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Bulk RNA-seq of CRISPRi ADGRG6-kd iAT2 following cigarette smoke exposure

ABSTRACT: Bulk RNA-seq of CRISPRi ADGRG6-kd iAT2 following cigarette smoke exposure

PROVIDER: PRJNA924805 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23100500_1.fastq.gz	Fastqsanger.gz
	SRR23100500_2.fastq.gz	Fastqsanger.gz
	SRR23100489_1.fastq.gz	Fastqsanger.gz
	SRR23100489_2.fastq.gz	Fastqsanger.gz
	SRR23100490_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of CRISPRi ADGRG6-kd iAT2 following cigarette smoke exposure

Project description:We performed bulk transcriptomic profiling of induced human pluripotent stem cells (iPSCs)-derived type 2 alveolar epithelial cells (iAT2). iPSCs stably expressed CRISPRi (dCas9-KRAB) under the control of doxycyline. iAT2s were transduced with a lentivirus expressing gRNA targeting the transcriptional start site of ADGRG6. Cells were treated with or without doxycyline to intiate CRISPRi-knockdown. Cells were plated at an air-liquid interface, then subsequently exposed to air or 5% cigarette smoke using a VitroCell smoke robot. Cells were harvested for bulk RNA sequencing 8 hours post cigarette smoke exposure

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Single-cell RNA-seq of CRISPRi ADGRG6-kd in iAT2

Project description:We performed single cell transcriptomic profiling of induced human pluripotent stem cells (iPSCs)-derived type 2 alveolar epithelial cells (iAT2). iPSCs stably expressed CRISPRi (dCas9-KRAB) under the control of doxycyline. iAT2s were transduced with a lentivirus expressing gRNA targeting the transcriptional start site of ADGRG6. Cells were treated with or without doxycyline to intiate CRISPRi-knockdown. Prior to capture, cells were labelled with hashing antibodies (HTO). Cells were captured for 10x Genomics Single cell capture (V3 protocol), and GEX and HTO libraries were sequenced. HTODemux function was used to demultiplex the samples. Knockdown of ADGRG6 caused cells to cluster separately from wild-type cells.

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Project description:We performed single cell transcriptomic profiling of induced human pluripotent stem cells (iPSCs)-derived type 2 alveolar epithelial cells (iAT2). iPSCs stably expressed CRISPRi (dCas9-KRAB) under the control of doxycyline. iAT2s were transduced with a lentivirus expressing gRNA targeting the transcriptional start site of DSP. Cells were treated with or without doxycyline to intiate CRISPRi-knockdown. Prior to capture, cells were labelled with hashing antibodies (HTO). Cells were captured for 10x Genomics Single cell capture (V3 protocol), and GEX and HTO libraries were sequenced. HTODemux function was used to demultiplex the samples. Knockdown of DSP caused cells to cluster separately from wild-type cells.

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mouse lung resistance or sensitivity to cigarette smoke

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Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.

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