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Article ; Online: Stimulation of soluble guanylate cyclase activity with riociguat promotes angiogenesis and improves neovascularization after limb ischemia.

Dhahri, Wahiba / Dussault, Sylvie / Raguema, Nozha / Desjarlais, Michel / Rivard, Alain

2023 Volume 372, Page(s) 32–40

Abstract: Background and aims: The NO-cGMP pathway is essential for angiogenesis, vasculogenesis and post-natal neovascularization. The key enzyme responsible for the synthesis of cGMP following binding of NO is soluble guanylate cyclase (sGC). Riociguat is the ... ...

Abstract	Background and aims: The NO-cGMP pathway is essential for angiogenesis, vasculogenesis and post-natal neovascularization. The key enzyme responsible for the synthesis of cGMP following binding of NO is soluble guanylate cyclase (sGC). Riociguat is the first member of a novel class of compounds known as sGC stimulators. We tested the hypothesis that stimulation of sGC with riociguat might improve neovascularization in response to ischemia. Methods: In vitro, the angiogenic effect of riociguat was tested in human umbilical vein endothelial cells (HUVECs). In vivo, neovascularization was investigated in a mouse model of limb ischemia. C57Bl/6 mice were treated by gavage with 3 mg/kg/day of riociguat for a total of 28 days. After two weeks of treatment, hindlimb ischemia was surgically induced by femoral artery removal. Results: In a matrigel assay in vitro, riociguat dose-dependently stimulates tubule formation in HUVECs. Cell migration (scratch assay) is also increased in HUVECs treated with riociguat. At the molecular level, riociguat treatment leads to rapid activation of the p44/p42 MAP kinase pathway in HUVECs. Inhibition of protein kinase G (PKG) activity supresses both p44/p42 MAP kinase activation and angiogenesis in HUVECs treated with riociguat. In vivo, treatment with riociguat improves blood flow recovery after ischemia (Laser Doppler imaging), and increases capillary density in ischemic muscles (CD31 immunostaining). Clinically, this is associated with a significant decrease of ambulatory impairment and ischemic damages. Interestingly, mice treated with riociguat also show a 94% increase in the number of bone marrow-derived pro-angiogenic cells (PACs) compared to control mice. Moreover, riociguat treatment is associated with a significant improvement of PAC functions including migratory capacity, adhesion to an endothelial monolayer, and integration into endothelial tubular networks. Conclusions: The sGC stimulator riociguat promotes angiogenesis and improves neovascularization after ischemia. The mechanism involves PKG-dependent activation of p44/p42 MAP kinase pathway, together with an improvement of PAC number and functions. sGC stimulation could constitute a novel therapeutic strategy to reduce tissue ischemia in patients with severe atherosclerotic diseases.
MeSH term(s)	Humans ; Mice ; Animals ; Soluble Guanylyl Cyclase/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Neovascularization, Pathologic ; Ischemia ; Human Umbilical Vein Endothelial Cells ; Neovascularization, Physiologic ; Hindlimb
Chemical Substances	Soluble Guanylyl Cyclase (EC 4.6.1.2) ; riociguat (RU3FE2Y4XI) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24)
Language	English
Publishing date	2023-03-27
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2023.03.017
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Article ; Online: Dual functions of ARP101 in targeting membrane type-1 matrix metalloproteinase: Impact on U87 glioblastoma cell invasion and autophagy signaling.

Desjarlais, Michel / Annabi, Borhane

Chemical biology & drug design

2018 Volume 93, Issue 3, Page(s) 272–282

Abstract: Membrane type-1 matrix metalloproteinase (MT1-MMP) possesses both extracellular proteolytic and intracellular signal-transducing functions in tumorigenesis. An imbalance in MT1-MMP expression and/or function triggers a metastatic, invasive, and therapy ... ...

