PUBLICATION
Alternative Splicing for Activation of Coagulation Factor XIII-A in the Fish Retina After Optic Nerve Injury
- Authors
- Sugitani, K., Koriyama, Y., Ogai, K., Furukawa, A., Kato, S.
- ID
- ZDB-PUB-180504-8
- Date
- 2018
- Source
- Advances in experimental medicine and biology 1074: 387-393 (Chapter)
- Registered Authors
- Keywords
- Alternative splicing, Explant culture, Factor XIII-A, Neurite outgrowth, Optic nerve regeneration, Retina, Thrombin, Transglutaminase, Wound healing, Zebrafish
- MeSH Terms
-
- Alternative Splicing*
- Animals
- Axons/ultrastructure
- Enzyme Activation
- Eye Proteins/biosynthesis
- Eye Proteins/genetics*
- Eye Proteins/physiology
- Factor XIIIa/metabolism*
- Gene Expression Regulation
- Goldfish
- Nerve Crush
- Nerve Regeneration
- Optic Nerve Injuries/genetics*
- Optic Nerve Injuries/metabolism
- Organ Culture Techniques
- Peptides/metabolism
- RNA, Messenger/biosynthesis
- RNA, Messenger/genetics*
- Real-Time Polymerase Chain Reaction
- Recombinant Proteins/metabolism
- Sequence Deletion
- Zebrafish
- Zebrafish Proteins/biosynthesis
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/physiology
- PubMed
- 29721968 Full text @ Adv. Exp. Med. Biol.
Citation
Sugitani, K., Koriyama, Y., Ogai, K., Furukawa, A., Kato, S. (2018) Alternative Splicing for Activation of Coagulation Factor XIII-A in the Fish Retina After Optic Nerve Injury. Advances in experimental medicine and biology. 1074:387-393.
Abstract
Factor XIII-A (FXIII-A), which has become known as cellular transglutaminase, plays important roles in mediating cross-linking reactions in various tissues. FXIII-A acts as one of the regeneration molecules in the fish retina and optic nerve after optic nerve injury and becomes activated at the site of injury within a few hours. Previous research has shown that activated FXIII-A induces neurite outgrowth from injured retinal ganglion cells and supports elongation of the regenerating optic nerve. However, the activation mechanism of FXIII-A remains unknown. Furthermore, the injured tissues do not express thrombin, a known activator of plasma FXIII. Here, we investigated the mRNA expression of FXIII-A based on two different regions, one encoding the activation peptide and the other encoding the enzymatic active site. We found that expression of the region encoding the activation peptide was markedly suppressed compared with the region encoding the active site. An overexpression study with a short-type FXIII-A cDNA lacking the activation peptide revealed induction of long neurite outgrowth in fish retinal explant cultures compared with full-length FXIII-A cDNA. The present findings suggest that alternative splicing may occur in the FXIII-A gene, resulting in deletion of the region encoding the activation peptide and thus allowing direct production of activated FXIII-A protein in the fish retina and optic nerve after optic nerve injury.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping