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2014 Fiscal Year Final Research Report

New strategy for protecting and therapy of neuronal cell degeneration by intranasal infusion of proteins and neuropeptide

Research Project

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Project/Area Number 25670767
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Emergency medicine
Research InstitutionShowa University

Principal Investigator

SHIODA SEIJI  昭和大学, 医学部, 教授 (80102375)

Co-Investigator(Kenkyū-buntansha) DOHI Kenji  東京慈恵会医科大学, 医学部, 准教授 (20301509)
OHTAKI Hirokazu  昭和大学, 医学部, 講師 (20349062)
NAKAMACHI Tomoya  富山大学, 大学院理工学研究部, 助教 (30433840)
Co-Investigator(Renkei-kenkyūsha) WARANABE Jun  昭和大学, 遺伝子組換え実験室, 助教 (50649069)
NONAKA Naoko  昭和大学, 歯学部, 准教授 (20307052)
ARATA Satoru  昭和大学, 遺伝子組換え実験室, 准教授 (20159502)
RAKWAL Randeep  昭和大学, 医学部, 兼任講師 (70590850)
Project Period (FY) 2013-04-01 – 2015-03-31
KeywordsPACAP / TSG-6 / 神経細胞死防御 / 神経再生 / 点鼻投与
Outline of Final Research Achievements

We studied the effect of PACAP on neuroregeneration and neurogenesis in mouse brain ischemia. We injected intraventricularly or intranasally TSG-6 in normal and PACAP gene deficient mice to study whether neuronal cell death was inhibited or not by use of morphological methods. As a result, it appeared that PACAP inhibited neuronal cell death after brain ischemia not depending on TSG-6 so it may be suggested that PACAP affects rescuing neuronal cell death without the effect of TSG-6 pathway. In our another study to search for the gene or gene product which PACAP may affect on protecting cell death in brain ischemia and spinal cord injury that it stimulated to induce CRMP2 protein, which is known as an axon outgrowth factor. It may be suggested that PACAP affects on stimulating CRMP2 protein to stimulate axon outgrowth in rodents as well as primates and humans and in future PACAP may be used for protecting of neuronal cell death after brain ischemia and/or spinal cord injury.

Free Research Field

医歯薬学

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Published: 2016-06-03  

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