The Effects of Insulin on Immortalized Rat Schwann Cells, IFRS1.

Tytuł:: The Effects of Insulin on Immortalized Rat Schwann Cells, IFRS1.
Autorzy:: Saiki T; Department of Pharmacy, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan.
Nakamura N; Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Miyabe M; Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Ito M; Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Minato T; Department of Clinical Laboratory, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan.
Sango K; Diabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Matsubara T; Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Naruse K; Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan.
Źródło:: International journal of molecular sciences [Int J Mol Sci] 2021 May 23; Vol. 22 (11). Date of Electronic Publication: 2021 May 23.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:: Insulin/*pharmacology
Schwann Cells/*drug effects
Animals ; Cell Division/drug effects ; Cell Line, Transformed ; Chromones/pharmacology ; Diabetic Neuropathies/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flavonoids/pharmacology ; Gene Expression Regulation/drug effects ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors ; Morpholines/pharmacology ; Myelin Proteins/biosynthesis ; Myelin Proteins/genetics ; Phosphatidylinositol 3-Kinases/drug effects ; Phosphorylation ; Protein Processing, Post-Translational/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Inbred F344 ; Receptor, Insulin/biosynthesis ; Receptor, Insulin/genetics ; Signal Transduction/drug effects
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Grant Information:: 21592506 Ministry of Education, Culture, Sports, Science and Technology
Contributed Indexing:: Keywords: Akt; Schwann cells; extracellular-signal-regulated kinase (ERK); insulin; myelin associated glycoprotein; myelin basic protein; myelin protein zero
Substance Nomenclature:: 0 (Chromones)
0 (Flavonoids)
0 (Insulin)
0 (Morpholines)
0 (Myelin Proteins)
31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
EC 2.7.10.1 (Receptor, Insulin)
EC 2.7.11.1 (Akt1 protein, rat)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
Entry Date(s):: Date Created: 20210602 Date Completed: 20210621 Latest Revision: 20210621
Update Code:: 20240104
PubMed Central ID:: PMC8197103
DOI:: 10.3390/ijms22115505
PMID:: 34071138
: Czasopismo naukowe

Pełny tekst

Schwann cells play an important role in peripheral nerve function, and their dysfunction has been implicated in the pathogenesis of diabetic neuropathy and other demyelinating diseases. The physiological functions of insulin in Schwann cells remain unclear and therefore define the aim of this study. By using immortalized adult Fischer rat Schwann cells (IFRS1), we investigated the mechanism of the stimulating effects of insulin on the cell proliferation and expression of myelin proteins (myelin protein zero (MPZ) and myelin basic protein (MBP). The application of insulin to IFRS1 cells increased the proliferative activity and induced phosphorylation of Akt and ERK, but not P38-MAPK. The proliferative potential of insulin-stimulated IFRS1 was significantly suppressed by the addition of LY294002, a PI3 kinase inhibitor. The insulin-stimulated increase in MPZ expression was significantly suppressed by the addition of PD98059, a MEK inhibitor. Furthermore, insulin-increased MBP expression was significantly suppressed by the addition of LY294002. These findings suggest that both PI3-K/Akt and ERK/MEK pathways are involved in insulin-induced cell growth and upregulation of MPZ and MBP in IFRS1 Schwann cells.

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