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Total RNA sequencing of AKAP12 knockdown cells

ABSTRACT: Total RNA sequencing of AKAP12 knockdown cells

PROVIDER: PRJNA616288 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11449189.fastq.gz	Fastqsanger.gz
	SRR11449190.fastq.gz	Fastqsanger.gz
	SRR11449191.fastq.gz	Fastqsanger.gz
	SRR11449192.fastq.gz	Fastqsanger.gz
	SRR11449193.fastq.gz	Fastqsanger.gz

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Total RNA sequencing of AKAP12 knockdown cells

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Modulation of AKAP12 in the liver regulates lipid homeostasis and inflammation

Project description:Dysregulation of lipid homeostasis is a feature of alcohol-associated liver disease (ALD). A-kinase anchoring protein 12 (AKAP12) is a scaffolding partner of the cAMP-dependent protein kinase, PKA that controls its spatiotemporal localization. Activation of PKA by cAMP inhibits lipogenesis and facilitates fatty acid oxidation (FAO). We examined how AKAP12’ could regulate alcohol-associated steatosis. Alcohol exposure reduced AKAP12’s interaction with PKA and suppressed PKA activation. Forced expression of AKAP12 overcame the suppression of PKA activity in human hepatocytes and in livers of mice exposed to alcohol. This led to a decrease in hepatic steatosis. Disrupting the scaffold of AKAP12 and PKA by CRISPR editing increased steatosis and inflammation. RNA sequencing analysis of hepatocytes from alchol fed mice and normal mice demonstrated key lipogenic and inflammatory pathways regulated by AKAP12 overexpression. RNA sequencing of total liver from mice with AKAP12-PKA binding site CRISPR editing or AKAP12 overexpression confirmed regulation of lipogenic and inflammatory pathways by AKAP12

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AKAP12 variant 1 knockout enhances vascular endothelial cell motility

Project description:This study investigates the role of AKAP12 in endothelial cell motility with a specific focus on AKAP12 variants, AKAP12v1 and AKAP12v2. Previous work has shown that AKAP12, a multivalent A-kinase anchoring protein that binds to PKA and several other proteins regulating protein phosphorylation, is expressed at low levels in most endothelia in vivo but is expressed at higher levels in cells in vitro. Here, we found that AKAP12 expression in endothelial cell (HUVEC) cultures was cell density-dependent, with the expression being highest in subconfluent cultures and lowest in confluent cultures. AKAP12 expression was also elevated in cells at the wound edge of wounded endothelial cell monolayers. Knockdown of variants 1 and 2 inhibited cell migration. However, CRISPR/Cas9 knockout of AKAP12v1 enhanced migration, indicating that the absence of this variant and the presence of AKAP12v2 likely alters the signaling events controlling cell motility. Further analysis using bulk RNA sequencing revealed that the loss of AKAP12v1 affected genes associated with cell migration and intercellular junctions. We propose that AKAP12v1 and AKAP12v2 play distinct yet complementary roles in endothelial cell migration and likely work together in controlling the signaling events associated with vascular repair and development.

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