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Yonggang Guo - One of the best experts on this subject based on the ideXlab platform.

  • microRNA-205-5p Promotes Unstable Atherosclerotic Plaque Formation In Vivo.
    Cardiovascular drugs and therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P 

  • microRNA 205 5p promotes unstable atherosclerotic plaque formation in vivo
    Cardiovascular Drugs and Therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P < 0.001). miR-205KI Apoe-/- mice exhibited lower serum levels of high-density lipoprotein cholesterol (HDL-C) (5.18 vs. 19.31 mg/dL, P < 0.001) and triglycerides (32.79 vs. 156.76 mg/dL, P < 0.001) with system-wide reversal of cholesterol transport. Macrophages derived from miR-205KI Apoe-/- mice exhibited ~ 20% lowered cholesterol efflux capability with enhanced pro-inflammatory gene expression through lipid raft formation. Bone marrow transplantation demonstrated that bone marrow (BM) donor cells with miR-205-5pKI simulated plaque formation independent of the recipients' miR-205-5p status. CONCLUSIONS miR-205-5p encourages unstable atherogenesis in vivo. miR-205-5p also adversely influences lipid metabolism and promotes a pro-inflammatory macrophage phenotype. Our findings advocate miR-205-5p as a potential therapeutic target for combating unstable atherogenesis.

Xiandong Meng - One of the best experts on this subject based on the ideXlab platform.

  • microRNA-205-5p Promotes Unstable Atherosclerotic Plaque Formation In Vivo.
    Cardiovascular drugs and therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P 

  • microRNA 205 5p promotes unstable atherosclerotic plaque formation in vivo
    Cardiovascular Drugs and Therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P < 0.001). miR-205KI Apoe-/- mice exhibited lower serum levels of high-density lipoprotein cholesterol (HDL-C) (5.18 vs. 19.31 mg/dL, P < 0.001) and triglycerides (32.79 vs. 156.76 mg/dL, P < 0.001) with system-wide reversal of cholesterol transport. Macrophages derived from miR-205KI Apoe-/- mice exhibited ~ 20% lowered cholesterol efflux capability with enhanced pro-inflammatory gene expression through lipid raft formation. Bone marrow transplantation demonstrated that bone marrow (BM) donor cells with miR-205-5pKI simulated plaque formation independent of the recipients' miR-205-5p status. CONCLUSIONS miR-205-5p encourages unstable atherogenesis in vivo. miR-205-5p also adversely influences lipid metabolism and promotes a pro-inflammatory macrophage phenotype. Our findings advocate miR-205-5p as a potential therapeutic target for combating unstable atherogenesis.

Evi S Lianidou - One of the best experts on this subject based on the ideXlab platform.

  • prognostic value of mature microRNA 21 and microRNA 205 overexpression in non small cell lung cancer by quantitative real time rt pcr
    Clinical Chemistry, 2008
    Co-Authors: Athina Markou, Emily Tsaroucha, Loukas Kaklamanis, Marianthi Fotinou, Vassilis Georgoulias, Evi S Lianidou
    Abstract:

    Background: microRNA (miRNA) expression profiles are being intensively investigated for their involvement in carcinogenesis. We evaluated the prognostic value of mature microRNA-21 (miR-21) and mature microRNA-205 (miR-205) overexpression in non–small cell lung cancer (NSCLC). Patients and methods: We studied 48 pairs of NSCLC fresh frozen tissue specimens collected at time of surgery and before chemotherapy. Highly specific amplification and quantification of mature miR-21 and mature miR-205 was achieved using looped real time RT-PCR. Results: miRNA expression, determined by real time RT-PCR, was defined by ΔΔCt measurements. We detected overexpression of mature miR-21 in 25 (52.0%) of the 48 NSCLC paired specimens and overexpression of miR-205 in 31 (64.6%). Overexpression was assessed after comparison of miRNA expression in NSCLC tissues and in their corresponding noncancerous tissues with respect to U6 expression. During the follow-up period, 29 of 48 (60.4%) patients relapsed, and 23 of 48 died (47.9%). Mature miR-21 was upregulated in 16 of 29 (55.2%) patients who relapsed and 15 of 23 (65.2%) patients who died. Mature miR-205 was overexpressed in 19 of 29 patients who relapsed (65.5%) and 15 of 23 patients who died (65.2%). Mature miR-21 overexpression correlated with overall survival (OS) of the patients ( P = 0.027), whereas overexpression of mature miR-205 did not. Conclusions: Our results suggest that overexpression of mature miR-21 is an independent negative prognostic factor for OS in NSCLC patients.

