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A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2

ABSTRACT: A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2

PROVIDER: PRJNA1052009 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27198685.fastq.gz	Fastqsanger.gz
	SRR27198686.fastq.gz	Fastqsanger.gz
	SRR27198687.fastq.gz	Fastqsanger.gz

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A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2

Project description:Liver fibrosis is an urgent clinical problem without effective treatment. Herein, we conduct a high-content screening on a natural “privileged” diterpenoid library to identify a potent anti-liver fibrosis lead DP. Leveraging photoaffinity labeling approach, apolipoprotein L2 (APOL2), an ER-rich protein, is identified as the direct target of DP. APOL2 is mainly expressed in activated hepatic stellate cells (HSCs) and could activate HSCs to synthesize ECM proteins. It can be induced by TGF-b1 and be antagonized by DP. Mechanistically, upon TGF-b1 stimulation, APOL2 binds ER Ca2+ pump SERCA2 to trigger ER stress, elevating its downstream PERK-HES1 axis to promote liver fibrosis, mildly dependent on the canonical TGF-b/Smad signaling. As a result, ablation of APOL2 significantly alleviates TGF-b1-stimulated HSCs activation, and abolishes anti-fibrosis effect of DP. Our findings not only define APOL2 as a novel therapeutic target for liver fibrosis, but also highlight DP as a promising lead for treatment of this symptom.

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A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2 (APOL2)-mediated endoplasmic reticulum (ER) stress

Project description:To investigate the functional role of APOL2 in liver fibrosis, we performed an unbiased immunoprecipitation-mass spectrometry (IP-MS) analysis for APOL2 in the TGF-β1-stimulated LX-2 cell lysates.

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Natural small molecule DP combats liver fibrosis by targeting APOL2

Project description:Liver fibrosis is an urgent clinical problem without effective treatment. Herein, we conducted a high-content screening on a natural “privileged” diterpenoid library to identify a potent anti-liver fibrosis lead DP. Leveraging photoaffinity labeling approach, apolipoprotein L2 (APOL2), an ER-rich protein, was identified as the direct target of DP. APOL2 is mainly expressed in activated hepatic stellate cells (HSCs) and could activate HSCs to synthesize ECM proteins. It can be induced by TGF-β1 and be antagonized by DP. Mechanistically, upon TGF-β1stimulation, APOL2 binds ER Ca2+ pump SERCA2 to trigger ER stress, elevating its downstream PERK-HES1 axis to promote liver fibrosis, mildly dependent on the canonical TGF-β/Smad signaling. As a result, ablation of APOL2 significantly alleviated TGF-β1-stimulated HSCs activation, and abolished anti-fibrosis effect of DP. Our findings not only define APOL2 as a novel therapeutic target for liver fibrosis, but also highlight DP as a promising lead for treatment of this symptom.

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