Adjuvant role of macrophages in stem cell-induced cardiac repair in rats

Lim, Soo Yeon; Cho, Dong Im; Jeong, Hyun‐Ja; Kang, Hyejin; Kim, Mi Ra; Cho, Meeyoung; Kim, Yong Sook; Ahn, Youngkeun

doi:10.1038/s12276-018-0171-5

Cited by 20 publications

(14 citation statements)

References 38 publications

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“…Moreover, an intact immune response is essential to achieve any improvement observed in cardiac function when injecting bone marrow derived progenitor cells into infarcted myocardium (261). Furthermore, bone marrow-derived MSCs achieve better improvement in cardiac function, fibrosis, and angiogenesis when administered in combination with co-cultured macrophages in rat MI, the improvements being associated with elevated anti-inflammatory macrophages and gene expression (262). Finally, the inflammatory response per se elicited during and owing to a stem cell-based therapy may be of paramount importance for the beneficial effects of the latter in a diseased heart (263).…”

Section: Exploitation Of Cardiac and Modified Extracardiac Cells And mentioning

confidence: 99%

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

Psarras

Beis

Nikouli

et al. 2019

Front. Cardiovasc. Med.

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Following an insult by both intrinsic and extrinsic pathways, complex cellular, and molecular interactions determine a successful recovery or inadequate repair of damaged tissue. The efficiency of this process is particularly important in the heart, an organ characterized by very limited regenerative and repair capacity in higher adult vertebrates. Cardiac insult is characteristically associated with fibrosis and heart failure, as a result of cardiomyocyte death, myocardial degeneration, and adverse remodeling. Recent evidence implies that resident non-cardiomyocytes, fibroblasts but also macrophages -pillars of the innate immunity- form part of the inflammatory response and decisively affect the repair process following a cardiac insult. Multiple studies in model organisms (mouse, zebrafish) of various developmental stages (adult and neonatal) combined with genetically engineered cell plasticity and differentiation intervention protocols -mainly targeting cardiac fibroblasts or progenitor cells-reveal particular roles of resident and recruited innate immune cells and their secretome in the coordination of cardiac repair. The interplay of innate immune cells with cardiac fibroblasts and cardiomyocytes is emerging as a crucial platform to help our understanding and, importantly, to allow the development of effective interventions sufficient to minimize cardiac damage and dysfunction after injury.

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Section: Exploitation Of Cardiac and Modified Extracardiac Cells And mentioning

confidence: 99%

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

Psarras

Beis

Nikouli

et al. 2019

Front. Cardiovasc. Med.

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“…In GBM, high expression of CD44 was identified in the proteogenomic profiling of GBM tissues [ 23 ] and further classified as a GBM cell surface antigen in a systematic analysis [ 31 ]. Interestingly, this transmembrane glycoprotein can be cleaved and secreted into the vasculatures, suggesting its potential to be developed as a diagnostic marker [ 67 ]. It has been reported that the activation of CD44 by its ligand promotes cancer stem cell-like phenotypes in GBM and increased therapeutic resistance [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

Integration of RNA-Seq and proteomics data identifies glioblastoma multiforme surfaceome signature

