High Levels of Endogenous Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Expression Correlate With Increased Cell Death in Human Pancreas

Şanlioğlu, Ahter Dilşad; Dirice, Ercument; Elpek, Özlem; Korcum, Aylin Fidan; Balcı, Mustafa Kemal; Omer, Abdulkadir; Griffith, Thomas S.; Şanlıoğlu, Salih

doi:10.1097/mpa.0b013e318158a4e5

Cited by 29 publications

(21 citation statements)

References 30 publications

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“…This may be due to the ratio of TRAIL death to decoy receptors on these cells. In fact, high levels of expression of decoy receptors have recently been demonstrated in human islets [54]. These results suggest that contrary to what was observed with FasL or TNF-a, TRAIL gene delivery into pancreatic islets may be therapeutically beneficial.…”

Section: Treatment Of Diabetescontrasting

confidence: 51%

Diabetes mellitus and apoptosis: inflammatory cells

et al. 2009

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Since the early observation that similarities between thyroiditis and insulitis existed, the important role played by inflammation in the development of diabetes has been appreciated. More recently, experiments have shown that inflammation also plays a prominent role in the development of target organ damage arising as complications, with both elements of the innate and the adaptive immune system being involved, and that cytokines contributing to local tissue damage may arise from both infiltrating and resident cells. This review will discuss the experimental evidence that shows that inflammatory cellmediated apoptosis contributes to target organ damage, from beta cell destruction to both micro-and macro-vascular disease complications, and also how alterations in leukocyte turnover affects immune function.

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Section: Treatment Of Diabetescontrasting

confidence: 51%

Diabetes mellitus and apoptosis: inflammatory cells

et al. 2009

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“…Natural immune cells and Th1 cytokines (Sanlioglu et al 2008b) play key roles in the generation of inflammation causing pancreatic tissue damage during the early phase of T1D (Sanlioglu et al 2008a). As VIP can skew the proinflammatory cytokine profile to an anti-inflammatory response, the extent to which VIP has any therapeutic effect on autoimmune model of diabetes has been tested.…”

Section: Vip-mediated Gene Transfer Studiesmentioning

confidence: 99%

Therapeutic potential of VIP vs PACAP in diabetes

Şanlioğlu

Karaçay²,

Balcı³

et al. 2012

Journal of Molecular Endocrinology

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Type 2 diabetes (T2D) is characterized by chronic insulin resistance and a progressive decline in beta-cell function. Although rigorous glucose control can reduce morbidity and mortality associated with diabetes, achieving optimal longterm glycemic control remains to be accomplished in many diabetic patients. As beta-cell mass and function inevitably decline in T2D, exogenous insulin administration is almost unavoidable as a final outcome despite the use of oral antihyperglycemic agents in many diabetic patients. Pancreatic islet cell death, but not the defect in new islet formation or beta-cell replication, has been blamed for the decrease in beta-cell mass observed in T2D patients. Thus, therapeutic approaches designed to protect islet cells from apoptosis could significantly improve the management of T2D, because of its potential to reverse diabetes not just ameliorate glycemia. Therefore, an ideal beta-cell-preserving agent is expected to protect beta cells from apoptosis and stimulate postprandial insulin secretion along with increasing beta-cell replication and/or islet neogenesis. One such potential agent, the islet endocrine neuropeptide vasoactive intestinal peptide (VIP) strongly stimulates postprandial insulin secretion. Because of its broad spectrum of biological functions such as acting as a potent anti-inflammatory factor through suppression of Th1 immune response, and induction of immune tolerance via regulatory T cells, VIP has emerged as a promising therapeutic agent for the treatment of many autoimmune diseases including diabetes.

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“…30 One of the potential markers useful for the follow-up of PDAC patients may be TRAIL. 31 However, it is unclear how the TRAIL/TRAIL receptor system contributes to carcinogenesis. Benign and malignant prostate cancer cells differentially display TRAIL and its receptors, and this profile was connected to prostate carcinogenesis.…”

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confidence: 99%