Tissue-specific and glucose-responsive expression of the pancreatic derived factor (PANDER) promoter

Burkhardt, Brant R.; Yang, Michael; Robert, Claudia E.; Greene, Scott R.; McFadden, Kile; Yang, Jichun; Wu, Jianmei; Gao, Zhiyong; Wolf, Bryan A.

doi:10.1016/j.bbaexp.2005.07.003

Cited by 34 publications

(70 citation statements)

References 37 publications

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“…Treatment with IFN-␥ or a combination of IL-1␤, TNF-␣, and IFN-␥ upregulates PANDER gene expression in mouse islets and in insulin secreting ␤-cell lines in a time-and dose-dependent manner (14), revealing that PANDER may function as a downstream signal in cytokine-mediated ␤-cell dysfunction and death. The PANDER promoter contains glucose-responsive elements and has a robust glucose response in pancreatic ␤-cell lines and in primary islet cells (45). This is similar to the insulin promoter (15), implying a potential role of PANDER in glucose homeostasis.…”

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confidence: 57%

Mechanisms of Glucose-Induced Secretion of Pancreatic-Derived Factor (PANDER or FAM3B) in Pancreatic β-Cells

et al. 2005

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Pancreatic-derived factor (PANDER) is an islet-specific cytokine present in both pancreatic ␣-and ␤-cells, which, in vitro, induces ␤-cell apoptosis of primary islet and cell lines. In this study, we investigated whether PANDER is secreted by pancreatic ␣-and ␤-cells and whether PANDER secretion is regulated by glucose and other insulin secretagogues. In mouse-derived insulin-secreting ␤-TC3 cells, PANDER secretion in the presence of stimulatory concentrations of glucose was 2.8 ؎ 0.4-fold higher (P < 0.05) than without glucose. Insulin secretion was similarly increased by glucose in the same cells. The total concentration of secreted PANDER in the medium was ϳ6 -10 ng/ml [IFN]-␥) play vital roles in ␤-cell dysfunction and death and in the development of type 1 diabetes (2-6). Recently, it was shown that glucose causes islet ␤-cells to produce IL-1␤, while the released IL-1␤ has a deleterious effect on human pancreatic islets (7,8). These studies suggest that production and release of cytokines from pancreatic islet cells are involved in ␤-cell dysfunction and death in hyperglycemia. To date, although several cytokines have been shown to be involved in ␤-cell dysfunction and death, the precise mechanisms of type 1 diabetes are still incompletely understood, suggesting that other potential factors may be involved.Pancreatic-derived factor (PANDER), also known as FAM3B (9,10), is one of four members of a new cytokine family recently identified using the algorithm ostensible recognition of folds (11) while searching for novel cytokines based on their predicted secondary structure. The rationale for this approach is that the secondary structure of cytokines is highly conserved through evolution. Many cytokines, such as IL

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confidence: 57%

Mechanisms of Glucose-Induced Secretion of Pancreatic-Derived Factor (PANDER or FAM3B) in Pancreatic β-Cells

et al. 2005

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“…Glucose-induced β-cell production of IL-1β induces glucotoxicity in human islets, and perhaps PANDER is induced in a similar pathway. Particularly since we have demonstrated that glucose can upregulate PANDER protein secretion and stimulate the PANDER promoter in both primary islets and β-cell lines (Yang et al, 2005;Burkhardt et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

PANDER-induced cell-death genetic networks in islets reveal central role for caspase-3 and cyclin-dependent kinase inhibitor 1A (p21)

Burkhardt

Greene

White

et al. 2006

Gene

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“…FAM3B can be sensitively regulated by glucose. Upon glucose stimulation, the secretion of cleaved FAM3B and production of full-length FAM3B are increased in both insulinoma cells and primary islets 19,20 ; the promoter activity and mRNA expression levels of FAM3B are up-regulated 21 . Glucose induces FAM3B gene expression via multiple signaling pathways that include Ca 2+ protein kinase A (PKA), Ca 2+ protein kinase C (PKC), ERK1/2, and cAMP-responsive element-binding protein (CREB) mechanisms.…”

Section: Introductionmentioning

confidence: 99%

FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p

Zhang

Chen

Zhang

et al. 2017

Sci Rep

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The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative factor. On the other hand, FAM3B (named PANDER for its secretory form) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. FAM3B is co-secreted with insulin from the β-cell upon glucose stimulation and regulates glucose homeostasis. In the present study, we sought to determine the roles of FAM3B in the regulation of VSMC physiology, especially under the hyperglycemic condition. We found that FAM3B expression was induced by hyperglycemia both in vivo and in vitro. FAM3B knockdown inhibited, whereas FAM3B overexpression accelerated VSMC proliferation and migration. At the molecular level, FAM3B inhibited miR-322-5p expression, and enforced expression of miR-322-5p antagonized FAM3B-induced VSMC proliferation and migration, suggesting that FAM3B facilitated VSMC pathological activation via miR-322-5p. Taken together, FAM3B mediates high glucose-induced VSMC proliferation and migration via inhibition of miR-322-5p. Thus, FAM3B may therefore serve as a novel therapeutic target for diabetes-related CVDs.

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Tissue-specific and glucose-responsive expression of the pancreatic derived factor (PANDER) promoter

Cited by 34 publications

References 37 publications

Mechanisms of Glucose-Induced Secretion of Pancreatic-Derived Factor (PANDER or FAM3B) in Pancreatic β-Cells

Mechanisms of Glucose-Induced Secretion of Pancreatic-Derived Factor (PANDER or FAM3B) in Pancreatic β-Cells

PANDER-induced cell-death genetic networks in islets reveal central role for caspase-3 and cyclin-dependent kinase inhibitor 1A (p21)

FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p

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