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Biological Correlates of Microwave
Published in Jitendra Behari, Radio Frequency and Microwave Effects on Biological Tissues, 2019
PKC plays a key role in a variety of pathologic states including oncogenesis (Nishizuka 1986; Harvey & French 2000) and in mediating cellular responses to extracellular stimuli involved in proliferation, differentiation, apoptosis and exocytotic release in a number of non-neuronal cells (Ohkusu et al. 1986). Several lines of evidence suggest that PKC modulates ion conductance by phosphorylating membrane proteins such as channels, pumps, and ion exchange proteins, besides its role in extrusion of Ca2+ immediately after its mobilization into cytosol. The enzyme has also been implicated in phosphorylation of several neuronal proteins, which are thought to regulate neurotransmitter release and long-term potentiation in memory formation (Suzuk 1994).
Chemical Carcinogenesis in Skin: Causation, Mechanism, and Role of Oncogenes
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
The molecular mechanism leading to tumor promotion by macrocyclic terpenoids such as phorbol esters, mezerein, and teleocidin involves phospholipase C-dependent activation of PKC. It is becoming increasingly clear that PKC is a receptor for these tumor promoters and that tumor promotion by these agents is mediated by their receptor binding. The receptor for these promoters is implicated in the transduction of altered and unscheduled signals of cellular proliferation. PKC is activated by TPA in vivo in the presence of Ca2+ and phospholipids forming a part of the signal transducing system. Recent evidences have shown that activation of phospholipase C by an external stimuli results in two separate arms of second messengers which include DAG and inositol 1,4,5 triphosphate.33 Inositol 1,4,5 triphosphate mobilizes Ca2+ from internal stores leading to the activation of calmodulin/Ca2+-dependent enzymes which may, in turn, lead to PKC activation via indirect mechanisms. So far, six isozymes of PKC are known, the majority of which are Ca2+ dependent.33 Recently some Ca2+ independent PKC are also described, one of which, nPKCTn, is predominantly expressed in murine skin.34 However, the isozyme of PKC involved in skin tumor promotion is not clearly defined. The activation of PKC phosphorylates various growth factor receptors which then receive unscheduled signals leading to the enhanced synthesis of DNA along with the amplified expression of oncogenes. The product of rasHa oncogene (p21) may also play a role in the modulation of activity of phospholipase C.33 The detailed description of oncogenes is provided separately in this chapter.
Marine Algae in Diabetes and Its Complications
Published in Se-Kwon Kim, Marine Biochemistry, 2023
The polyol pathway of glucose metabolism plays a crucial function in the development of neuropathy (Gabbay, 1973). It is an alternative route of glucose metabolism in which the enzyme aldose reductase catalyzes the reduction of glucose to sorbitol, then to fructose by sorbitol dehydrogenase. Aldose reductase (AR) requires NADPH as a co-factor, and sorbitol dehydrogenase (SDH) needs NAD+. During hyperglycemia, sorbitol accumulates in AR-containing tissues, as it is impermeable to the cell membranes and cannot diffuse out and, hence, creates hyperosmotic stress on the cell, thereby inducing neuropathic pain (Niimi et al., 2021; Kinoshita and Nishimura, 1988). Treatment with inhibitors of aldose reductase has been shown to prevent various complications, including nephropathy, neuropathy, and cataractin animal models (Oates and Mylari, 1999). It is reported that the AR inhibitor epalrestat prevents high glucose–induced smooth muscle cell proliferation and hypertrophy (Yasunari et al., 1995), thereby preventing their dysfunction and remodeling (Tawata et al., 1992). Accumulation of intracellular sorbitol and fructose due to polyol activation leads to diminution of other organic electrolytes like taurine and myo-inositol that regulate cellular osmolality (Stevens et al., 1993). Lessening of myo-inositol in the peripheral nerves gets in the way of phosphoinositide production, leading to inadequate diacylglycerol to sustain the content of protein kinase C (PKC) essential for Na+/K+-ATPase activation (Zhu and Eichberg, 1990; Greene et al., 1987). Amendments in PKC activation also interfere with an important myelin protein’s (PO) phosphorylation of peripheral nerves and play an important pathogenetic role in primary segmental demyelination (Row-Rendleman and Eichberg, 1994). Enhanced activity of vascular PKC-β is thought to play a noteworthy role in microvascular complications.
A new Ni(II)-based coordination polymer: structural characterization and protective effect on type 2 diabetes by regulating PKC and MAPK expression
Published in Inorganic and Nano-Metal Chemistry, 2020
Qin Li, Xiuzhen Shi, Qiong Luo, Aili Guo, Yijing Guo
During the procession of the diabetic disease, there is usually combined with an abnormal expression of the pkc and mapk in HepG2 cell. The pkc and mapk gene were now regarded as the important mediator in the progression of diabetic disease. The activation of PKC pathway could damage the liver cells and promote the development of diabetic complication via increasing the level of oxidative stress. Thus, in this experiment, the real-time RT-PCR detection was performed to detect the influence of nano 1 on the pkc and mapk expression in HepG2 cell. As results showed in Figure 4, we can see that there was a significantly increase of the pkc and mapk expression which increased to about 5 fold of the control group. While, after nano 1 treatment, the up-regulated level of the pkc and mapk genes was returned back to the normal level, which is similar with the control group. This result indicated the protective effect of nano 1 in high-glucose induced diabetes by reducing the pkc and mapk expression in HepG2 cell.
Ceramide pathway: A novel approach to cancer chemotherapy
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Mahdi Mashhadi Akbar Boojar, Masoud Mashhadi Akbar Boojar, Sepide Golmohammad
Among the various PKC subtypes, at least two of them are influenced by the ceramide messaging pathway: PKCα and PKCζ. PKCα is one of the common types of PKC family that requires calcium liberation in cytoplasm and diacylglycerol in a cytoplasmic membrane for signaling, in order to activate ultimately many cell survival factors, including p38 and MAP-kinase [42]. Ceramide by dephosphorylating this sub-group suppresses all related pathways. On the other hand, ceramide, by increasing the activity of PKCζ, delays the rearrangement of the Bcl-x gene family as one of the most critical apoptotic suppressors, thus causing cellular death [2].