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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Interleukin-6 deficiency modulates testicular function by increasing the expression of suppressor of cytokine signaling 3 (SOCS3) in mice

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Autor(es):
Alves-Silva, Thais [1, 2] ; Freitas, Geanne Arantes [3, 4] ; Rodrigues Hungaro, Talita Guerreiro [1, 5] ; Arruda, Adriano Cleis [1, 5] ; Oyama, Lila Missae [6] ; Werneck Avellar, Maria Christina [4] ; Araujo, Ronaldo Carvalho [1, 2, 5]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Fed Univ Sao Paulo UNIFESP, Biophys Dept, Lab Genet & Exercise Metab, Sao Paulo - Brazil
[2] Fed Univ Sao Paulo UNIFESP, Mol Biol Program, Sao Paulo - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo - Brazil
[4] Fed Univ Sao Paulo UNIFESP, Pharmacol & Mol Biol Inst, Sao Paulo - Brazil
[5] Fed Univ Sao Paulo UNIFESP, Nephrol Program, Sao Paulo - Brazil
[6] Fed Univ Sao Paulo UNIFESP, Lab Nutr & Endocrine Physiol, Physiol Dept, Sao Paulo - Brazil
Número total de Afiliações: 6
Tipo de documento: Artigo Científico
Fonte: SCIENTIFIC REPORTS; v. 11, n. 1 JUN 1 2021.
Citações Web of Science: 0
Resumo

Several cytokines have been reported to participate in spermatogenesis, including interleukin-6 (IL6). However, not many studies have been conducted on the loss of Il6 on the male reproductive tract. Nonetheless, there is considerable knowledge regarding the pathological and physiological role of IL6 on spermatogenesis. In this way, this study evaluated the impact of Il6 deficiency on mice testicles in the absence of infection or inflammation. We showed that Il6 deficiency increases daily sperm production, the number of spermatids, and the testicular testosterone and dihydrotestosterone levels. Besides that, mice with a deleted Il6 (IL6KO) showed increased testicular SOCS3 levels, with no changes in pJAK/JAK and pSTAT3/STAT3 ratios. It is worth noting that the aforementioned pathway is not the only pathway to up-regulate SOCS3, nor is it the only SOCS3 target, thus proposing that the increase of SOCS3 in the testis occurs independently of the JAK-STAT signaling in IL6KO mice. Therefore, we suggest that the lack of Il6 drives androgenic production by increasing SOCS3 in the testis, thus leading to an increase in spermatogenesis. (AU)

Processo FAPESP: 15/24399-5 - Modulação da herança genética pelo treinamento físico induzida pela interleucina-6
Beneficiário:Thaís Alves da Silva
Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
Processo FAPESP: 15/20082-7 - Sistema calicreína cininas no exercício físico e metabolismo
Beneficiário:Ronaldo de Carvalho Araújo
Modalidade de apoio: Auxílio à Pesquisa - Temático