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Bo Yu - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of microrna 143 3p attenuates myocardial hypertrophy by inhibiting inflammatory response
    Cell Biology International, 2018
    Co-Authors: Bo Yu, Yanan Zhao, Hongli Zhang
    Abstract:

    : MicroRNA-143-3p (Mir-143-3p) is involved in the initiation of inflammatory response and the progression of cardiovascular diseases. Myocardial hypertrophy is a common symptom in numerous cardiovascular diseases. In the current study, we attempted to demonstrate the role of Mir-143-3p in the development of myocardial hypertrophy by focusing on its association with inflammation. Myocardial hypertrophy was induced by transverse aortic constriction (TAC) method in vivo and by H2 O2 administration in vitro. The expression status of Mir-143-3p and downstream effectors were detected in animal heart tissues and H9c2 cells. Furthermore, the effect of Mir-143-3p inhibition on H2 O2 -induced changes in ERK5/PPARδ/NF-κB axis was assessed. TAC induced oxidative stress and inflammation in rat heart tissues, which was associated with the increased expressions of Mir-143-3p and p-ERK5. However, the up-regulated expression of Mir-143-3p had no effect on the expression of ERK5, which was a direct target of Mir-143-3p. The results of in vitro assays showed that H2 O2 administration increased the levels of Mir-143-3p and p-EKR5 and induced the activation of NF-κB pathway. After the inhibition of Mir-143-3p, the activation of EKR5 and NF-κB pathway was suppressed, whereas the expression of PPARδ was up-regulated. The current study demonstrated that Mir-143-3p is crucial to the initiation of inflammatory response induced by myocardial hypertrophy. The activation of ERK5 following Mir-143-3p up-regulation appears to be a complementary response to induce the subsequent anti-inflammatory signaling transduction, which needed further exploration.

  • regulation of intraocular pressure by microrna cluster mir 143 145
    Scientific Reports, 2017
    Co-Authors: Xinyu Li, Fangkun Zhao, Guorong Li, Coralia Luna, Guigang Li, Qinbo Zhou, Yuguang He, Bo Yu
    Abstract:

    Glaucoma is a major cause of irreversible blindness worldwide. Elevated intraocular pressure (IOP), which causes optic nerve damage and retinal ganglion cell death, is the primary risk factor for blindness in glaucoma patients. IOP is controlled by the balance between aqueous humor secretion from the ciliary body (CB) and its drainage through the trabecular meshwork (TM). How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unknown. Here we show that Mir-143 and miR-145 expression is enriched in the smooth muscle and trabecular meshwork in the eye. Targeted deletion of Mir-143/145 in mice results in significantly reduced IOP, consistent with an ~2-fold increase in outflow facilities. However, aqueous humor production in the same mice appears to be normal based on a microbeads-induced glaucoma model. Mechanistically, we found that Mir-143/145 regulates actin dynamics and the contractility of TM cells, consistent with its regulation of actin-related protein complex (ARPC) subunit 2, 3, and 5, as well as myosin light chain kinase (MLCK) in these cells. Our data establish Mir-143/145 as important regulators of IOP, which may have important therapeutic implications in glaucoma.

Fangkun Zhao - One of the best experts on this subject based on the ideXlab platform.

  • regulation of intraocular pressure by microrna cluster mir 143 145
    Scientific Reports, 2017
    Co-Authors: Xinyu Li, Fangkun Zhao, Guorong Li, Coralia Luna, Guigang Li, Qinbo Zhou, Yuguang He, Bo Yu
    Abstract:

    Glaucoma is a major cause of irreversible blindness worldwide. Elevated intraocular pressure (IOP), which causes optic nerve damage and retinal ganglion cell death, is the primary risk factor for blindness in glaucoma patients. IOP is controlled by the balance between aqueous humor secretion from the ciliary body (CB) and its drainage through the trabecular meshwork (TM). How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unknown. Here we show that Mir-143 and miR-145 expression is enriched in the smooth muscle and trabecular meshwork in the eye. Targeted deletion of Mir-143/145 in mice results in significantly reduced IOP, consistent with an ~2-fold increase in outflow facilities. However, aqueous humor production in the same mice appears to be normal based on a microbeads-induced glaucoma model. Mechanistically, we found that Mir-143/145 regulates actin dynamics and the contractility of TM cells, consistent with its regulation of actin-related protein complex (ARPC) subunit 2, 3, and 5, as well as myosin light chain kinase (MLCK) in these cells. Our data establish Mir-143/145 as important regulators of IOP, which may have important therapeutic implications in glaucoma.

