Leptin impairs myogenesis in C2C12 cells through JAK/STAT and MEK signaling pathways
PBN-AR
Instytucja
Instytut Medycyny Doświadczalnej i Klinicznej im. Mirosława Mossakowskiego Polskiej Akademii Nauk
Informacje podstawowe
Główny język publikacji
en
Czasopismo
CYTOKINE
ISSN
1043-4666
EISSN
Wydawca
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI
URL
Rok publikacji
2013
Numer zeszytu
2
Strony od-do
445-454
Numer tomu
61
Identyfikator DOI
Liczba arkuszy
1,72
Słowa kluczowe
en
Leptin
Insulin
Myogenesis
C2C12 muscle cells
SOCS3/JAK/STAT3 pathway
Streszczenia
Język
en
Treść
Reduced lean body mass in genetically obese (ob/ob) or anorectic/cachectic subjects prcimpted us to verify the hypothesis whether leptin, white adipose tissue cytokine, might be a negative organizer of myogenesis. Recombinant leptin (100 ng/mL) stimulated mitogenesis together with the raise in (TY204)-Y-202/ P-ERK1/2 protein expression. Concomitantly, it impaired cell viability and muscle fiber formation from C2C12 mouse myoblasts. Detailed acute and chronic studies with the use of metabolic inhibitors revealed that both JAK/STAT3 and MEK/MAPK but not P13-K/AKT/GSK-313 signaling pathways were activated by leptin, and that STAT3 ((YP)-P-705-STAT3) and MEK ((TYP)-Y-202/-P-204-ERK1/2) mediate these effects. In contrary, insulin evoked PI3-K-dependent phosphorylation of ART (S-473) and GSK-3 beta (S-9) and insulin surpassed leptin-dependent inhibition of myogenic differentiation in PI3-K-dependent manner. GSK-3 beta seems to play dual role in muscle development. Insulin-dependent effect on GSK-3 beta ((SP)-P-9-GSK-3 beta) led to accelerated myotube construction. In contrary, leptin through MEK-dependent manner caused GSK-3 beta phosphorylation ((YP)-P-216-GSK-3 beta) with resultant drop in myoblast fusion. Summing up, partially opposite effects of insulin and leptin on skeletal muscle growth emphasize the importance of interplay between these cytokines. They determine how muscle mass is gained or lost. (C) 2012 Elsevier Ltd. All rights reserved.
Cechy publikacji
ORIGINAL_ARTICLE
Inne
System-identifier
599508
CrossrefMetadata from Crossref logo
Cytowania
Liczba prac cytujących tę pracę
Brak danych
Referencje
Liczba prac cytowanych przez tę pracę
Brak danych