Effects of Excessive Retinoic Acid on C2C12 Myogenesis

Liu, Bo; Li, Nan; Jiang, Yuling; Liu, Chao; Ma, Le; Xiao, Jing

doi:10.2485/jhtb.25.97

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…This provides insights into the infection dynamics in cell types resembling skeletal muscle and cardiomyocytes. We demonstrated morphological and molecular changes confirming successful differentiation of H9c2 cells into myotubes [11,21]. Cardiac myotubes displayed larger cell surface area compared to skeletal myotubes, as noted previously during myoblast differentiation [21].…”

Section: Discussionsupporting

confidence: 82%

In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology

Contreras-Ortiz,

Hernández-Mendoza,

Márquez-Dueñas

et al. 2024

PLoS Negl Trop Dis

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Chagas disease predominantly affects the heart, esophagus, and colon in its chronic phase. However, the precise infection mechanisms of the causal agent Trypanosoma cruzi in these tissue types remain incompletely understood. This study investigated T. cruzi infection dynamics in skeletal (SM) and cardiac myotubes (CM) differentiated from H9c2(2–1) myoblasts (control). SM and CM were generated using 1% fetal bovine serum (FBS) without or with retinoic acid, respectively. Initial invasion efficiencies and numbers of released parasites were equivalent between undifferentiated and differentiated cells (~0.3–0.6%). Concomitantly, parasite motility patterns were similar across cell lines. However, CM demonstrated significantly higher infection kinetics over time, reaching 13.26% infected cells versus 3.12% for SM and 3.70% for myoblasts at later stages. Cellular automata modeling suggested an enhanced role for cell-to-cell transmission in driving the heightened parasitism observed in CM. The increased late-stage susceptibility of CM, potentially mediated by cell-to-cell transfer mechanisms of the parasite, aligns with reported clinical tropism patterns. The myotube infection models provide novel insights into Chagas disease pathogenesis that are not fully attainable through in vivo examination alone. Expanding knowledge in this area could aid therapeutic development for this neglected illness.

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Section: Discussionsupporting

confidence: 82%

In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology

Contreras-Ortiz,

Hernández-Mendoza,

Márquez-Dueñas

et al. 2024

PLoS Negl Trop Dis

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“…To induce myogenic differentiation, GM was replaced by differentiation medium (DM) containing high-glucose DMEM supplemented with 2% horse serum (HyClone, Logan, UT, USA) after C2C12 cells reached 80~90% confluence. RA supplement in medium was prepared as previously described [ 27 ]. All media were changed every 2 days.…”

Section: Methodsmentioning

confidence: 99%

Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ

Liu

et al. 2017

Skeletal Muscle

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BackgroundWe previously reported that Wnt5a/CaMKIIδ (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Our latest study found that the expression of miR-31-5p, which was predicted to target the 3′UTR of CamkIIδ, was raised in the RA-treated embryonic tongue. Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIδ pathway through miR-31-5p in embryonic tongue.MethodsC2C12 myoblast line was employed as an in vitro model to examine the suppression of miR-31-5p on CamkIIδ expression, through which RA impaired the myoblast proliferation and differentiation in embryonic tongue.ResultsRA stimulated the expression of miR-31-5p in both embryonic tongue and C2C12 myoblasts. Luciferase reporter assay confirmed that the 3′UTR of CamkIIδ was a target of miR-31-5p. MiR-31-5p mimics disrupted CamkIIδ expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA.ConclusionsExcess RA can stimulate miR-31-5p expression to suppress CamkIIδ, which represses the proliferation and differentiation of tongue myoblasts.Electronic supplementary materialThe online version of this article (doi:10.1186/s13395-017-0126-x) contains supplementary material, which is available to authorized users.

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“…Retinoic acid treatment of human embryonic stem cells expanded the premyogenic progenitor population, promoting the Pax3 -positive myoblast population and elevating the expression of MyoD , myogenin, and mesenchyme homeobox 1 (Meox1) [ 97 ]. In addition, a high dose level of retinoic acid supplementation in the C2C12 cell line still stimulated the myogenic differentiation, but the MyHC protein level was obviously decreased [ 98 ].…”

Section: Vitamin a Myoblast Hyperplasia And Myotube Differentiationmentioning

confidence: 99%

Vitamin A regulates intramuscular adipose tissue and muscle development: promoting high-quality beef production

Peng

Smith

Lee

2021

J Animal Sci Biotechnol

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During growth in cattle, the development of intramuscular adipose tissue and muscle is dependent upon cell hyperplasia (increased number of adipocytes) and hypertrophy (increased size of adipocytes). Based on the results of previous studies, other adipose tissue depots (e.g., perirenal and subcutaneous) develop from the fetal stage primarily as brown adipose tissue. The hyperplastic stage of intramuscular adipose is considered to develop from late pregnancy, but there is no evidence indicating that intramuscular adipose tissue develops initially as brown adipose tissue. Hyperplastic growth of intramuscular adipose continues well into postweaning and is dependent on the timing of the transition to grain-based diets; thereafter, the late-stage development of intramuscular adipose tissue is dominated by hypertrophy. For muscle development, hyperplasia of myoblasts lasts from early (following development of somites in the embryo) to middle pregnancy, after which growth of muscle is the result of hypertrophy of myofibers. Vitamin A is a fat-soluble compound that is required for the normal immunologic function, vision, cellular proliferation, and differentiation. Here we review the roles of vitamin A in intramuscular adipose tissue and muscle development in cattle. Vitamin A regulates both hyperplasia and hypertrophy in in vitro experiments. Vitamin A supplementation at the early stage and restriction at fattening stage generate opposite effects in the beef cattle. Appropriate vitamin A supplementation and restriction strategy increase intramuscular adipose tissue development (i.e., marbling or intramuscular fat) in some in vivo trials. Besides, hyperplasia and hypertrophy of myoblasts/myotubes were affected by vitamin A treatment in in vitro trials. Additionally, some studies reported an interaction between the alcohol dehydrogenase-1C (ADH1C) genotype and vitamin A feed restriction for the development of marbling and/or intramuscular adipose tissue, which was dependent on the timing and level of vitamin A restriction. Therefore, the feed strategy of vitamin A has the visible impact on the marbling and muscle development in the cattle, which will be helpful to promote the quality of the beef.

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Effects of Excessive Retinoic Acid on C2C12 Myogenesis

Cited by 7 publications

References 15 publications

In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology

In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology

Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ

Vitamin A regulates intramuscular adipose tissue and muscle development: promoting high-quality beef production

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