SOCS3 silencing attenuates eosinophil functions in asthma patients

Eosinophils are one of the key inflammatory cells in asthma. Eosinophils can exert a wide variety of actions through expression and secretion of multiple molecules. Previously, we have demonstrated that eosinophils purified from peripheral blood from asthma patients express high levels of suppressor of cytokine signaling 3 (SOCS3). In this article, SOCS3 gene silencing in eosinophils from asthmatics has been carried out to achieve a better understanding of the suppressor function in eosinophils. SOCS3 siRNA treatment drastically reduced SOCS3 expression in eosinophils, leading to an inhibition of the regulatory transcription factors GATA-3 and FoxP3, also interleukin (IL)-10; in turn, an increased STAT3 phosphorilation was observed. Moreover, SOCS3 abrogation in eosinophils produced impaired migration, adhesion and degranulation. Therefore, SOCS3 might be regarded as an important regulator implicated in eosinophil mobilization from the bone marrow to the lungs during the asthmatic process.

Medienart:

E-Artikel

Erscheinungsjahr:

2015

Erschienen:

2015

Enthalten in:

Zur Gesamtaufnahme - volume:16

Enthalten in:

International journal of molecular sciences - 16(2015), 3 vom: 10. März, Seite 5434-51

Sprache:

Englisch

Beteiligte Personen:

Zafra, Ma Paz [VerfasserIn]
Cañas, Jose A [VerfasserIn]
Mazzeo, Carla [VerfasserIn]
Gámez, Cristina [VerfasserIn]
Sanz, Veronica [VerfasserIn]
Fernández-Nieto, Mar [VerfasserIn]
Quirce, Santiago [VerfasserIn]
Barranco, Pilar [VerfasserIn]
Ruiz-Hornillos, Javier [VerfasserIn]
Sastre, Joaquín [VerfasserIn]
del Pozo, Victoria [VerfasserIn]

Links:

Volltext

Themen:

130068-27-8
FOXP3 protein, human
Forkhead Transcription Factors
GATA3 Transcription Factor
Interleukin-10
Journal Article
Research Support, Non-U.S. Gov't
SOCS3 protein, human
STAT3 Transcription Factor
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins

Anmerkungen:

Date Completed 25.11.2015

Date Revised 13.11.2018

published: Electronic

Citation Status MEDLINE

doi:

10.3390/ijms16035434

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM24701608X