Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury. We constructed a minipig surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. Lung tissues from minipig with sham operation (one sample), left side lung tissues (the operated side)(one sample) and right side lung tissues (the non-operated side)(one sample) from minipig with lung ischemia-reperfusion were submitted for gene expression array analysis.
Project description:Alveolar epithelial type 2 (AT2) cells are facultative progenitor cells that drive adult alveolar regeneration after acute lung injury. Using transcriptomic analyses from in vivo mouse injury models, we define the role of Tfcp2l1 in regulating AT2 cell behavior during lung regeneration.
Project description:Alveolar epithelial type 2 (AT2) cells are facultative progenitor cells that drive adult alveolar regeneration after acute lung injury. Using transcriptomic analyses from in vivo mouse injury models, we define the role of Tfcp2l1 in regulating AT2 cell behavior during lung regeneration.
Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury.
Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury. MH.S-miR127 and MH.S-Sico cells were cultured for RNA extraction.Total RNA were assessed for quality with Agilent 2100 Bioanalyzer G2939A (Agilent Technologies,Santa Clara, CA)) and Nanodrop 8000 spectrophotometer (Thermo Scientific/Nanodrop, Wilmington, DE). Hybridization targets were prepared with MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems/Ambion, Austin, TX) from total RNA, hybridized to GeneChip® Mouse Genome 430 2.0 arrays in Affymetrix GeneChip® hybridization oven 645, washed in Affymetrix GeneChip® Fluidics Station 450 and scanned with Affymetrix GeneChip® Scanner 7G according to standard Affymetrix GeneChip® Hybridization, Wash, and Stain protocols. (Affymetrix, Santa Clara,CA).
Project description:Infection of the lung with Influenza A virus results in a regenerative phase following the acute lung injury phase. The involvement of mesenchymal niche cells in supporting epithelial stem and progenitor cells in the regeneration process is still unclear. The aim of this study was to investigate the transcriptomic changes occurring in resident mesenchymal cells during injury and regeneration.
