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Medium Design for Cell Culture Processing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
A group of compounds generally referred to as retinoids possess vitamin A activities. Their forms are retinol, retinal, retinoic acids, and ester. Their most important role is the vision function, with retinal serving as the photosensitive chromophore through a covalent link to the photoreceptor protein rhodopsin. In addition to operating as a vitamin, the retinoic acid derived from retinol plays a role in the regulation of transcriptional regulation in embryo development and in stem cell differentiation. Vitamin B is used to guide the differentiation process of specific lineages.
Multiple biotherapy effects of salidroside on tumors
Published in Domenico Lombardo, Ke Wang, Advances in Materials Science and Engineering, 2021
X.P. Wang, D.Y. Yuan, W.H. Li, Y. Tian
Inducing the differentiation of cancer cells does not directly kill cancer cells, but prevents cancer cells from progression and induces them to develop into normal cells under the function of some differentiation inducers. At present, retinoic acid (RA) is the most widely used differentiation inducer in clinical practice. RA is used in the treatment of a variety of malignant tumors, such as acute leukemia, thyroid cancer and breast cancer [19, 20]. The initiation of cell differentiation is regulated by oncogenes such as c-myc and p53 [21, 22]. As a proto-oncogene, c-myc participates in the process of cancer growth, proliferation, invasion and migration. In transformation cells, the expression of c-myc gene will increase, but with the differentiation of cells, the expression of c-myc gene will decrease, and the ability to promote cell proliferation will be lost. The research found that salidroside could cooperate with RA to down-regulate c-myc and promote apoptosis of gastric cancer cells, to achieve the effect of treating gastric cancer [23]. When hepatocellular cells were treated with different concentrations of salidroside, the DNA content of the salidroside treatment group was lower than that of the control group, and the expression of c-myc decreased with the increase of the concentration of salidroside. Morphological observation also showed that the volume of the cells increased significantly in HCC cells with high expression of c-myc, especially the enlargement of nuclei and deep staining, however, when the expression of c-myc was low after treated with salidroside, the differentiation of HCC cells was better [24]. Therefore, salidroside can inhibit the expression of proto-oncogene c-myc, and promote cancer cells to develop towards normal cells, which can indeed induce differentiation of cancer cells.
Retinoic acid and the genetics of positional information
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Malcolm Maden, David Chambers, James Monaghan
We now have a beginning of an understanding of the gene pathways, cell type, and cellular location of the genetics of positional information during limb regeneration that is drawn together in Figure 7.7. It is the fibroblasts, the stem cells of the blastema, that are the effectors of positional information in the blastema. Retinoic acid, perhaps in a concentration gradient deriving from the apical cap of the blastema, acts in the nucleus of blastemal cells via RARγ to upregulate and downregulate many genes with a variety of cellular functions. One group of genes comprises the Hox genes, which have classically been associated with positional specification, but few downstream targets, which could play a role in the realization of positional specification, have been identified. Perhaps, their targets are more transcription factors. On the other hand, the transcription factor MEIS has been shown to act on the Prod1 enhancer to upregulate it, and the PROD1 protein translocates to the cell membrane, where it is present in an amount depending on the location of the cell in the proximodistal axis of the limb. PROD1 interacts with EGFR in the cell membrane to signal back into the cytoplasm via ERK1/2 to upregulate MMP9 that is secreted into the extracellular space (signal 1). PROD1 also binds to nAG, the neurotrophic factor in the extracellular environment, and that interaction signals back into the cytoplasm to stimulate proliferation of the cell (signal 2). PROD1 also interacts with PROD1 on the surface of the adjacent cell, and the detection of concentration differences (perhaps by receptor occupancy Morais da Silva et al. 2002) results in a signal back into the cytoplasm of both cells to respond to positional differences (signal 3). These latter signals are likely to result in the upregulation of developmental signaling molecules such as FGF8 and SHH (Nacu et al. 2016), which are at least two of the intercellular signals responding to the detection of positional differences.
Retinoic acid as a teratogen: IX-Induction of fetal skeletal anomalies and alteration in the utero-placental expression pattern of EGFR during mice development
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Ahmed Said, Abdel-Rahman S. Sultan, Reda A. Ali, Mohsen A. Moustafa
Retinoic acid (RA), a bioactive vitamin A metabolite, is a signaling molecule, tightly regulated during embryogenesis; indispensable for the formation of many organs, including body axis, spinal cord, eyes, limbs, heart, and kidneys [7–10]. RA is also a valuable compound in the therapy of cystic acne among other numerous dermatologic disorders [11–13]. In target cells, RA acts as a ligand for nuclear retinoic acid receptors (RARs), which form heterodimers with retinoid X receptors (RXRs). The complex binds to a regulatory DNA segment, the retinoic acid response element (RARE), to control transcription of RA target genes. Maternal retinoic acid excess or deficiency during pregnancy cause abnormalities both in human infants [9,14] and in rodents [15], indicating that retinoic acid levels must be within a specific range for normal development [16]. Rat fetuses in mothers reared on vitamin A-deficient diets demonstrate an array of anomalies collectively known as ‘fetal vitamin A deficiency’ (VAD) syndrome, which comprises hind-brain, eye, ear, heart, lung, diaphragm, kidney, testis, limb and skeletal defects [17]. Similarly, mice with compound null mutations of RA nuclear receptors [18,19] and RA-synthesizing enzymes have malformations resembling the VAD syndrome [20]. Notably, excess vitamin A/RA in humans and animal models causes malformations resembling the fetal VAD syndrome [21,22].