Abstract	Membrane type-1 matrix metalloproteinase (MT1-MMP) possesses both extracellular proteolytic and intracellular signal-transducing functions in tumorigenesis. An imbalance in MT1-MMP expression and/or function triggers a metastatic, invasive, and therapy resistance phenotype. MT1-MMP is involved in extracellular matrix (ECM) proteolysis, activation of latent MMPs, as well as in autophagy signaling in human hepatoma and glioblastoma cells. A low autophagy index in tumorigenesis has been inferred by recent studies where autophagic capacity was decreased during tumor progression. Here, we establish ARP101 as a dual-function small-molecule inhibitor against MT1-MMP ECM hydrolysis and autophagy signal-transducing functions in a model of grade IV glioblastoma cells. ARP101 inhibited concanavalin-A-mediated proMMP-2 activation into MMP-2, as well as MT1-MMP auto-proteolytic processing. When overexpressing recombinant Wt MT1-MMP, ARP101 inhibited proMMP-2 activation and triggered the formation of MT1-MMP oligomers that required trafficking to the plasma membrane. ARP101 further induced cell autophagy as reflected by increased formation of acidic vacuole organelles, LC3 puncta, and autophagy-related protein ATG9 transcription. These were all significantly reversed upon siRNA-mediated gene silencing of MT1-MMP. ARP101 can thus concomitantly inhibit MT1-MMP extracellular catalytic function and exploit its intracellular transducing signal function to trigger autophagy-mediated cell death in U87 glioblastoma cancer cells.
MeSH term(s)	Autophagy/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Concanavalin A/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Matrix Metalloproteinase 14/chemistry ; Matrix Metalloproteinase 14/genetics ; Matrix Metalloproteinase 14/metabolism ; Matrix Metalloproteinase 2/genetics ; Matrix Metalloproteinase 2/metabolism ; RNA Interference ; RNA, Small Interfering/metabolism ; Signal Transduction/drug effects ; Sulfonamides/pharmacology
Chemical Substances	ARP101 compound ; RNA, Small Interfering ; Sulfonamides ; Concanavalin A (11028-71-0) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 14 (EC 3.4.24.80)
Language	English
Publishing date	2018-10-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2216600-2
ISSN	1747-0285 ; 1747-0277
ISSN (online)	1747-0285
ISSN	1747-0277
DOI	10.1111/cbdd.13410
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Article ; Online: Novel Function of Nogo-A as Negative Regulator of Endothelial Progenitor Cell Angiogenic Activity: Impact in Oxygen-Induced Retinopathy.

Ruknudin, Pakiza / Nazari, Ali Riza / Wirth, Maelle / Lahaie, Isabelle / Bajon, Emmanuel / Rivard, Alain / Chemtob, Sylvain / Desjarlais, Michel

International journal of molecular sciences

2023 Volume 24, Issue 17

Abstract: Endothelial Progenitor Cells (EPCs) can actively participate in revascularization in oxygen-induced retinopathy (OIR). Yet the mechanisms responsible for their dysfunction is unclear. Nogo-A, whose function is traditionally related to the inhibition of ... ...

Abstract	Endothelial Progenitor Cells (EPCs) can actively participate in revascularization in oxygen-induced retinopathy (OIR). Yet the mechanisms responsible for their dysfunction is unclear. Nogo-A, whose function is traditionally related to the inhibition of neurite function in the central nervous system, has recently been documented to display anti-angiogenic pro-repellent properties. Based on the significant impact of EPCs in retinal vascularization, we surmised that Nogo-A affects EPC function, and proceeded to investigate the role of Nogo-A on EPC function in OIR. The expression of Nogo-A and its specific receptor NgR1 was significantly increased in isolated EPCs exposed to hyperoxia, as well as in EPCs isolated from rats subjected to OIR compared with respective controls (EPCs exposed to normoxia). EPCs exposed to hyperoxia displayed reduced migratory and tubulogenic activity, associated with the suppressed expression of prominent EPC-recruitment factors SDF-1/CXCR4. The inhibition of Nogo-A (using a Nogo-66 neutralizing antagonist peptide) or siRNA-NGR1 in hyperoxia-exposed EPCs restored SDF-1/CXCR4 expression and, in turn, rescued the curtailed neovascular functions of EPCs in hyperoxia. The in vivo intraperitoneal injection of engineered EPCs (Nogo-A-inhibited or NgR1-suppressed) in OIR rats at P5 (prior to exposure to hyperoxia) prevented retinal and choroidal vaso-obliteration upon localization adjacent to vasculature; coherently, the inhibition of Nogo-A/NgR1 in EPCs enhanced the expression of key angiogenic factors VEGF, SDF-1, PDGF, and EPO in retina; CXCR4 knock-down abrogated suppressed NgR1 pro-angiogenic effects. The findings revealed that hyperoxia-induced EPC malfunction is mediated to a significant extent by Nogo-A/NgR1 signaling via CXCR4 suppression; the inhibition of Nogo-A in EPCs restores specific angiogenic growth factors in retina and the ensuing vascularization of the retina in an OIR model.
MeSH term(s)	Animals ; Rats ; Oxygen/adverse effects ; Nogo Proteins/genetics ; Hyperoxia/complications ; Endothelial Progenitor Cells ; Retinal Diseases
Chemical Substances	Oxygen (S88TT14065) ; Nogo Proteins
Language	English
Publishing date	2023-08-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241713185
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Article: Nutraceutical Targeting of Inflammation-Modulating microRNAs in Severe Forms of COVID-19: A Novel Approach to Prevent the Cytokine Storm.