  • Regulation of intraocular pressure by microRNA cluster Mir-143/145.
    Scientific reports, 2017
    Co-Authors: Fangkun Zhao, Coralia Luna, Qinbo Zhou, Mei Xin, Eric N. Olson
    Abstract:

    Glaucoma is a major cause of irreversible blindness worldwide. Elevated intraocular pressure (IOP), which causes optic nerve damage and retinal ganglion cell death, is the primary risk factor for blindness in glaucoma patients. IOP is controlled by the balance between aqueous humor secretion from the ciliary body (CB) and its drainage through the trabecular meshwork (TM). How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unknown. Here we show that Mir-143 and miR-145 expression is enriched in the smooth muscle and trabecular meshwork in the eye. Targeted deletion of Mir-143/145 in mice results in significantly reduced IOP, consistent with an ~2-fold increase in outflow facilities. However, aqueous humor production in the same mice appears to be normal based on a microbeads-induced glaucoma model. Mechanistically, we found that Mir-143/145 regulates actin dynamics and the contractility of TM cells, consistent with its regulation of actin-related protein complex (ARPC) subunit 2, 3, and 5, as well as myosin light chain kinase (MLCK) in these cells. Our data establish Mir-143/145 as important regulators of IOP, which may have important therapeutic implications in glaucoma.

Xinyu Li - One of the best experts on this subject based on the ideXlab platform.

  • regulation of intraocular pressure by microrna cluster mir 143 145
    Scientific Reports, 2017
    Co-Authors: Xinyu Li, Fangkun Zhao, Guorong Li, Coralia Luna, Guigang Li, Qinbo Zhou, Yuguang He, Bo Yu
    Abstract:

    Glaucoma is a major cause of irreversible blindness worldwide. Elevated intraocular pressure (IOP), which causes optic nerve damage and retinal ganglion cell death, is the primary risk factor for blindness in glaucoma patients. IOP is controlled by the balance between aqueous humor secretion from the ciliary body (CB) and its drainage through the trabecular meshwork (TM). How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unknown. Here we show that Mir-143 and miR-145 expression is enriched in the smooth muscle and trabecular meshwork in the eye. Targeted deletion of Mir-143/145 in mice results in significantly reduced IOP, consistent with an ~2-fold increase in outflow facilities. However, aqueous humor production in the same mice appears to be normal based on a microbeads-induced glaucoma model. Mechanistically, we found that Mir-143/145 regulates actin dynamics and the contractility of TM cells, consistent with its regulation of actin-related protein complex (ARPC) subunit 2, 3, and 5, as well as myosin light chain kinase (MLCK) in these cells. Our data establish Mir-143/145 as important regulators of IOP, which may have important therapeutic implications in glaucoma.

Deepak Srivastava - One of the best experts on this subject based on the ideXlab platform.

  • mir 145 and mir 143 regulate smooth muscle cell fate and plasticity
    Nature, 2009
    Co-Authors: Kimberly R Cordes, Neil T Sheehy, Mark P White, Emily C Berry, Sarah U Morton, Alecia N Muth, Tinghein Lee, Joseph M Miano, Kathryn N Ivey, Deepak Srivastava
    Abstract:

    MicroRNAs (miRNAs) are regulators of myriad cellular events, but evidence for a single miRNA that can efficiently differentiate multipotent stem cells into a specific lineage or regulate direct reprogramming of cells into an alternative cell fate has been elusive. Here we show that miR-145 and Mir-143 are co-transcribed in multipotent murine cardiac progenitors before becoming localized to smooth muscle cells, including neural crest stem-cell-derived vascular smooth muscle cells. miR-145 and Mir-143 were direct transcriptional targets of serum response factor, myocardin and Nkx2-5 (NK2 transcription factor related, locus 5) and were downregulated in injured or atherosclerotic vessels containing proliferating, less differentiated smooth muscle cells. miR-145 was necessary for myocardin-induced reprogramming of adult fibroblasts into smooth muscle cells and sufficient to induce differentiation of multipotent neural crest stem cells into vascular smooth muscle. Furthermore, miR-145 and Mir-143 cooperatively targeted a network of transcription factors, including Klf4 (Kruppel-like factor 4), myocardin and Elk-1 (ELK1, member of ETS oncogene family), to promote differentiation and repress proliferation of smooth muscle cells. These findings demonstrate that miR-145 can direct the smooth muscle fate and that miR-145 and Mir-143 function to regulate the quiescent versus proliferative phenotype of smooth muscle cells.

Mansoor Husain - One of the best experts on this subject based on the ideXlab platform.

  • c-Myb regulates transcriptional activation of Mir-143/145 in vascular smooth muscle cells.
    PloS one, 2018
    Co-Authors: Mark Chandy, Tao Wang, Masayoshi Ishida, Eric A. Shikatani, Omar El-mounayri, Lawrence Changsu Park, Talat Afroze, Philip A. Marsden, Mansoor Husain
    Abstract:

    Background MicroRNAs (miR) are small non-coding RNAs that regulate diverse biological functions. The bicistronic gene Mir-143/145 determines cell fate and phenotype of vascular smooth muscle cells (VSMC), in part, by destabilizing Elk-1 mRNA. The transcription factor c-Myb also regulates differentiation and proliferation of VSMC, and here we test whether these effects may be mediated by Mir-143/145. Methods & results Flow cytometry of cardiovascular-directed d3.75 embryoid bodies (EBs) isolated smooth muscle progenitors with specific cell surface markers. In c-myb knockout (c-myb -/-) EB, these progenitors manifest low levels of Mir-143 (19%; p