Search Results
You are looking at 1 - 2 of 2 items for
- Author: S Morimoto x
- Refine by access: All content x
Search for other papers by K Zeki in
Google Scholar
PubMed
Search for other papers by I Morimoto in
Google Scholar
PubMed
Search for other papers by T Arao in
Google Scholar
PubMed
Search for other papers by S Eto in
Google Scholar
PubMed
Search for other papers by U Yamashita in
Google Scholar
PubMed
This study provides the first report that the same cytokine (interleukin-1 (IL-1)) can induce opposite effects on cyclin-dependent kinases (Cdks) and Cdk inhibitors (Cdkis) in the G1 phase even in the same type of cancer cells (papillary thyroid carcinoma cells). Cell cycle analysis revealed an increase in NIM1 cells and a decrease in NPA cells in the S and G2+M phases after treatment with IL-1alpha. The addition of IL-1alpha to NIM1 cells reduced the expression of p16 and p21 protein and induced the expression of Cdk2 and Cdk4 protein, which leads to the phosphorylation of retinoblastoma protein. The addition of IL-1alpha to NPA cells induced the expression of p27 protein and reduced the expression of Cdk2 protein, which leads to induction of p107 protein expression. It is of interest that p21 protein expression was not observed in NPA cells. These results suggest that several Cdks and Cdkis play a regulatory role in the G1 cell cycle progression and arrest induced by IL-1alpha in thyroid carcinoma cell lines.
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by S Morimoto in
Google Scholar
PubMed
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by C A Mendoza-Rodríguez in
Google Scholar
PubMed
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by M Hiriart in
Google Scholar
PubMed
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by M E Larrieta in
Google Scholar
PubMed
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by P Vital in
Google Scholar
PubMed
Facultad de Química and
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacan 04510, D F México, México
Search for other papers by M A Cerbón in
Google Scholar
PubMed
Beta-cell apoptosis is responsible for the development of insulin-dependent diabetes mellitus in the streptozotocin (STZ) rat model. It has been demonstrated that steroid hormones possess antioxidant and protective antiapoptotic effects in many tissues. The aim of the present study was to investigate the early apoptotic damage induced by STZ in rat pancreas, and the effect of testosterone in preventing apoptosis of pancreatic β cells. Intact and castrated adult male Wistar rats were subjected to a unique injection of STZ 60 mg/kg (body weight) in citrate buffer, and the kinetics of apoptosis in β cells was assessed. Insulin and glucose were measured by RIA and a glucometer respectively, and in pancreatic tissue by immunohistochemistry. At 6 h after STZ injection, a marked increase in apoptotic β cells was detected; however, glucose and insulin serum levels were not significantly different from the controls. The castrated animals presented higher percentages of apoptotic β cells (65.75 ± 5.42%) than intact males (20.6 ± 4.38%) and castrated, testosterone-substituted males (30.66 ± 1.38%). The decrease in apoptotic β cells induced by testosterone was reversed by the antiandrogen flutamide (67.69 ± 3.45%). The overall results indicate that early apoptotic damage produced by STZ in castrated animals was reversed by testosterone, suggesting that this hormone exerts a natural protective effect in rat pancreas. This effect could help to explain some sexual differences in diabetes mellitus incidence in man, reinforcing the idea that new approaches in steroid hormone therapies should be considered for treatment of this disease.
