Apoptotic, injury-induced cell death in cultured mouse murine motor neurons
Section snippets
Acknowledgements
We thank Ray Salcedo and Keith Ratzlaff for expert technical assistance, Dr. Neil Cashman for providing the NSC19 cells, and Dr. Dennis Wallace for statistics discussion. This study was supported, in part, by the Jackson Foundation, USUHS (DVHIP), the ALS and Spinal Cord Injury Fund of The Kansas University Endowment Association, The Research Institute, Inc., of the University of Kansas Medical Center, and the Medical Research Service of the Department of Veterans Affairs.
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2016, Brain ResearchCitation Excerpt :Antibody to murine PAR1 was a generous gift of Drs. Patricia Andrade-Gordon and Michael D’Andrea (R. W. Johnson Pharmaceutical Research Institute, Spring House, PA). As in our previously-published studies (Citron et al., 1997; Smirnova et al., 1998a; Smirnova et al., 1998b), we used motor neuron-like NSC19 (or NSC34) cells (initially a gift from Dr. N. Cashman, Montreal Neurologic Hospital, Montreal, Canada), a mouse-mouse neural hybrid cell line produced through fusion of the aminopterin-sensitive neuroblastoma N18TG2 with motor neuron-enriched embryonic day 12-14 spinal cord cells, (Cashman et al., 1992). Relevant to our experiments, a prior report utilized these same cells to estimate the effects of HNE on glutamate transport (Pedersen et al., 1999).
VEGF protects rat cortical neurons from mechanical trauma injury induced apoptosis via the MEK/ERK pathway
2011, Brain Research BulletinCitation Excerpt :In several studies, the survival effects of VEGF in primary neuronal cultures are mediated by the anti-apoptotic pathway involving the MEK/ERK pathway [21,27]. Mechanical trauma injury induced cell death with apoptotic features in cultured neurons [4]. Our study indicates that pretreatment with VEGF prevented scratch-induced neuronal death.
Differentially expressed genes of the carpet shell clam Ruditapes decussatus against Perkinsus olseni
2009, Fish and Shellfish ImmunologyCitation Excerpt :Further investigations are needed to elucidate this aim, and will be the objective of a separate publication. Apoptosis or programmed cell death (that essentially acts on the elimination of unwanted cells [5,14]) can play an important role in the progression of disease, and normally occurs when a cell is damaged, infected or senescent [45] and also plays an important role during the elimination of harmful cells [14]. The DAD-1 (defender against apoptotic cell death) is involved, among other processes, in the genetic control of apoptosis inhibiting it [33], and it is known to be a highly conserved gene among humans, mice, clawed frogs, plants, and even recently have been characterized in arachnids, and in the marine invertebrate A. irradians [53] and S. purpuratus (GenBank accession number XP001178079) suggesting that this gene could have similar biochemical functions in animal and plants.
Keratinocyte Growth Factor 1 Inhibits Wound Edge Epithelial Cell Apoptosis In Vitro
2004, Journal of Investigative DermatologyCitation Excerpt :Previously, it was found using mouse motor neurons in culture that sister cells undergo apoptosis adjacent to those at the “epicenter” of the scratch injury. This was restricted only to those neurons proximal to the scratch, early after injury, suggesting that a “death signal” or wave of apoptosis is produced by injured cells moving outward from the injury and not by factors diffusing from the wound edge cells (Citron et al, 1997). Signaling processes have also been detected radiating from scrape-wounded intestinal epithelial cell cultures.