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  • Keratin K has been identified as the

    2020-08-04

    Keratin 8 (K8) has been identified as the first intermediate filament expressed during development in amphibians and mammals. In zebrafish, a type II cytokeratin 8 (zf-K8) cDNA has been cloned. zf-K8 gene was maternally inherited and expressed in all surface cells throughout the embryonic stages older than blastula. In these embryonic stages, zf-K8 was also expressed in presumptive intestinal cells and the pectoral fin, and in the adult, its expression was observed in the colorectal luminal cells and superficial cell layers of skin and fins, and scales (Imboden et al., 1997). Cyt-1 was reported as a novel type I cytokeratin, which was expressed in the outer enveloping layer in zebrafish embryos (Sagerstrom et al., 1996). We report the identification of a novel type I cytokeratin gene, dorsal aorta and pronephric duct keratin type-1 gene (DAPK-1) from zebrafish cDNA, and the expression in early dorsal aorta and pronephric duct. DAPK-1 cDNA (1.3 kb) contains an open reading frame for 431 amino acids. Comparative studies of amino ctab medical abbreviation sequence revealed 87% identity between the goldfish keratin (GK) and the zebrafish DAPK-1. Application of DAPK-1 as a marker gene for dorsal aorta and pronephric duct also was discussed.
    Materials and methods
    Results and discussion
    Acknowledgements
    Introduction Stroke is a leading cause of mortality worldwide and is the leading cause of disability in the United States, representing a high-cost burden [1], [2]. Several experimental animal models of stroke are available in which reproducible injuries can be obtained through a combination of ischemia [3] and hypoxia [4], effectively mimicking the human condition. Ischemic stroke is caused by a disruption of blood flow that deprives the afflicted brain region of oxygen and nutrients, resulting in membrane depolarization and glutamate release [5]. Exposure to glutamate has been associated with a form of calcium-dependent delayed cell death linked to neurotoxicity [6], [7]. A mechanism of calcium-mediated neuronal death has been hypothesized in ischemia [8], central to which is the observation that hypoxia leads to the translocation of calcium from extracellular to intracellular spaces [9]. Death-associated protein kinase (DAPK) is an intracellular calcium/calmodulin (CaM)-regulated protein kinase (CaMK) whose mRNA levels increase in regions of tissue damage in an animal model of cerebral ischemia [10]. DAPK mRNA levels are also increased in the developing hippocampus [10], reaching maximal levels between embryonic day 22 and postnatal day 7. This represents the period of brain development characterized by apoptotic cell death [11], [12], [13], suggesting a role for DAPK in the regulation of apoptotic cell death during development. Consistent with this, cell culture models have demonstrated the involvement of DAPK in neuronal apoptosis that requires its intact catalytic domain [14], [15]. These findings raise the possibility that inhibition of the DAPK catalytic activity might forestall apoptotic neuronal death following ischemia. The targeting of DAPK in stroke is attractive, particularly because DAPK appears to function early in pathways of apoptosis [16], [17], potentially prior to the commitment of a cell to death.