The proliferation/migration ability mediated by CD151/PI3K/AKT pathway determines the therapeutic effect of hUC-MSCs transplantation on rheumatoid arthritis.
Clin Exp Hypertens
; 46(1): 2366270, 2024 Dec 31.
Article
en En
| MEDLINE
| ID: mdl-38864268
ABSTRACT
OBJECTIVE:
To elucidate the underlying mechanism by which the proliferation and migration abilities of human umbilical cord mesenchymal stem cells (hUC-MSCs) determine their therapeutic efficacy in rheumatoid arthritis treatment.METHODS:
The DBA/1J mice were utilized to establish a collagen-induced RA (CIA) mouse model and to validate the therapeutic efficacy of hUC-MSCs transfected with CD151 siRNA. RNA-seq, QT-PCR and western blotting were utilized to evaluate the mRNA and protein levels of the PI3K/AKT pathway, respectively.RESULTS:
IFN-γ significantly enhanced the proliferation and migration abilities of hUC-MSCs, up-regulating the expression of CD151, a gene related to cell proliferation and migration. Effective inhibition of this effect was achieved through CD151 siRNA treatment. However, IFN-γ did not affect hUC-MSCs differentiation or changes in cell surface markers. Additionally, transplantation of CD151-interfered hUC-MSCs (siRNA-CD151-hUC-MSCs) resulted in decreased colonization in the toes of CIA mice and worse therapeutic effects compared to empty vector treatment (siRNA-NC-hUC-MSCs).CONCLUSION:
IFN-γ facilitates the proliferation and migration of hUC-MSCs through the CD151/PI3K/AKT pathway. The therapeutic efficacy of siRNA-CD151-hUC-MSCs was found to be inferior to that of siRNA-NC-hUC-MSCs.Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Artritis Reumatoide
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Transducción de Señal
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Movimiento Celular
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Fosfatidilinositol 3-Quinasas
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Trasplante de Células Madre Mesenquimatosas
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Proliferación Celular
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Proteínas Proto-Oncogénicas c-akt
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Células Madre Mesenquimatosas
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Ratones Endogámicos DBA
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Clin Exp Hypertens
Año:
2024
Tipo del documento:
Article
País de afiliación:
China