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ibidi μ-slide 15 well 3d  (ibidi GmbH)

 
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    ibidi GmbH ibidi μ-slide 15 well 3d
    Ibidi μ Slide 15 Well 3d, supplied by ibidi GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%BC-slide+with+15+wells/pm40619121-120-1-6?v=ibidi+GmbH
    Average 90 stars, based on 1 article reviews
    ibidi μ-slide 15 well 3d - by Bioz Stars, 2026-08
    90/100 stars

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    In acute MI, the exacerbation of Mito-ROS leads to mitochondrial dysfunction and a decrease in ATP production, leading to an increase in AMP/ATP ratio, which results in phosphorylation of AMPKα at Threonine 172. Over time, the unmet need for ATP results in impaired angiogenesis and loss of capillaries in the heart, affecting blood supply and myocardial healing. This leads to cardiac maladaptation, resulting in impaired cardiac function associated with larger infarcted tissue area after acute MI. When JP4-039 is introduced after acute MI, its mitochondria-targeted ROS and electron scavenging activities result in a reduction of Mito-ROS and increased expression of mitochondrial complexes I and V. Thus, treatment with JP4-039 results in increased ATP supply and reduced phosphorylation of AMPKα at Threonine 172 in comparison to untreated mice after MI, suggesting an improvement of the AMP/ATP balance. The increase in ATP supply promoted by JP4-039 may contribute to angiogenesis associated with an improved cardiac function and reduction of infarct size after an acute MI. Created with BioRender.com.

    Journal: PLOS One

    Article Title: Mitochondria-targeted ROS scavenger JP4-039 improves cardiac function in a post-myocardial infarction animal model and induces angiogenesis in vitro

    doi: 10.1371/journal.pone.0320703

    Figure Lengend Snippet: In acute MI, the exacerbation of Mito-ROS leads to mitochondrial dysfunction and a decrease in ATP production, leading to an increase in AMP/ATP ratio, which results in phosphorylation of AMPKα at Threonine 172. Over time, the unmet need for ATP results in impaired angiogenesis and loss of capillaries in the heart, affecting blood supply and myocardial healing. This leads to cardiac maladaptation, resulting in impaired cardiac function associated with larger infarcted tissue area after acute MI. When JP4-039 is introduced after acute MI, its mitochondria-targeted ROS and electron scavenging activities result in a reduction of Mito-ROS and increased expression of mitochondrial complexes I and V. Thus, treatment with JP4-039 results in increased ATP supply and reduced phosphorylation of AMPKα at Threonine 172 in comparison to untreated mice after MI, suggesting an improvement of the AMP/ATP balance. The increase in ATP supply promoted by JP4-039 may contribute to angiogenesis associated with an improved cardiac function and reduction of infarct size after an acute MI. Created with BioRender.com.

    Article Snippet: Human coronary artery endothelial cells (HCAEC), or MHEC with prolonged overexpression of NOX2 were plated into a 15-well µ-slide Angiogenesis (ibidi GmbH, Gräfelfing, Germany) precoated with Cultrex® basement membrane extract (BME, R&D Systems, Minneapolis, MN) at a density of 10 4 cells/well (passage 4), following manufacturer protocol [ ].

    Techniques: Expressing, Comparison