differentially modulated and their potential role in modulating cardiac function in MSC exosome treated ischemic mice hearts. Our analysis shows ischemic stress modulating transcriptional regulators and factors such as HSF1 and HIF1A in the infarct and peri-infarct areas of ischemic hearts which is mitigated by MSC exosomes. Similarly, STAT3 and SMAD3 are also modulated by MSC exosomes. Interestingly, NOTCH1 and β-catenin were detected in the ischemic hearts. The differential expression of these regulators and factors drives changes in various biological process governed in the ischemic cardiac cells.We believe these studies will advance our understanding of cardiac dysfunction occurring in the ischemic hearts and lay the groundwork for further studies on the modulation of cardiac function during ischemia by MSC exosomes.
Keywords	Mesenchymal stem cell exosomes ; Myocardial ischemia ; Post-ischemic fibrosis ; Proteomics ; Transcription factors ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	610
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Rajshekhar A. Kore / Jeffrey C. Henson / Rabab N. Hamzah / Robert J. Griffin / Alan J. Tackett / Zufeng Ding / Jawahar L. Mehta

Scientific Reports, Vol 12, Iss 1, Pp 1-

Molecular events in MSC exosome mediated cytoprotection in cardiomyocytes

2022 Volume 3

Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: MSC exosome-mediated cardioprotection in ischemic mouse heart comparative proteomics of infarct and peri-infarct areas.

Kore, Rajshekhar A / Wang, Xianwei / Ding, Zufeng / Griffin, Robert J / Tackett, Alan J / Mehta, Jawahar L

Molecular and cellular biochemistry

2021 Volume 476, Issue 4, Page(s) 1691–1704

Abstract: Mesenchymal stem cell (MSC) exosomes may limit cardiac injury, and even reverse cardiac damage in animal models of ischemia. To understand exosome-mediated improvement in cardiac function we examined the proteomic alternations in the MSC exosome-treated ... ...

Abstract	Mesenchymal stem cell (MSC) exosomes may limit cardiac injury, and even reverse cardiac damage in animal models of ischemia. To understand exosome-mediated improvement in cardiac function we examined the proteomic alternations in the MSC exosome-treated mice hearts subjected to left coronary artery (LCA) ligation, with particular emphasis on peri-infarct areas. At 7 days after LCA ligation, left ventricular end systolic thickness, infarct size and survival of mice were studied. Mass spectrometric analysis of infarct and peri-infarct areas was carried out. Expression of inflammatory markers (LOX-1 and NLRP3) and cell death markers (Bax, Bcl-2, Caspases 1 and 3 and GSDMD) were investigated by Western blots and immunofluorescence. Proteomic analysis of the infarct and peri-infarct areas in saline-treated hearts revealed differentially expressed proteins involved in inflammation and apoptotic cell death, while showing depletion of processes governing cell death. Exosome treatment significantly improved the proteomic profile in both infarct and peri-infarct areas, more so in the peri-infarct areas. The infarct size was smaller (9 ± 1%), and cardiac contractile function (fractional shortening) was preserved in the exosome-treated mice (28 ± 2%). Survival of exosome-treated mice was also better. White blood cell accumulation in and around the infarct area, expression of LOX-1 and NLRP3 inflammasome, and markers of cell death (cleaved Caspase-3, Caspase-1, GSDMD, Bcl-2 and Bax) were dramatically reduced by MSC exosome treatment (all p < 0.01). In cultured primary mouse cardiomyocytes, treatment with MSC exosomes essentially reversed inflammation-induced pro-apoptotic and inflammatory signals (p < 0.01). MSC exosomes exert their cardioprotective effects by suppressing inflammation and pro-apoptotic processes, particularly in the peri-infarct areas, resulting in preservation of cardiac function after LCA ligation.
MeSH term(s)	Animals ; Cell Line, Transformed ; Exosomes/metabolism ; Exosomes/pathology ; Exosomes/transplantation ; Humans ; Male ; Mesenchymal Stem Cells/metabolism ; Mesenchymal Stem Cells/pathology ; Mice ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Infarction/prevention & control
Language	English
Publishing date	2021-01-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-020-04029-6
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Article: Phosphorylation negatively regulates exosome mediated secretion of cryAB in glioma cells.

Kore, Rajshekhar A / Abraham, Edathara C

Biochimica et biophysica acta

2015 Volume 1863, Issue 2, Page(s) 368–377

Abstract: Exosomes mediate secretion of crystallin alphaB (cryAB), a well characterized molecular chaperone with anti-apoptotic activity. However, the mechanisms governing its packaging and secretion remained unexplored. In glioma cells, notwithstanding extensive ... ...

