Extracellular vesicles and exosome: insight from physiological regulatory perspectives

Waqas, Muhammad; Javid, Muhammad Arshad; Nazir, Muhammad Mudasser; Niaz, Nasir; Nisar, Muhammad; Manzoor, Zahid; Bhatti, Sheraz Ahmed; Hameed, Sajid; Khaliq, Muhammad Haseeb

doi:10.1007/s13105-022-00877-6

Cited by 26 publications

(22 citation statements)

References 63 publications

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“…The EV phenotype is characterized by the presence on their surface of typical maternal receptors [ 60 ]. The most common integrin receptor αIIβ3 present on PLT surfaces was favored as a PEV marker.…”

Section: Discussionmentioning

confidence: 99%

Platelet Extracellular Vesicles Are Taken up by Canine T Lymphocytes but Do Not Play a Role in Their Proliferation, Differentiation and Cytokine Production In Vitro

Żmigrodzka

Pingwara

Winnicka

2022

IJMS

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Eukaryotic and prokaryotic cells in physiological and pathological conditions form membrane-bound extracellular vesicles, known as EVs. The ability of these submicron structures to transfer their cargoes (miRNA, DNA, protein, cytokines, receptors, etc.) into recipient cells is described. Recent data revealed that platelet-derived extracellular vesicles (PEVs) crosstalk promotes cancer growth and metastasis formation. Moreover, they exert immunosuppressive activities on phagocytes. This EV subpopulation is the most abundant amongst all types in circulation. According to the authors’ best knowledge, there is no information regarding the impact of PEVs on canine lymphocytes. The aim of this study was to evaluate the influence of PEVs on lymphocyte proliferation, phenotype and cytokine production in vitro. In the study, it was demonstrated (i) that PEVs interact differently with lymphocyte subsets and are preferentially associated with T-lymphocytes PBMC, while (ii) they are rarely detected in association with B-lymphocytes, and there is evidence that (iii) PEV uptake is observed after 7 h of co-culturing with lymphocytes. In addition, obtained data support the notion that PEVs do not influence in vitro lymphocyte proliferation, differentiation and cytokine production in a canine model.

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Section: Discussionmentioning

confidence: 99%

Platelet Extracellular Vesicles Are Taken up by Canine T Lymphocytes but Do Not Play a Role in Their Proliferation, Differentiation and Cytokine Production In Vitro

Żmigrodzka

Pingwara

Winnicka

2022

IJMS

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“…Exosomes are released continuously from cells, whereas microvesicles and apoptotic bodies are released predominantly by activated or apoptotic cells. EVs are generated by plasma membrane blebbing, which induces the externalization of phosphatidylserine, normally located exclusively in the cytoplasmic leaflet [ 21 ].…”

Section: The Endotheliummentioning

confidence: 99%

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

Six

Guillaume

Jacob

et al. 2022

IJMS

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The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19.

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Section: Seahorse Metabolic Analysis Also Indicated That Expression O...mentioning

confidence: 99%

“…Exosomes become an attractive focus of cancer research recently [11]. The exosomes are extracellular vesicles (EVs) originated from endosomes, with diameters ranging between 30 and 150 nm, and are frequently detected in the urine, blood, and other samples of cerebrospinal fluid [11]. Exosomes could carry cargoes containing multiple cellular components, such as proteins, lipids, DNAs, transposable elements, and RNAs (either coding and non-coding).…”

Section: Seahorse Metabolic Analysis Also Indicated That Expression O...mentioning

confidence: 99%

“…It was reported that TAMs resided in LSCC microenvironment, were associated with disease prognosis and induced to M2 differentiation [9,10]. Cells, including macrophages, produce and secret small cell vesicles with diameters measured between 30 and 150 nm, called exosomes, for exchange of material with other cells [11]. In tumors, exosomes actively participate in the communication between cancer cells and tumor niche cells, that influence on the survival, growth and metastasis of tumors [12].…”

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confidence: 99%

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Exosomes from M2 macrophages promoted glycolysis in FaDu cells by inhibiting PDLIM2 expression to stabilize PFKL

Wang¹,

Li²,

Zhou³

et al. 2022

neo

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Laryngeal squamous cell carcinoma (LSCC) is one of the most prevalent malignant diseases worldwide. LSCC patients suffer from a severe decline in life quality, due to the essential roles of the larynx in basic functions in a human body. The overarching goa l of the present study is to explore whether exosome from M2 macrophages promotes LSCC by targeting glycolysis. In the current study, the expression of PDLIM2, an E3 ubiquitin ligase, in clinical samples was monitored by quantitative PCR and immunohistochemical examination. Extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were measured by the Seahorse machine. Cell proliferation was measured by using Cell Counting Kit-8. A luciferase assay was performed to verify the regulation of miRNA on its target gene. The results showed that PDLIM2 exhibited downregulation in LSCC clinical samples and was associated with stage and differentiation of tumors in patients. In FaDu cell line, PDLIM2 inhibited cell proliferation and glycolysis but pro moted the ubiquitination of PFKL. Exosomes from M2-type macrophages delivered miR-222-3p into LSCC cells to suppress PDLIM2 expression, leading to the elevated expression of PFKL and enhanced glycolysis which accelerated the proliferation of FaDu cells. The findings from cultured cells were supported by a subcutaneous tumor growth model in nude mice. Collectively, our data provided a snapshot of the miR-222-3p/PDLIM2/PFKL axis in LSCC tumorigenesis, and in concert with the importance of TAM exosomes and glycolysis, could be potentially translated to LSCC clinics.

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Extracellular vesicles and exosome: insight from physiological regulatory perspectives

Cited by 26 publications

References 63 publications

Platelet Extracellular Vesicles Are Taken up by Canine T Lymphocytes but Do Not Play a Role in Their Proliferation, Differentiation and Cytokine Production In Vitro

Platelet Extracellular Vesicles Are Taken up by Canine T Lymphocytes but Do Not Play a Role in Their Proliferation, Differentiation and Cytokine Production In Vitro

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

Exosomes from M2 macrophages promoted glycolysis in FaDu cells by inhibiting PDLIM2 expression to stabilize PFKL

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