Desjarlais, Michel / Wirth, Maëlle / Lahaie, Isabelle / Ruknudin, Pakiza / Hardy, Pierre / Rivard, Alain / Chemtob, Sylvain

Frontiers in pharmacology

2020 Volume 11, Page(s) 602999

Abstract: The coronavirus disease 2019 (COVID-19) pandemic has become the number one health problem worldwide. As of August 2020, it has affected more than 18 million humans and caused over 700,000 deaths worldwide. COVID-19 is an infectious disease that can lead ... ...

Abstract	The coronavirus disease 2019 (COVID-19) pandemic has become the number one health problem worldwide. As of August 2020, it has affected more than 18 million humans and caused over 700,000 deaths worldwide. COVID-19 is an infectious disease that can lead to severe acute respiratory syndrome. Under certain circumstances, the viral infection leads to excessive and uncontrolled inflammatory response, which is associated with the massive release of inflammatory cytokines in pulmonary alveolar structures. This phenomenon has been referred to as the "cytokine storm," and it is closely linked to lung injury, acute respiratory syndrome and mortality. Unfortunately, there is currently no vaccine available to prevent the infection, and no effective treatment is available to reduce the mortality associated with the severe form of the disease. The cytokine storm associate with COVID-19 shows similarities with those observed in other pathologies such as sepsis, acute respiratory distress syndrome, acute lung injury and other viral infection including severe cases of influenza. However, the specific mechanisms that cause and modulate the cytokine storm in the different conditions remain to be determined. micro-RNAs are important regulators of gene expression, including key inflammatory cytokines involved in the massive recruitment of immune cells to the lungs such as IL1β, IL6, and TNFα. In recent years, it has been shown that nutraceutical agents can modulate the expression of miRs involved in the regulation of cytokines in various inflammatory diseases. Here we review the potential role of inflammatory-regulating-miRs in the cytokine storm associated with COVID-19, and propose that nutraceutical agents may represent a supportive therapeutic approach to modulate dysregulated miRs in this condition, providing benefits in severe respiratory diseases.
Language	English
Publishing date	2020-12-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.602999
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Article: MicroRNA Expression Profiling of Bone Marrow-Derived Proangiogenic Cells (PACs) in a Mouse Model of Hindlimb Ischemia: Modulation by Classical Cardiovascular Risk Factors.

Desjarlais, Michel / Dussault, Sylvie / Rivera, José Carlos / Chemtob, Sylvain / Rivard, Alain

Frontiers in genetics

2020 Volume 11, Page(s) 947

Abstract: Background: Classical cardiovascular risk factors (CRFs) are associated with impaired angiogenic activities of bone marrow-derived proangiogenic cells (PACs) related to peripheral artery diseases (PADs) and ischemia-induced neovascularization. MicroRNAs ...