et al. 2021

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Background Glioblastoma multiforme (GBM) is a highly lethal, stage IV brain tumour with a prevalence of approximately 2 per 10,000 people globally. The cell surface proteins or surfaceome serve as information gateway in many oncogenic signalling pathways and are important in modulating cancer phenotypes. Dysregulation in surfaceome expression and activity have been shown to promote tumorigenesis. The expression of GBM surfaceome is a case in point; OMICS screening in a cell-based system identified that this sub-proteome is largely perturbed in GBM. Additionally, since these cell surface proteins have ‘direct’ access to drugs, they are appealing targets for cancer therapy. However, a comprehensive GBM surfaceome landscape has not been fully defined yet. Thus, this study aimed to define GBM-associated surfaceome genes and identify key cell-surface genes that could potentially be developed as novel GBM biomarkers for therapeutic purposes. Methods We integrated the RNA-Seq data from TCGA GBM (n = 166) and GTEx normal brain cortex (n = 408) databases to identify the significantly dysregulated surfaceome in GBM. This was followed by an integrative analysis that combines transcriptomics, proteomics and protein-protein interaction network data to prioritize the high-confidence GBM surfaceome signature. Results Of the 2381 significantly dysregulated genes in GBM, 395 genes were classified as surfaceome. Via the integrative analysis, we identified 6 high-confidence GBM molecular signature, HLA-DRA, CD44, SLC1A5, EGFR, ITGB2, PTPRJ, which were significantly upregulated in GBM. The expression of these genes was validated in an independent transcriptomics database, which confirmed their upregulated expression in GBM. Importantly, high expression of CD44, PTPRJ and HLA-DRA is significantly associated with poor disease-free survival. Last, using the Drugbank database, we identified several clinically-approved drugs targeting the GBM molecular signature suggesting potential drug repurposing. Conclusions In summary, we identified and highlighted the key GBM surface-enriched repertoires that could be biologically relevant in supporting GBM pathogenesis. These genes could be further interrogated experimentally in future studies that could lead to efficient diagnostic/prognostic markers or potential treatment options for GBM.

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“…It was also shown to increase GBM resistance to radiation therapy [ 25 ]. A recent study demonstrated that a soluble CD44 protein secreted by the GBM cells is the link between GBM and neurodegenerative disorders, as it induces neuronal degeneration through the activation of tau pathology in the brain, which is known to be the underlying mechanism of some neurodegenerative disorders such as Alzheimer’s disease [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Glioblastoma CUSA Fluid Protein Profiling: A Comparative Investigation of the Core and Peripheral Tumor Zones

Rocca¹,

Simboli

Vincenzoni

et al. 2020

Cancers

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The present investigation aimed to characterize the protein profile of cavitating ultrasound aspirator fluid of newly diagnosed and recurrent glioblastoma comparing diverse zones of collection, i.e., tumor core and tumor periphery, with the aid of 5-aminolevulinic acid fluorescence. The samples were pooled and analyzed in triplicate by LC-MS following the shotgun proteomic approach. The identified proteins were then grouped to disclose elements exclusive and common to the tumor state or tumor zones and submitted to gene ontology classification and pathway overrepresentation analysis. The proteins common to the distinct zones were further investigated by relative quantitation, following a label free approach, to disclose possible differences of expression. Nine proteins, i.e., tubulin 2B chain, CD59, far upstream element-binding, CD44, histone H1.4, caldesmon, osteopontin, tropomyosin chain and metallothionein-2, marked the core of newly diagnosed glioblastoma with respect to tumor periphery. Considering the tumor zone, including the core and the fluorescence positive periphery, the serine glycine biosynthesis, pentose phosphate, 5-hydroxytryptamine degredation, de novo purine biosynthesis and huntington disease pathways resulted statistically significantly overrepresented with respect to the human genome of reference. The fluorescence negative zone shared several protein elements with the tumor zone, possibly indicating the presence of pathological aspects of glioblastoma rather than of normal brain parenchyma. On the other hand, its exclusive protein elements were considered to represent the healthy zone and, accordingly, exhibiting no pathways overrepresentation. On the contrary to newly diagnosed glioblastoma, pathway overrepresentation was recognized only in the healthy zone of recurrent glioblastoma. The TGFβ signaling pathway, exclusively classified in the fluorescence negative periphery in newly diagnosed glioblastoma, was instead the exclusive pathway classified in the tumor core of recurrent glioblastoma. These results, preliminary obtained on sample pools, demonstrated the potential of cavitron ultrasonic surgical aspirate fluid for proteomic profiling of glioblastoma able to distinguish molecular features specific of the diverse tumor zones and tumor states, possibly contributing to the understanding of the highly infiltrative capability and recurrent rate of this aggressive brain tumor and opening to potential clinical applications to be further investigated.

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Adjuvant role of macrophages in stem cell-induced cardiac repair in rats

Cited by 20 publications

References 38 publications

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

Integration of RNA-Seq and proteomics data identifies glioblastoma multiforme surfaceome signature

Glioblastoma CUSA Fluid Protein Profiling: A Comparative Investigation of the Core and Peripheral Tumor Zones

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