Dataset Information

Differential label free quantiation of Sec24D interactome, Boyce Lab

ABSTRACT: Relative quantitative analysis of Sec24D interactions using nanoscale liquid chromotography coupled with MS1 based LFQ on an Orbitrap Astral.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Erik Soderblom

LAB HEAD: Michael Boyce

PROVIDER: PXD058582 | Pride | 2026-04-01

REPOSITORIES: Pride

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			Action	DRS
	20231106_104241_10260_Hirata_110623.sne	Other
	Hirata_etal_Read_Me_013126.pdf	Pdf
	Hirata_etal_Read_Me_013126.txt	Txt
	ID108704_01_OA10034_10260_110223.raw	Raw
	ID108705_01_OA10034_10260_110223.raw	Raw

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Project description:Acute pancreatitis (AP), a severe inflammatory disorder of the pancreas, lacks effective pharmacological treatment. The disease is primarily driven by necrosis of pancreatic acinar cells (PACs), which intensifies inflammation and organ injury. This study explores the potential of BCL2 inhibitors, specifically Navitoclax and Venetoclax, to shift cell death pathways from necrosis to apoptosis and thereby mitigate disease severity. Ex vivo models using cerulein or ethanol/palmitoleic acid (EtOH/POA) showed that both inhibitors significantly reduced necrosis, increased apoptosis, and improved PAC viability and ATP levels. In mouse models of AP, both drugs promoted apoptosis and decreased tissue necrosis, with Venetoclax showing superior efficacy and safety. Venetoclax markedly reduced disease severity in two AP models without affecting healthy tissue or inducing thrombocytopenia. In contrast, Navitoclax caused apoptosis even in healthy tissue and triggered thrombocytopenia. Importantly, both drugs attenuated pathological Ca2+ responses in PACs and upregulated the expression of Ca²⁺-binding proteins S100A8/A9 and the chemokine CCL8. The latter may mediate enhanced apoptotic clearance and limit secondary necrosis, supporting the therapeutic shift from necrosis to apoptosis. Proteomic analyses revealed extensive drug-induced remodeling. In the short-term AP model, both inhibitors altered expression of proteins linked to intracellular compartments and extracellular signaling, reflecting cellular adaptation. In CP, Navitoclax strongly upregulated ECM and lysosomal proteins while downregulating ribosomal components – indicating intensified fibrosis and suppressed protein synthesis. Venetoclax had milder effects and did not worsen fibrosis. Despite Navitoclax’s efficacy toward activated pancreatic stellate cells in vitro, it exacerbated fibrosis and tissue atrophy in CP in vivo, likely due to ongoing parenchymal damage and stellate cell activation. Together, these findings demonstrate that selective BCL2 inhibition with Venetoclax promotes apoptosis, reduces necrosis, and improves outcomes in AP, supporting its repurposing as a therapeutic strategy. However, BCL2 inhibition does not benefit CP and may aggravate fibrosis, underscoring the need for context-specific approaches.

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Differential label free quantiation of Sec24D interactome, Boyce Lab

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