Abstract	Background: Classical cardiovascular risk factors (CRFs) are associated with impaired angiogenic activities of bone marrow-derived proangiogenic cells (PACs) related to peripheral artery diseases (PADs) and ischemia-induced neovascularization. MicroRNAs (miRs) are key regulators of gene expression, and they are involved in the modulation of PAC function and PAC paracrine activity. However, the effects of CRFs on the modulation of miR expression in PACs are unknown. Aims and methods: We used a model of hindlimb ischemia and next-generation sequencing to perform a complete profiling of miRs in PACs isolated from the bone marrow of mice subjected to three models of CRFs: aging, smoking (SMK) and hypercholesterolemia (HC). Results: Approximately 570 miRs were detected in PACs in the different CRF models. When excluding miRs with a very low expression level (<100 RPM), 40 to 61 miRs were found to be significantly modulated by aging, SMK, or HC. In each CRF condition, we identified downregulated proangiogenic miRs and upregulated antiangiogenic miRs that could contribute to explain PAC dysfunction. Interestingly, several miRs were similarly downregulated (e.g., miR-542-3p, miR-29) or upregulated (e.g., miR-501, miR-92a) in all CRF conditions. Conclusion: This study describes for the first time the effects of CRFs on the modulation of miR profile in PACs related to PAD and ischemia-induced neovascularization. We found that several angiogenesis-modulating miRs are similarly altered in different CRF conditions. Our findings constitute a solid framework for the identification of miRs that could be targeted in PACs in order to improve their angiogenic function and for the future development of novel therapies to improve neovascularization and reduce tissue damage in patients with severe PAD.
Language	English
Publishing date	2020-08-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.00947
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Article ; Online: Reduced expression of microRNA-130a promotes endothelial cell senescence and age-dependent impairment of neovascularization.

Dhahri, Wahiba / Dussault, Sylvie / Légaré, Éliane / Rivard, François / Desjarlais, Michel / Mathieu, Raphael / Rivard, Alain

Aging

2020 Volume 12, Issue 11, Page(s) 10180–10193

Abstract: Aging is associated with impaired neovascularization in response to ischemia. MicroRNAs are small noncoding RNAs emerging as key regulators of physiological and pathological processes. Here we investigated the potential role of microRNAs in endothelial ... ...

Abstract	Aging is associated with impaired neovascularization in response to ischemia. MicroRNAs are small noncoding RNAs emerging as key regulators of physiological and pathological processes. Here we investigated the potential role of microRNAs in endothelial cell senescence and age-dependent impairment of neovascularization. Next generation sequencing and qRT-PCR analyses identified miR-130a as a pro-angiogenic microRNA which expression is significantly reduced in old mouse aortic endothelial cells (ECs). Transfection of young ECs with a miR-130a inhibitor leads to accelerated senescence and reduced angiogenic functions. Conversely, forced expression of miR-130a in old ECs reduces senescence and improves angiogenesis. In a mouse model of hindlimb ischemia, intramuscular injection of miR-130a mimic in older mice restores blood flow recovery and vascular densities in ischemic muscles, improves mobility and reduces tissue damage. miR-130a directly targets antiangiogenic homeobox genes MEOX2 and HOXA5. MEOX2 and HOXA5 are significantly increased in the ischemic muscles of aging mice, but forced expression of miR-130a reduces the expression of these factors. miR-130a treatment after ischemia is also associated with increased number and improved functional activities of pro-angiogenic cells (PACs). Forced expression of miR-130a could constitute a novel strategy to improve blood flow recovery and reduce ischemia in older patients with ischemic vascular diseases.
MeSH term(s)	Age Factors ; Aged ; Aging/genetics ; Animals ; Aorta/cytology ; Cell Movement/drug effects ; Cell Movement/genetics ; Cellular Senescence/drug effects ; Cellular Senescence/genetics ; Disease Models, Animal ; Endothelial Cells/drug effects ; Endothelial Cells/pathology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/pathology ; Hindlimb/blood supply ; Homeodomain Proteins/genetics ; Human Umbilical Vein Endothelial Cells ; Humans ; Ischemia/pathology ; Mice ; MicroRNAs/agonists ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/metabolism ; Neovascularization, Physiologic/drug effects ; Neovascularization, Physiologic/genetics ; Primary Cell Culture ; Transcription Factors/genetics ; Young Adult
Chemical Substances	Homeodomain Proteins ; Hoxa5 protein, mouse ; MIRN130 microRNA, human ; MIRN130 microRNA, mouse ; Meox2 protein, mouse ; MicroRNAs ; Transcription Factors
Language	English
Publishing date	2020-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.103340
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Article ; Online: MicroRNA-150 Modulates Ischemia-Induced Neovascularization in Atherosclerotic Conditions.

