These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regulation of inositol 1,4,5-triphosphate receptor, type 1 (IP3R1) in hypoxic/reperfusion injury of white matter.
    Author: Kesherwani V, Agrawal SK.
    Journal: Neurol Res; 2012 Jun; 34(5):504-11. PubMed ID: 22643045.
    Abstract:
    OBJECTIVE: Calcium overloading is responsible for initiating the cell death in neuronal tissue after hypoxic injury. Inositol 1,4,5-triphosphate receptors (IP3Rs) is an important calcium channel which regulates cellular calcium homeostasis. IP3R1 is widely expressed in brain and spinal tissue. In the present study, we have studied the regulation of IP3R1 in hypoxic/reperfusion injury of spinal cord dorsal column in vitro. METHODS: Dorsal columns were isolated from the spinal cord of adult rats and injury was induced by exposing to hypoxic condition for 1 hour. After injury, reperfusion was carried out for 0, 2, 4, and 8 hours. Tissues were collected and processed for western blotting, immunohistochemistry and real-time PCR. RESULTS: In the present study, we have found increased expression of IP3R1 after hypoxic/reperfusion injury of spinal cord dorsal column in vitro. Maximum expression of IP3R1 has been seen at 4 hours after hypoxia. Double immunofluorescence studies show the localization of IP3R1 in axons and astrocytes. Further identifying the signaling pathway involved in the regulation, we found Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitor KN-62 and c-Jun N-terminal kinase (JNK) inhibitor SP600125 reduced the expression of IP3R1 suggesting the role of CaMKII and JNK in the regulation of IP3R1 expression. We did not find role of ERK and p38 in the regulation IP3R1 expression in hypoxic/reperfusion injury of dorsal column in vitro. DISCUSSION: The result presented in this study showed that IP3R1 expression is increased in hypoxic/reperfusion injury of spinal cord white matter and it is regulated by the CaMKII-JNK pathway.
    [Abstract] [Full Text] [Related] [New Search]