Proteomics

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AKT/PACS2 participates in renal vascular hyperpermeability by regulating endothelial fatty acid oxidation in diabetic mice


ABSTRACT: HUVECs were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA) and cultured in an Endothelial Cell Medium (Invitrogen, Carlsbad, CA, USA) containing 5% fetal bovine serum at 37°C in a 5% CO2 incubator. Cells were treated with 30 mM glucose and 0.1 mM palmitic acid (P0500, Sigma-Aldrich, USA) dissolved in 0.5% bovine serum albumin (BSA) for 48 h to simulate HGHF treatment. The Akt inhibitor MK-2206 2HCl was purchased from Selleck Chemicals (S1078, Houston, TX, USA).

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Blood Vessel Endothelial Cell

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: Zhihao Shu  

LAB HEAD: Zhihao Shu

PROVIDER: PXD033227 | Pride | 2022-08-12

REPOSITORIES: Pride

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CONTROL-3.raw Raw
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Publications

AKT/PACS2 Participates in Renal Vascular Hyperpermeability by Regulating Endothelial Fatty Acid Oxidation in Diabetic Mice.

Shu Zhihao Z   Chen Shuhua S   Xiang Hong H   Wu Ruoru R   Wang Xuewen X   Ouyang Jie J   Zhang Jing J   Liu Huiqin H   Chen Alex F AF   Lu Hongwei H  

Frontiers in pharmacology 20220705


Diabetes is a chronic metabolic disorder that can cause many microvascular and macrovascular complications, including diabetic nephropathy. Endothelial cells exhibit phenotypic and metabolic diversity and are affected by metabolic disorders. Whether changes in endothelial cell metabolism affect vascular endothelial function in diabetic nephropathy remains unclear. In diabetic mice, increased renal microvascular permeability and fibrosis, as well as increased MAMs and PACS2 in renal endothelial c  ...[more]

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