Desjarlais, Michel / Dussault, Sylvie / Dhahri, Wahiba / Mathieu, Raphael / Rivard, Alain

Arteriosclerosis, thrombosis, and vascular biology

2017 Volume 37, Issue 5, Page(s) 900–908

Abstract: Objective: Hypercholesterolemia is an atherosclerotic condition that is associated with impaired neovascularization in response to ischemia. This study sought to define the role of microRNAs in that pathophysiology.: Approach and results: Next- ... ...

Abstract	Objective: Hypercholesterolemia is an atherosclerotic condition that is associated with impaired neovascularization in response to ischemia. This study sought to define the role of microRNAs in that pathophysiology. Approach and results: Next-generation sequencing and quantitative reverse transcription polymerase chain reaction analyses identified miR-150 as a proangiogenic microRNA, which expression is significantly reduced in the ischemic muscles of hypercholesterolemic apolipoprotein E-deficient (ApoE Conclusions: Hypercholesterolemia is associated with reduced expression of miR-150, impaired Src signaling, and inefficient neovascularization in response to ischemia. Forced expression of miR-150 using a miR mimic could constitute a novel therapeutic strategy to improve ischemia-induced neovascularization in atherosclerotic conditions.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/physiopathology ; Cells, Cultured ; Disease Models, Animal ; Female ; Fenoterol ; Genetic Predisposition to Disease ; Hindlimb ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Hypercholesterolemia/genetics ; Hypercholesterolemia/metabolism ; Ischemia/genetics ; Ischemia/metabolism ; Ischemia/physiopathology ; Lipoproteins, LDL/pharmacology ; Mice, Inbred C57BL ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Skeletal/blood supply ; Neovascularization, Physiologic ; Nitric Oxide Synthase Type III/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Signal Transduction ; Transfection ; src-Family Kinases/metabolism
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Apolipoproteins E ; Lipoproteins, LDL ; MIRN150 microRNA, human ; MicroRNAs ; Mirn150 microRNA, mouse ; SRCIN1 protein, human ; oxidized low density lipoprotein ; Fenoterol (22M9P70OQ9) ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39) ; src-Family Kinases (EC 2.7.10.2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2017-03-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.117.309189
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Article: MicroRNA-96 Promotes Vascular Repair in Oxygen-Induced Retinopathy-A Novel Uncovered Vasoprotective Function.

Desjarlais, Michel / Wirth, Maëlle / Rivera, José Carlos / Lahaie, Isabelle / Dabouz, Rabah / Omri, Samy / Ruknudin, Pakiza / Borras, Celine / Chemtob, Sylvain

Frontiers in pharmacology

2020 Volume 11, Page(s) 13

Abstract: Background and aims: Vascular degeneration is a hallmark in the pathogenesis of oxygen-induced retinopathy (OIR). Dysregulation of microRNAs (miRNAs), key regulators of genes expressions, has been implicated in the regulation of ocular angiogenesis. ... ...

Abstract	Background and aims: Vascular degeneration is a hallmark in the pathogenesis of oxygen-induced retinopathy (OIR). Dysregulation of microRNAs (miRNAs), key regulators of genes expressions, has been implicated in the regulation of ocular angiogenesis. However, miRNAs specific functions in impaired vascular development during OIR are poorly understood. Herein, we identified miR-96 as one of the most highly expressed miRNAs in the retina and choroid during vascular development and investigated the potential role of miR-96 on microvascular degeneration in a rat OIR model. Methods and results: Next generation sequencing (NGS) and qRT-PCR analysis showed that miR-96 maintain high levels of expression during ocular vascular development. Nevertheless, miR-96 was significantly downregulated in the retina and choroid of OIR rats (80% O Conclusion: This study demonstrates that miR-96 regulates the expression of angiogenic factors (VEGF/ANG-2) associated to the maintenance of retinal and choroidal microvasculature during physiological and pathological conditions. Intravitreal supplementation of miR-96 mimic could constitute a novel therapeutic strategy to improve vascular repair in OIR and other ischemic retinopathies.
Language	English
Publishing date	2020-02-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.00013
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Article: Tyrosine-Protein Phosphatase Non-receptor Type 9 (PTPN9) Negatively Regulates the Paracrine Vasoprotective Activity of Bone-Marrow Derived Pro-angiogenic Cells: Impact on Vascular Degeneration in Oxygen-Induced Retinopathy.

