In summary, the present study suggests that Panobinostat Traf2 down-regulates BMP signaling pathway, and that the accumulation of Smad1 under TNF-α stimulation in the nucleus is associated with Traf2, therefore, there is cross-talk between the TNF-α and BMP signaling pathways. However, the role of the interaction between Smad4 and Traf2 is unknown. Smad4 protein may serve as a scaffold protein able to react immediately to various stimuli such as TNF-α.
Acknowledgments
This work was supported by the Sato Fund and the Uemura Fund, Nihon University School of Dentistry, Tokyo, Japan.
Keywords
Apoptosis; Beta-cell; Exendin-4; GLP-1; Proliferation; Diabetes
Introduction
The pancreatic beta-cell mass and the capacity of beta-cells to secrete insulin are controlled under physiological conditions to the metabolic demand of the body. Failure of the pancreas to provide appropriate insulin secreting capacity due to decreased beta-cell mass and function is one of the underlying mechanisms of the onset and deterioration of type 2 diabetes [1] and [2]. Thus, finding means to preserve beta-cell mass and function may be useful for the treatment of diabetes. In this regard, agonists of glucagon-like peptide-1 receptor (GLP-1R) are promising anti-diabetic agents, since activation of GLP-1R has been reported to preserve beta-cell mass by stimulating beta-cell proliferation, inhibiting beta-cell apoptosis in addition to enhancing glucose-induced insulin secretion [3], [4] and [5].
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We investigated OSCC cell lines from tissues with
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