Asset Details
Do you wish to reserve the book?
Neuroprotective effect of TAT PTD-Ngb fusion protein on primary cortical neurons against hypoxia-induced apoptosis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Neuroprotective effect of TAT PTD-Ngb fusion protein on primary cortical neurons against hypoxia-induced apoptosis
Do you wish to request the book?
Neuroprotective effect of TAT PTD-Ngb fusion protein on primary cortical neurons against hypoxia-induced apoptosis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Neuroprotective effect of TAT PTD-Ngb fusion protein on primary cortical neurons against hypoxia-induced apoptosis
2013
Overview
Hypoxic–ischemic injury increases neuroglobin (Ngb) expression in the brain. In our previous study, we have generated a transactivator-of-transcription protein-transduction domain-neuroglobin fusion protein (TAT PTD-Ngb) that successfully mediated exogenous Ngb expression in the primary neurons. In this study, we further investigated the role of TAT PTD-Ngb in protecting neurons against hypoxia-induced apoptosis and explored the possible mechanism. The primary cultured neurons were divided into four groups: (1) the normal group (no hypoxic injury); (2) the vehicle group (vehicle treatment and hypoxia injury); (3) the TAT PTD-Ngb group (TAT PTD-Ngb treatment and hypoxia injury); and (4) the Ngb group (Ngb treatment and hypoxia injury). Translocation of TAT PTD-Ngb into neurons was detected using fluorescent immunostaining against His-tag as early as 30 min after incubation. MTT assay showed that the TAT PTD-Ngb group had significantly increased cell viability compared to the vehicle or Ngb group after hypoxia. The result of transmission electron microscopy (TEM) also displayed rescued ultrastructure in TAT PTD-Ngb neurons compared to that of apoptotic neurons. In addition, TAT PTD-Ngb neurons showed significantly increased expression of anti-apoptotic Bcl-2 protein and decreased activities of caspase-3 and caspase-9 in response to hypoxia. These results suggest that TAT PTD-Ngb fusion protein protects primary cortical neurons against hypoxia-induced injury possibly through suppressing mitochondria apoptotic pathway.
Publisher
Springer Milan,Springer Nature B.V
Subject
/ Gene Expression Regulation - drug effects
/ Gene Products, tat - pharmacology
/ Male
/ Medicine
/ Microtubule-Associated Proteins - metabolism
/ Nerve Tissue Proteins - pharmacology
/ Neuroprotective Agents - pharmacology
/ Proto-Oncogene Proteins c-bcl-2 - metabolism
/ Rats
