Susan C. Olson's research while affiliated with New York Medical College and other places
What is this page?
This page lists the scientific contributions of an author, who either does not have a ResearchGate profile, or has not yet added these contributions to their profile.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
Publications (7)
Coronary heart disease (CHD) is a leading cause of death in many developed countries. Evidence has long implicated endothelial injury and inflammation as apical events in the pathogenesis of atherosclerosis, the primary cause of CHD. Numerous risk factors contribute to a damaged, inflamed endothelium. Conversely, cardioprotective agents targeting t...
Population studies suggest that moderate red wine intake correlates with reduced risk of cardiovascular disease (CVD); cardioprotection may attribute to consumption of red wine polyphenol resveratrol. Since inflammation plays a key role in CVD, we investigated modulation of inflammation by resveratrol and its metabolites by determining the expressi...
We previously reported that all-trans retinoic acid (RA) and fenretinide (4HPR) suppress HL-60 leukemia cell growth and cause partial cell arrest in the G1-to-S phase. Moreover, 4HPR but not RA induces apoptosis in HL-60 cells. To investigate further the observed biological effects, cyclin D1 and cdk4 expression and the level of phosphorylation of...
We previously reported that all-trans retinoic acid (RA) and fenretinide (4HPR) suppress HL-60 leukemia cell growth and cause partial cell arrest in the G1-to-S phase. Moreover, 4HPR but not RA induces apoptosis in HL-60 cells. To investigate further the observed biological effects, cyclin D1 and cdk4 expression and the level of phosphorylation of...
Neutrophils play a major role host defense against invading microbes. Recent studies have emphasized the importance of the phospholipase D (PLD) in the signalling cascade leading to neutrophil activation. Phospholipase D catalyzes the hydrolysis of phospholipids to generate phosphatidic acid with secondarily generation of diradylglycerol; both of t...
Receptor-linked activation of phospholipase D has been demonstrated recently in a variety of intact cell types including granulocytes, but little is known about the enzyme, its cofactor requirements, and regulation. Using [3H]alkyllysophosphatidylcholine to prelable an endogenous phosphatidylcholine substrate pool in conjunction with transphosphati...
Agents which elevate cellular cAMP (prostaglandin E2, theophylline, and forskolin) or mimic cAMP action (dibutyryl cAMP) are known to inhibit human neutrophil activation (superoxide generation and secretion) by receptor-linked agonists such as formyl-methionyl-leucyl-phenylalanine (fMLP). Herein, we show that these agents also markedly inhibit fMLP...
Citations
... Endothelial cell injury and inflammation have an important role in the development of atherosclerosis [46]. It has been reported that miRNA-22 is downregulated in coronary artery disease and other diseases involve an inflammatory response. ...
... 4-HPR has a very broad range (0.7-10 M) of cytotoxicity and may have different effects dependent on the concentration and type of cancer cell used (Formelli et al., 2008). In neuroblastoma cells, high concentrations of 4-HPR (>5 M) have been shown to induce apoptosis and necrosis (Wang et al., 2001a) while lower concentrations (< 3 M) of 4-HPR have been reported to induce G 1 -S arrest and hypophosphorylation of Rb (DiPietrantonio et al., 1998; Kraveka et al., 2007; Wu et al., 2001). For neuroblastoma patients enrolled on a Phase I pediatric trial the mean plasma steady-state concentration on day 7 was as 9.9 mol/L with the maximal tolerated dosage of 2,475 mg/m 2 per day (Villablanca et al., 2006). ...
Reference: Bioactive Sphingolipids in Neuroblastoma
... (E)-Resveratrol has been shown to inhibit the pathways of NF-κB activation, which results in down-regulation of the inflammatory signal (Soleas et al. 2001, Tian et al. 2016). An in-vitro study conducted with pulmonary artery endothelial cell cultures has proposed a mechanism for the anti-inflammatory response of (E)resveratrol in humans (Yang et al. 2011). The study identified eotaxin-1 as a vital component of the inflammatory signaling pathway, and its expression in the cells is induced by cytokines such as IL-13 and TNF-α. ...
... Upon adipogenic differentiation, high cAMP levels lead to activation of C/EBPα and PPARγ , and also drive aP2 expression 45,46 . Previous reports showed that cAMP or cAMP-increasing agents inhibit PLD activity in vitro and in vivo [47][48][49] . In agreement with these reports, we observed that cAMP decreased PLD activity (Fig. 1h), suggesting that PLD is a downstream target of cAMP in adipogenesis. ...
... PLD is the enzyme that catalyzes phosphatidylcholine (PC) and phosphatidic acid (PA) is the main product. The activation of PLD is Ca 2+ -dependent (Olson et al. 1991) and PA participates in the release of cytokine (Abe et al. 2012;Taketomi and Murakami 2017) and of exosome (Laulagnier et al. 2004;Mazzeo et al. 2016) directly or through its downstream molecular, such as phohphoinositide 3-kinase (PI3K). We showed that PLD inhibition, PLDsiRNA and PI3K inhibition all decreased NAMPT release in microglia. ...
... PKC is activated by both DAG and IP3 generated by PLC. PKC then elicits its function by activation of Phospholipase D (PLD) and Arf6 ( Figure 1A) (114,115). Both Arf6 and PLD subsequently activate PIPKIg (also known as PIP5K1C) which increases phosphatidylinositol 4,5 (PIP 2 ) levels at the inner plasma membrane (104,(114)(115)(116)(117), resulting in the recruitment and activation of Talin-1 via its PIP 2 binding F2 domain and subsequent binding to the NPXY motif of the CD18 cytoplasmic tail ( Figure 1A) (104,109,112,118). ...
... N-(4-Hydroxyphenyl) retinamide (4HPR, also known as fenretinide) is a low-toxicity synthetic retinoid that has been proven to have anti-cancer properties in a wide array of malignancies [7][8][9]. 4HPR is a ligand that binds with the retinoic acid receptor, resulting in activation of many genes that contribute to apoptosis in cancer cells [10]. In glioblastoma, 4HPR induces the intrinsic pathway of apoptosis due to promotion of the mitochondrial release of cytochrome c into the cytosol and subsequent downstream activation of caspase-3 [11]. ...
