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• W3154865189 abstract "The obligate intracellular pathogen Chlamydia trachomatis is the causative agent oftrachoma related blindness and the sexually transmitted pelvic inflammatory disease.Being an obligate intracellular pathogen, C. trachomatis has an intricate dependencyon the survival of the host cell. This relationship is indispensible owing to the fact thatthe pathogen spends a considerable fraction of its biphasic lifecycle within acytoplasmic vacuole inside the host cell, the so-called chlamydial inclusion. Thecellular apoptotic-signalling network is governed by several finely tuned regulatorycascades composed of pro- and anti-apoptotic proteins that respond to changes inthe cellular homeostasis. In order to facilitate its intracellular survival, Chlamydia hasbeen known to inhibit the premature apoptosis of the host cell via the stabilization ofseveral host anti-apoptotic proteins such as cIAP2 and Mcl-1. While the pro- andanti-apoptotic proteins are the major regulators of the host apoptotic signallingnetwork, a class of the small non-coding RNAs called microRNAs (miRNAs) hasincreasingly gained focus as a new level of regulatory control over apoptosis.This work investigates the changes in the host miRNA expression profile postChlamydia infection using a high throughput miRNA deep sequencing approach.Several miRNAs previously associated with the modulation for apoptotic signallingwere differentially expressed upon Chlamydia infection in human endothelial cells. Ofthe differentially regulated miRNAs, miR-30c-5p was of particular interest since it hadbeen previously shown to target the tumor suppressor protein p53. Our lab andothers have previously demonstrated that Chlamydia can downregulate the levels ofp53 by promoting its proteasomal degradation. This work demonstrates thatChlamydia infection promotes p53 downregulation by increasing the abundance ofmiR-30c-5p and a successful infection cycle is hindered by a loss of miR-30c-5p.Over the last decade, dedicated research aimed towards a better understanding ofapoptotic stimuli has greatly improved our grasp on the subject. While extrinsicstress, deprivation of survival signals and DNA damage are regarded as majorproponents of apoptotic induction, a significant responsibility lies with themitochondrial network of the cell. Mitochondrial function and dynamics are crucial tocell fate determination and dysregulation of either is decisive for cell survival andpathogenesis of several diseases. The ability of the mitochondrial network to performits essential tasks that include ATP synthesis, anti-oxidant defense, and calciumhomeostasis amongst numerous other processes critical to cellular equilibrium is tiedclosely to the fission and fusion of individual mitochondrial fragments. It is, thus,8unsurprising that mitochondrial dynamics is closely linked to apoptosis. In fact, manyof the proteins involved regulation of mitochondrial dynamics are also involved inapoptotic signalling. The mitochondrial fission regulator, Drp1 has previously beenshown to be transcriptionally regulated by p53 and is negatively affected by a miR-30c mediated inhibition of p53. Our investigation reveals a significant alteration in themitochondrial dynamics of Chlamydia infected cells affected by the loss of Drp1. Weshow that loss of Drp1 upon chlamydial infection is mediated by the miR-30c-5pinduced depletion of p53 and results in a hyper-fused architecture of themitochondrial network.While it is widely accepted that Chlamydia depends on the host cell metabolism forits intracellular growth and development, the role of mitochondria in an infected cell,particularly with respect to its dynamic nature, has not been thoroughly investigated.This work attempts to illustrate the dependence of Chlamydia on miR-30c-5p inducedchanges in the mitochondrial architecture and highlight the importance of thesemodulations for chlamydial growth and development." @default.
• W3154865189 created "2021-04-26" @default.
• W3154865189 creator A5001706792 @default.
• W3154865189 date "2018-01-01" @default.
• W3154865189 modified "2023-09-23" @default.
• W3154865189 title "The Role of MicroRNAs in (Chlamydia) Infection" @default.
• W3154865189 hasPublicationYear "2018" @default.
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