  • Prognostic Value of Mature microRNA-21 and microRNA-205 Overexpression in Non–Small Cell Lung Cancer by Quantitative Real-Time RT-PCR
    Clinical chemistry, 2008
    Co-Authors: Athina Markou, Emily Tsaroucha, Loukas Kaklamanis, Marianthi Fotinou, Vassilis Georgoulias, Evi S Lianidou
    Abstract:

    Background: microRNA (miRNA) expression profiles are being intensively investigated for their involvement in carcinogenesis. We evaluated the prognostic value of mature microRNA-21 (miR-21) and mature microRNA-205 (miR-205) overexpression in non–small cell lung cancer (NSCLC). Patients and methods: We studied 48 pairs of NSCLC fresh frozen tissue specimens collected at time of surgery and before chemotherapy. Highly specific amplification and quantification of mature miR-21 and mature miR-205 was achieved using looped real time RT-PCR. Results: miRNA expression, determined by real time RT-PCR, was defined by ΔΔCt measurements. We detected overexpression of mature miR-21 in 25 (52.0%) of the 48 NSCLC paired specimens and overexpression of miR-205 in 31 (64.6%). Overexpression was assessed after comparison of miRNA expression in NSCLC tissues and in their corresponding noncancerous tissues with respect to U6 expression. During the follow-up period, 29 of 48 (60.4%) patients relapsed, and 23 of 48 died (47.9%). Mature miR-21 was upregulated in 16 of 29 (55.2%) patients who relapsed and 15 of 23 (65.2%) patients who died. Mature miR-205 was overexpressed in 19 of 29 patients who relapsed (65.5%) and 15 of 23 patients who died (65.2%). Mature miR-21 overexpression correlated with overall survival (OS) of the patients ( P = 0.027), whereas overexpression of mature miR-205 did not. Conclusions: Our results suggest that overexpression of mature miR-21 is an independent negative prognostic factor for OS in NSCLC patients.

Rui Yi - One of the best experts on this subject based on the ideXlab platform.

  • microRNA-205 controls neonatal expansion of skin stem cells by modulating the PI(3)K pathway
    Nature Cell Biology, 2013
    Co-Authors: Dongmei Wang, Li Wang, Zhaojie Zhang, Evan O’loughlin, Rui Yi
    Abstract:

    Skin stem cells (SCs) are specified and rapidly expanded to fuel body growth during early development. However, the molecular mechanisms that govern the amplification of skin SCs remain unclear. Here we report an essential role for miR-205, one of the most highly expressed microRNAs in skin SCs, in promoting neonatal expansion of these cells. Unlike most mammalian miRNAs, genetic deletion of miR-205 causes neonatal lethality with severely compromised epidermal and hair follicle growth. In the miR-205 knockout skin SCs, phospho-Akt is significantly downregulated, and the SCs prematurely exit the cell cycle. In the hair follicle, this accelerates the transition of the neonatal SCs towards quiescence. We identify multiple miR-205-targeted negative regulators of PI(3)K signalling that mediate the repression of phospho-Akt and restrict the proliferation of SCs. Our findings reveal an essential role for miR-205 in maintaining the expansion of skin SCs by antagonizing negative regulators of PI(3)K signalling. Skin stem cells are amplified in early development. Yi and colleagues found that miR-205 promotes neonatal skin stem cell expansion by directly targeting negative regulators of PI(3)K–Akt signalling to maintain proliferation.

  • microRNA 205 controls neonatal expansion of skin stem cells by modulating the pi 3 k pathway
    Nature Cell Biology, 2013
    Co-Authors: Dongmei Wang, Li Wang, Zhaojie Zhang, Evan Oloughlin, Rui Yi
    Abstract:

    Skin stem cells are amplified in early development. Yi and colleagues found that miR-205 promotes neonatal skin stem cell expansion by directly targeting negative regulators of PI(3)K–Akt signalling to maintain proliferation.

Jianjiao Yin - One of the best experts on this subject based on the ideXlab platform.

  • microRNA-205-5p Promotes Unstable Atherosclerotic Plaque Formation In Vivo.
    Cardiovascular drugs and therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P 

  • microRNA 205 5p promotes unstable atherosclerotic plaque formation in vivo
    Cardiovascular Drugs and Therapy, 2020
    Co-Authors: Xiandong Meng, Jianjiao Yin, Yonggang Guo
    Abstract:

    PURPOSE Atherosclerosis is a narrowing of the arteries caused by plaque buildup. microRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p's role in promoting atherosclerotic progression. METHODS Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe-/-) mice. This miR-205KI Apoe-/- murine model was employed to study the impact of miR-205-5p in Apoe-/- mice susceptible to atherosclerotic plaque formation. RESULTS miR-205KI Apoe-/-mice developed larger, more unstable plaques relative to their Apoe-/- counterparts (0.45 vs. 0.26 mm2, P < 0.001). miR-205KI Apoe-/- mice exhibited lower serum levels of high-density lipoprotein cholesterol (HDL-C) (5.18 vs. 19.31 mg/dL, P < 0.001) and triglycerides (32.79 vs. 156.76 mg/dL, P < 0.001) with system-wide reversal of cholesterol transport. Macrophages derived from miR-205KI Apoe-/- mice exhibited ~ 20% lowered cholesterol efflux capability with enhanced pro-inflammatory gene expression through lipid raft formation. Bone marrow transplantation demonstrated that bone marrow (BM) donor cells with miR-205-5pKI simulated plaque formation independent of the recipients' miR-205-5p status. CONCLUSIONS miR-205-5p encourages unstable atherogenesis in vivo. miR-205-5p also adversely influences lipid metabolism and promotes a pro-inflammatory macrophage phenotype. Our findings advocate miR-205-5p as a potential therapeutic target for combating unstable atherogenesis.