Pancreatic Pericytes Support β-Cell Function in a Tcf7l2-Dependent Manner
نویسندگان
چکیده
منابع مشابه
Neonatal pancreatic pericytes support β-cell proliferation
OBJECTIVE The maintenance and expansion of β-cell mass rely on their proliferation, which reaches its peak in the neonatal stage. β-cell proliferation was found to rely on cells of the islet microenvironment. We hypothesized that pericytes, which are components of the islet vasculature, support neonatal β-cell proliferation. METHODS To test our hypothesis, we combined in vivo and in vitro app...
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متن کاملTruncated forms of RUNX3 unlike full length protein alter cell proliferation in a TGF-β context dependent manner
The Runt related transcription factors (RUNX) are recognized as key players in suppressing or promoting tumor growth. RUNX3, a member of this family, is known as a tumor suppressor in many types of cancers, although such a paradigm was challenged by some researchers. The TGF-β pathway governs major upstream signals to activate RUNX3. RUNX3 protein consists of several regions and domains. The Ru...
متن کاملSelective disruption of Tcf7l2 in the pancreatic β cell impairs secretory function and lowers β cell mass
Type 2 diabetes (T2D) is characterized by β cell dysfunction and loss. Single nucleotide polymorphisms in the T-cell factor 7-like 2 (TCF7L2) gene, associated with T2D by genome-wide association studies, lead to impaired β cell function. While deletion of the homologous murine Tcf7l2 gene throughout the developing pancreas leads to impaired glucose tolerance, deletion in the β cell in adult mic...
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Objective: Pancreatic b-cell dysfunction is described to be present at the diagnosis of type 2 diabetes mellitus (T2DM) and progressively deteriorated with disease duration. However, its progression is variable and potentially influenced by several factors. The Magnesium (Mg) deficiency mediates insulin resistance but reports regarding its role in pancreatic β-cell dysfunction are scarce and co...
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ژورنال
عنوان ژورنال: Diabetes
سال: 2017
ISSN: 0012-1797,1939-327X
DOI: 10.2337/db17-0697