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Life Sciences

Apoptosis

Wright State University

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Potential Drug Treatment For Duchenne Muscular Dystrophy Which Could Be Through Upregulation Of Lipin1, Rajsi Y. Thaker Jan 2021

Potential Drug Treatment For Duchenne Muscular Dystrophy Which Could Be Through Upregulation Of Lipin1, Rajsi Y. Thaker

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Duchenne muscular dystrophy (DMD) is a genetic disorder leading to progressive muscle degeneration and weakness due to mutation in dystrophin gene, which is very important for maintaining muscle membrane integrity. Dystrophin is the largest gene in the human genome therefore more prone to mutation. There is currently no cure for DMD. Our lab recently found that Lipin1 deficient myofibers showed upregulation of necroptosis correlated with the loss of muscle membrane integrity. Our primary approach for ameliorating dystrophic phenotype in DMD is through reduction of necroptosis using drugs which can potentially upregulate Lipin1 expression. In this study, we identified two drugs …


Apoptosis And Necrosis Drive Muscle Fiber Loss In Lipin1 Deficient Skeletal Muscle, Sandhya Ramani Sattiraju Jan 2020

Apoptosis And Necrosis Drive Muscle Fiber Loss In Lipin1 Deficient Skeletal Muscle, Sandhya Ramani Sattiraju

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Mutations in lipin1 are suggested to be a common cause of massive rhabdomyolysis episodes in children, however, the molecular mechanism involved in the regulation of myofiber death by lipin1 is not known. In this study, we utilized the skeletal muscle from cell-type-specific lipin1 knockout (Lipin1Myf5cKO) mice to define cell death pathways involved in lipin1 deficient muscles. We observed a significant increase in centrally nucleated fibers and embryonic myosin heavy chain (EMyHC)-positive regenerating fibers in Lipin1Myf5cKO mice compared to wild-type (WT) mice, indicating an increased cycle of degeneration and regeneration in lipin1 deficient muscles. Lipin1 deficient muscles had significantly elevated pro-apoptotic …


The Expression Of Major Histocompatibility Class I And Major Histocompatibility Class Ii On Macrophages In The Presence Of Aryl Hydrocarbon Antagonist (Ch-223191), Caitlin Wilson Jan 2016

The Expression Of Major Histocompatibility Class I And Major Histocompatibility Class Ii On Macrophages In The Presence Of Aryl Hydrocarbon Antagonist (Ch-223191), Caitlin Wilson

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Macrophages are crucial for ridding the body of debris and foreign cells. The aryl hydrocarbon receptor (AhR) also plays a critical role in immunity. This study examined the effect of the AhR on the expression of major histocompatiability complex class I (MHCI) and MHC class II (MHCII) in two murine macrophage cell lines. This study used Raw264.7 and J774A.1 murine macrophage cell lines. The Raw264.7 cells are from male BALB/c mice while the J774A.1 cells are from female BALB/cN mice. The addition of the AhR anatagonist CH-223191 (AhRa) showed that the AhR does not significantly impact MHCI expression. However, MHCII …


Interaction Between Na/ K-Atpase And Bcl-2 Proteins Bclxl And Bak, Tariq M. Alqahtani Jan 2015

Interaction Between Na/ K-Atpase And Bcl-2 Proteins Bclxl And Bak, Tariq M. Alqahtani

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In silico analysis predicts interaction between the Na/ K-ATPase (NKA) and Bcl-2 protein canonical motifs BH3 and BH1. Such interaction is consistent with NKA inhibition by the benzo-phenanthridine alkaloid chelerythrine (CHE), a BH3 mimetic, in human lens epithelial cells (HLEC). This report establishes proof of concept: co-immuno-precipitation and immuno-colocalization showed unequivocal and direct interaction between NKA and Bcl-2 proteins. Particularly, NKA-antibodies co-immunoprecipitated BclXl and BAK in three different epithelial cell lines, HLECs and A549 lung cancer cells, whereas anti-Bcl-2 antibodies failed to pull down NKA. The molecular mass of the BAK proteins pulled down by antibodies against NKA and BclXl …


Effects Of Direct Mechanical Ventricular Actuation On The Apoptotic Signaling Of A Failing Heart, Scott Kerns Jan 2009

Effects Of Direct Mechanical Ventricular Actuation On The Apoptotic Signaling Of A Failing Heart, Scott Kerns

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Cardiovascular disease accounts for more than 40% of all deaths in the United States (AHA-2004 report). A non blood contacting ventricular assist device (VAD) can be used to treat heart failure without the complications that arise from blood contacting VADs. This study used cellular markers of heart failure as indicators of heart function in an attempt to assess if direct mechanical ventricular actuation (DMVA) support lessened the impact of heart failure in rabbits. Cell signaling proteins were monitored using enzyme activity measurements and quantitative immunoblotting with antibodies against intrinsic and extrinsic apoptotic pathways during heart failure with and without DMVA …