scholarly journals Silk Fibroin Promotes the Regeneration of Pancreatic β-Cells in the C57BL/KsJ-Leprdb/db Mouse

Molecules ◽  
2020 ◽  
Vol 25 (14) ◽  
pp. 3259
Author(s):  
So-young Park ◽  
Boyoung Kim ◽  
Yun Kyung Lee ◽  
Sueun Lee ◽  
Jin Mi Chun ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Silk Fibroin ◽  
Apoptotic Cell ◽  
Nuclear Antigen ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
In Vivo Models

Diabetes mellitus is a chronic metabolic disease, and its progression leads to serious complications. Although various novel therapeutic approaches for diabetes mellitus have developed in the last three decades, its prevalence has been rising more rapidly worldwide. Silk-related materials have been used as anti-diabetic remedies in Oriental medicine and many studies have shown the effects of silk fibroin (SF) in both in vitro and in vivo models. In our previous works, we reported that hydrolyzed SF improved the survival of HIT-T15 cells under high glucose conditions and ameliorated diabetic dyslipidemia in a mouse model. However, we could not provide a precise molecular mechanism. To further evaluate the functions of hydrolyzed SF on the pancreatic β-cell, we investigated the effects of hydrolyzed SF on the pancreatic β-cell proliferation and regeneration in the mouse model. Hydrolyzed SF induced the expression of the proliferating cell nuclear antigen (PCNA) and reduced the apoptotic cell population in the pancreatic islets. Hydrolyzed SF treatment not only induced the expression of transcription factors involved in the pancreatic β-cell regeneration in RT-PCR results but also increased neurogenin3 and Neuro D protein levels in the pancreas of those in the group treated with hydrolyzed SF. In line with this, hydrolyzed SF treatment generated insulin mRNA expressing small cell colonies in the pancreas. Therefore, our results suggest that the administration of hydrolyzed SF increases the pancreatic β-cell proliferation and regeneration in C57BL/KsJ-Leprdb/db mice.

scholarly journals MicroRNAs 106b and 222 Improve Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes via Pancreatic β-Cell Proliferation

EBioMedicine ◽  
2017 ◽  
Vol 15 ◽  
pp. 163-172 ◽  
Author(s):  
Sohei Tsukita ◽  
Tetsuya Yamada ◽  
Kei Takahashi ◽  
Yuichiro Munakata ◽  
Shinichiro Hosaka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Obesity-Induced miR-455 Upregulation Promotes Adaptive Pancreatic β-cell Proliferation Through the CPEB1/CDKN1B Pathway

2022 ◽  
Author(s):  
Ada Admin ◽  
Qianxing Hu ◽  
Jinming Mu ◽  
Yuhong Liu ◽  
Yue Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Expansion ◽  
Binding Protein ◽  
Pancreatic Β Cell ◽  
Loss Of Function ◽  
Metabolic Demand ◽  
Β Cell ◽  
Element Binding Protein ◽  
Mirna Pathway

Pancreatic β-cell adapt to compensate for increased metabolic demand during obesity. Although the microRNA (miRNA) pathway has an essential role in β-cell expansion, whether it is involved in adaptive proliferation is largely unknown. First, we report that EGR2 binding to the miR-455 promoter induced miR-455 upregulation in the pancreatic islets of obesity mouse models. Then, in vitro gain- or loss-of-function studies showed that miR-455 overexpression facilitated β-cell proliferation. Knockdown of miR-455 in ob/ob mice via pancreatic intraductal infusion prevented compensatory β-cell expansion. Mechanistically, our results revealed that increased miR-455 expression inhibits the expression of its target cytoplasmic polyadenylation element binding protein 1 (CPEB1), an mRNA binding protein that plays an important role in regulating insulin resistance and cell proliferation. Decreased CPEB1 expression inhibits elongation of the poly-A tail and the subsequent translation of Cdkn1b mRNA, reducing the CDKN1B expression level and finally promoting β-cell proliferation. Taken together, our results show that the miR-455/CPEB1/CDKN1B pathway contributes to adaptive proliferation of β-cells to meet metabolic demand during obesity.

scholarly journals Generation and Characterization of a Novel Mouse Model That Allows Spatiotemporal Quantification of Pancreatic β-Cell Proliferation

Diabetes ◽  
2020 ◽  
Vol 69 (11) ◽  
pp. 2340-2351 ◽  
Author(s):  
Shinsuke Tokumoto ◽  
Daisuke Yabe ◽  
Hisato Tatsuoka ◽  
Ryota Usui ◽  
Muhammad Fauzi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Administration of mulberry leaves maintains pancreatic β-cell mass in obese/type 2 diabetes mellitus mouse model

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Patlada Suthamwong ◽  
Manabu Minami ◽  
Toshiaki Okada ◽  
Nonomi Shiwaku ◽  
Mai Uesugi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mouse Model ◽  
Cell Mass ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Mulberry Leaves

scholarly journals Glucose homeostasis changes and pancreatic β-cell proliferation after switching to cyclosporin in tacrolimus-induced diabetes mellitus

2015 ◽  
Vol 35 (3) ◽  
pp. 264-272
Author(s):  
Ana Elena Rodríguez-Rodríguez ◽  
Javier Triñanes ◽  
Esteban Porrini ◽  
Silvia Velázquez-García ◽  
Cecilia Fumero ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cell Proliferation ◽  
Glucose Homeostasis ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Intermittent Hypoxia Exacerbates Pancreatic β-Cell Dysfunction in A Mouse Model of Diabetes Mellitus

SLEEP ◽  
2013 ◽  
Vol 36 (12) ◽  
pp. 1849-1858 ◽  
Author(s):  
Shariq I. Sherwani ◽  
Carolyn Aldana ◽  
Saif Usmani ◽  
Christopher Adin ◽  
Sainath Kotha ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Mouse Model ◽  
Intermittent Hypoxia ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

scholarly journals Obesity-Induced miR-455 Upregulation Promotes Adaptive Pancreatic β-cell Proliferation Through the CPEB1/CDKN1B Pathway

Diabetes ◽  
2022 ◽  
Author(s):  
Qianxing Hu ◽  
Jinming Mu ◽  
Yuhong Liu ◽  
Yue Yang ◽  
Yue Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Expansion ◽  
Binding Protein ◽  
Pancreatic Β Cell ◽  
Loss Of Function ◽  
Metabolic Demand ◽  
Β Cell ◽  
Element Binding Protein ◽  
Mirna Pathway

Pancreatic β-cell adapt to compensate for increased metabolic demand during obesity. Although the microRNA (miRNA) pathway has an essential role in β-cell expansion, whether it is involved in adaptive proliferation is largely unknown. First, we report that EGR2 binding to the miR-455 promoter induced miR-455 upregulation in the pancreatic islets of obesity mouse models. Then, in vitro gain- or loss-of-function studies showed that miR-455 overexpression facilitated β-cell proliferation. Knockdown of miR-455 in ob/ob mice via pancreatic intraductal infusion prevented compensatory β-cell expansion. Mechanistically, our results revealed that increased miR-455 expression inhibits the expression of its target cytoplasmic polyadenylation element binding protein 1 (CPEB1), an mRNA binding protein that plays an important role in regulating insulin resistance and cell proliferation. Decreased CPEB1 expression inhibits elongation of the poly-A tail and the subsequent translation of Cdkn1b mRNA, reducing the CDKN1B expression level and finally promoting β-cell proliferation. Taken together, our results show that the miR-455/CPEB1/CDKN1B pathway contributes to adaptive proliferation of β-cells to meet metabolic demand during obesity.

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