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Study of Nutraceuticals in Cancer Treatment: An In Silico Approach
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Co-expression network figures are drawn using R package igraph. Only the top 20 genes with the highest correlations are shown in Figure 6.5. Co-expressed genes are C1QBP, COX10, CTDNEP1, EIF4A1, EIF5AL1, ELAC2, GEMIN4, METTL16, MYBBP1A, NDEL1, NUP88, PFAS, PITPNA, PLD2, RPA1, RPL26, SCO1, SENP3, TP53, TSR1, andYWHAE.
Genome-wide DNA methylation profiles analysis in primary warm autoimmune hemolytic anemia patients
Published in Hematology, 2023
Manjun Zhao, Yang Zhang, Jin Yang, Lei Chen, Ziying Zhang, Huaquan Wang, Zonghong Shao, Limin Xing
PLD on the surface of mammalian cells catalyzes the hydrolysis of phosphatidylcholine to produce choline and phosphatidic acid, which function as secondary messengers to transmit signals and promote the transport of vesicles [21]. Among the PLD protein family, PLD1 and PLD2 are two major subtypes that have been extensively studied. Lymphocyte adhesion and transport through the endothelial barrier are key factors that mediate the development of central nervous system immune diseases such as multiple sclerosis. PLD1 expression is elevated in the lymphocytes of patients with multiple sclerosis, where it plays a central role in immune cell migration [22]. PLD-2 signaling promotes chemotaxis, migration, and cytoskeletal remodeling of immune cells, which participate in the pathogenesis of multiple AIDs [23]. It has been reported that PLD2 mutations may be involved in familial systemic lupus erythematosus by inhibiting PLD2-RAS signaling and downregulating Ras activity [24].
Expression and clinical significance of phospholipase D1 in de novo acute myeloid leukemia
Published in Hematology, 2020
Ying Lu, Jiasi Zhou, Renzhi Pei, Fenglin Li, Jie Jin, Lei Jiang
Phospholipase D (PLD) is a membrane protein that hydrolyzes phosphatidylcholine to phosphatidic acid and choline [3]. PLD1 and PLD2, two mammalian isoforms of PLD, have been proposed to play important roles in cancer. For instance, PLD1 is overexpressed in human breast cancer tissues and inhibition of either PLD1 or PLD2 enhances the sensitivity of breast cancer cells to radiotherapy [4,5]. Increased PLD expression or activity is also found in colorectal and prostate cancers, although the underlying mechanism remains unclear [6,7]. When wild-type melanoma and lung carcinoma cells are implanted in PLD1 deficiency mice, tumor growth, angiogenesis, and metastasis are impaired, indicating a critical role of PLD1 in tumor microenvironment [8]. However, a subset of chronic lymphocytic leukemia unresponsive to chemokine is characterized by defective activation of PLD1, suggesting that the function of PLD1 is not always pro-oncogenic [9,10].
The Key Role of Initiation Timing on Stroke Rehabilitation by Remote Ischemic Conditioning with Exercise (RICE)
Published in Neurological Research, 2023
Qingzhu Wang, Alexandra Wehbe, Melissa Wills, Fengwu Li, Xiaokun Geng, Yuchuan Ding
PLD2, located at the plasma membrane, drives axon growth and promotes nerve repair and reconstruction after injury [46,47]. A study conducted by Lee et al. found that upregulation of PLD2 in the hippocampus played a neuroprotective role in inducing ischemic tolerance after ischemic preconditioning [48]. In a recent study investigating tumor progression, it was found that HIF-1α could induce the expression of PLD2 [49]. A different study conducted by Sung et al. found that PLD2 could function as a mediator of mTOR activation [50]. In this study, we demonstrated that RICE, similar to exercise or RIC monotherapy, upregulates PLD2. Ischemic rats with RICE showed an additional increase in PLD2 mRNA expression. However, levels of PLD2 protein in the RICE group showed no statistical difference compared to the RIC and exercise group. We hypothesized that RICE only affected PLD2 at the level of transcription, and not at the level of translation, which may be regulated by other factors. mTOR is downstream of PLD2 [51]. Both RIC and exercise have also been shown to activate the mTOR pathway and improve motor memory and learning [52,53]. Previous studies have shown that activation of mTOR is crucial for spinogenesis, synaptic transmission, axonal myelination, and various neuronal functions. mTOR kinase, via the phosphorylation of 4EBP1 and P70S6K, plays a vital role in the regulation of cell growth, proliferation, transcription, protein synthesis, and ribosome biosynthesis, and is involved in cortical neural remodeling as well as motor learning [53,54]. The results from our study indicate that RICE with exercise initiated at 5 days, akin to exercise or RIC monotherapy, activates mTOR and its downstream substrates, P70S6K and 4EBP1, providing more evidence that the RICE regimen may be a useful intervention to improve motor and cognitive deficits. Therefore, the results from our study suggest a potential link within HIF-1α/PLD2/mTOR pathway that contributes to post-stroke synapse plasticity. Future endeavours should seek to expand the understanding of these proteins and the ways in which they are affected by different stimuli in the hours and days after stroke.