Desjarlais, Michel / Ruknudin, Pakiza / Wirth, Maëlle / Lahaie, Isabelle / Dabouz, Rabah / Rivera, José Carlos / Habelrih, Tiffany / Omri, Samy / Hardy, Pierre / Rivard, Alain / Chemtob, Sylvain

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 679906

Abstract: Background and aim: Insufficient post-ischemic neovascularization is an initial key step in the pathogenesis of Oxygen-Induced Retinopathy (OIR). During neovascularization, pro-angiogenic cells (PACs) are mobilized from the bone marrow and integrate ... ...

Abstract	Background and aim: Insufficient post-ischemic neovascularization is an initial key step in the pathogenesis of Oxygen-Induced Retinopathy (OIR). During neovascularization, pro-angiogenic cells (PACs) are mobilized from the bone marrow and integrate into ischemic tissues to promote angiogenesis. However, the modulation of PAC paracrine activity during OIR and the specific mechanisms involved remain to be explored. Because Tyrosine-protein phosphatase non-receptor type 9 (PTPN9) is reported to be a negative regulator of stem cell differentiation and angiogenesis signaling, we investigated its effect on PAC activity in the context of OIR. Methods and results: In a rat model of OIR, higher levels of PTPN9 in the retina and in bone marrow derived PACs are associated with retinal avascular areas, lower levels of the mobilization factor SDF-1 and decreased number of CD34 Conclusion: Our results suggest that hyperoxia alters the paracrine proangiogenic activity of BM-PACs by inducing PTPN9, which can contribute to impair post-ischemic revascularization in the context of OIR. Targeting PTPN9 restores PAC angiogenic properties, and provide a new target for vessel integrity in ischemic retinopathies.
Language	English
Publishing date	2021-05-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.679906
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Article ; Online: Forced expression of microRNA-146b reduces TRAF6-dependent inflammation and improves ischemia-induced neovascularization in hypercholesterolemic conditions.

Desjarlais, Michel / Dussault, Sylvie / Rivard, François / Harel, Sharon / Sanchez, Veronica / Hussain, Sabah N A / Rivard, Alain

Atherosclerosis

2019 Volume 289, Page(s) 73–84

Abstract: Background and aims: MicroRNA (miR)-146 is a key regulator of inflammation, endothelial activation and atherosclerosis. This study sought to define its potential role for the modulation of ischemia-induced neovascularization in atherosclerotic ... ...

Abstract	Background and aims: MicroRNA (miR)-146 is a key regulator of inflammation, endothelial activation and atherosclerosis. This study sought to define its potential role for the modulation of ischemia-induced neovascularization in atherosclerotic conditions. Methods: Next generation sequencing and qRT-PCR analyses were used to compare microRNA expression in the ischemic muscles of hypercholesterolemic ApoE-deficient (ApoE Results: We found that miR-146b (but not miR-146a) is significantly reduced in the ischemic muscles of ApoE Conclusions: Hypercholesterolemia is associated with reduced expression of miR-146b, which increases TRAF6-dependent inflammation and is associated with poor neovascularization in response to ischemia. Forced expression of miR-146b using a miR mimic could constitute a novel therapeutic strategy to improve ischemia-induced neovascularization in atherosclerotic conditions.
MeSH term(s)	Animals ; Blood Flow Velocity ; Cell Movement ; Cell Proliferation ; Hindlimb/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypercholesterolemia/metabolism ; Inflammation/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Ischemia/physiopathology ; Lipoproteins, LDL/metabolism ; Mice ; Mice, Knockout, ApoE ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neovascularization, Pathologic/metabolism ; Reactive Oxygen Species/metabolism ; Sequence Analysis, RNA ; THP-1 Cells ; TNF Receptor-Associated Factor 6/genetics
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Lipoproteins, LDL ; MIRN146 microRNA, human ; MicroRNAs ; Mirn146 microRNA, mouse ; Reactive Oxygen Species ; TNF Receptor-Associated Factor 6 ; TRAF6 protein, mouse ; Tifab protein, human ; oxidized low density lipoprotein
Language	English
Publishing date	2019-08-23
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2019.08.010
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