ApoA1 impairs macrophage activation of Akt following CCL5 stimulation. Given the consistent effects of apoA1 on monocyte and macrophage chemotaxis in vitro and in vivo, we were interested to identify the mechanistic basis of these findings.

Oct 1, 2022 · Moreover, the phosphorylation of eNOS, PI3K, and Akt begins when ApoA1 binds to the ATPase on the endothelium membrane, converting ATP into APD and activating the P2Y1 receptor, all of which promote the proliferation of endothelial cells and prevent apoptosis.

Apolipoprotein A-I (ApoA-I), the major protein component of high density lipoprotein (HDL), widely known for regulating cholesterol trafficking and for protecting against cardiovascular disease (CVD), may also modulate inflammatory and immune responses [1].

Jan 28, 2019 · The ApoA1 mimetic peptide strongly suppresses Akt signaling in ovarian cancer cells. After overnight serum starvation, SKOV3 cells were treated with the ApoA1 mimetic peptide (50 or 100 μg/mL). Untreated SKOV3 cells were used as control.

Jul 26, 2022 · APOA1 treatment downregulated the phosphorylation of phosphatidylinositol 3-kinase (PI3K)/AKT, p38, and NF-κB signaling, whereas BLT-1 reversed the function of APOA1 in IRBP-specific CD4 + T cells (Figs. 5 A–H).

Scavenger receptor class B member I (SR-BI), a high-affinity receptor for apolipoprotein A-I (apoA-I)/high-density lipoprotein (HDL), inhibits nuclear factor-κB (NF-κB) translocation and decreases the plasma levels of inflammatory mediators via the PI3K/Akt pathway.

Aug 2, 2021 · We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell...

Nov 21, 2014 · ATP-binding cassette transporter A1 (ABCA1) plays an essential role in mediating cholesterol efflux to apolipoprotein A-I (apoA-I), a major housekeeping mechanism for cellular cholesterol homeostasis. After initial engagement with ABCA1, apoA-I directly interacts with the plasma membrane to acquire cholesterol.

ANGPTL4 gene induction by HDL was direct and was blocked in the presence of inhibitors for the AKT or the p38 MAP kinases. TgHDL-apoA-I caused phosphorylation of the transcription factor forkhead box O1 (FOXO1) and its translocation from the nucleus to the cytoplasm.

Nov 10, 2022 · Genetic overexpression reduced, and ApoA1 knockout increased necrotic core formation and RIPK3 and MLKL within atherosclerotic plaques. Macrophages were protected against necroptosis by HDL and this protection required SR-B1, PDZK1, and PI3K/Akt pathway.