Abstract	Exosomes mediate secretion of crystallin alphaB (cryAB), a well characterized molecular chaperone with anti-apoptotic activity. However, the mechanisms governing its packaging and secretion remained unexplored. In glioma cells, notwithstanding extensive phosphorylation of cryAB at Ser59 followed by Ser45 (Ser19 is largely unphosphorylated), we discovered that the majority of secreted exosomal cryAB is nonphosphorylated. Transient ectopic expression of a yellow fluorescent protein (YFP) tagged triple phosphomimic (3-SD) cryAB construct in cryAB absent glioma cells led to the formation of large cytosolic inclusions. Our findings demonstrate that mimicking phosphorylation significantly reduces cryAB secretion via exosomes. Moreover, decreased colocalization of 3-SD YFP-cryAB with multivesicular endosome (MVE) and exosome marker, CD63 or Rab27, a small GTPase regulating exocytosis of MVEs, suggests that phosphorylation deters packaging of cryAB in vesicles bound for secretion as exosomes. Additionally, we found that preventing O-GlcNAcylation on cryAB also curtailed its colocalization with CD63 and Rab27 resulting in reduced exosomal secretion. Thus, our study points to O-GlcNAcylation and lack of phosphorylation as being the selective processes involved in the packaging and secretion of cryAB via exosomes.
MeSH term(s)	Blotting, Western ; Cell Line, Tumor ; Exosomes/metabolism ; Exosomes/ultrastructure ; Glioma/genetics ; Glioma/metabolism ; Glioma/pathology ; Glycosylation ; Humans ; Luminescent Proteins/genetics ; Luminescent Proteins/metabolism ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Multivesicular Bodies/metabolism ; Mutation ; Phosphorylation ; Serine/genetics ; Serine/metabolism ; Tetraspanin 30/metabolism ; alpha-Crystallin B Chain/genetics ; alpha-Crystallin B Chain/metabolism ; rab GTP-Binding Proteins/metabolism ; rab27 GTP-Binding Proteins
Chemical Substances	CD63 protein, human ; Luminescent Proteins ; Tetraspanin 30 ; alpha-Crystallin B Chain ; rab27 GTP-Binding Proteins ; Serine (452VLY9402) ; RAB27A protein, human (EC 3.6.1.-.) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2015-11-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2015.11.027
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Article ; Online: Proteomic basis of modulation of postischemic fibrosis by MSC exosomes.

Kore, Rajshekhar A / Wang, Xianwei / Henson, Jeffrey Curran / Ding, Zufeng / Jamshidi-Parsian, Azemat / Mehta, Jawahar L

American journal of physiology. Regulatory, integrative and comparative physiology

2021 Volume 321, Issue 5, Page(s) R639–R654

Abstract: After an ischemic event, there is activation of fibroblasts leading to scar formation. It is critical to limit the profibrotic remodeling and activate the reparative remodeling phase to limit cardiac diastolic dysfunction. Mesenchymal stem cell (MSC) ... ...

Abstract	After an ischemic event, there is activation of fibroblasts leading to scar formation. It is critical to limit the profibrotic remodeling and activate the reparative remodeling phase to limit cardiac diastolic dysfunction. Mesenchymal stem cell (MSC) exosomes offer significant protection against ischemia-related systolic dysfunction. Here, we studied if MSC exosomes would offer protection against profibrotic events in mouse hearts subjected to acute ischemia [1 h left coronary artery (LCA) occlusion] or chronic ischemia (7 days LCA occlusion). After acute ischemia, there was activation of inflammatory signals, more in the peri-infarct than in the infarct area, in the saline (vehicle)-treated mice. At the same time, there was expression of cardiac remodeling signals (vimentin, collagens-1 and -3, and fibronectin), more in the infarct area. Treatment with MSC exosomes before LCA ligation suppressed inflammatory signals during acute and chronic ischemia. Furthermore, exosome treatment promoted pro-reparative cardiac extracellular matrix (ECM) remodeling in both infarct and peri-infarct areas by suppressing fibronectin secretion and by modulating collagen secretion to reduce fibrotic scar formation through altered cellular signaling pathways. Proteomics study revealed intense expression of IL-1β and activation of profibrotic signals in the saline-treated hearts and their suppression in MSC exosome-treated hearts. To our knowledge, this is the first report on the infarct and peri-infarct area proteomics of ischemic mice hearts to explain MSC exosome-mediated suppression of scar formation in the ischemic mouse hearts.
MeSH term(s)	Animals ; Blotting, Western ; Cell Line ; Cell Movement ; Disease Models, Animal ; Electrophoresis, Polyacrylamide Gel ; Exosomes/metabolism ; Exosomes/transplantation ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosis ; Humans ; Inflammation Mediators/metabolism ; Interleukin-1beta/metabolism ; Male ; Mass Spectrometry ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/metabolism ; Mice, Inbred C57BL ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/pathology ; Myocardial Ischemia/surgery ; Myocardium/metabolism ; Myocardium/pathology ; Proteome ; Proteomics ; Ventricular Remodeling ; Mice
Chemical Substances	Extracellular Matrix Proteins ; IL1B protein, mouse ; Inflammation Mediators ; Interleukin-1beta ; Proteome
Language	English
Publishing date	2021-08-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00124.2021
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