MCPIP1 is a novel link between diabetogenic conditions and impaired insulin secretory capacity

Tyka, Karolina; Jörns, Anne; Dunst, Alessia; Tang, Yadi; Bryde, Tenna Holgersen; Mehmeti, Ilir; Walentinsson, Anna; Marselli, Lorella; Cnop, Miriam; Tyrberg, Björn; Marzec, Michał; Gurgul-Convey, Ewa

doi:10.1016/j.bbadis.2021.166199

Cited by 4 publications

(4 citation statements)

References 46 publications

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“…Therefore, new therapeutic biomarkers must be identified. previous studies have reported that MCPIP1 serves important biological roles in lipid homeostasis (30), insulin secretion (31) and the inflammatory response (32), and also regulates the development of certain diseases, such as hidradenitis suppurativa (33), primary biliary cholangitis (34), skin inflammation (35) and clear cell renal cell carcinoma (36). Previous studies have reported that neuroinflammation is a risk factor for depression (42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

MCPIP1 alleviates depressive‑like behaviors in mice by inhibiting the TLR4/TRAF6/NF‑κB pathway to suppress neuroinflammation

An,

Xia,

et al. 2023

Mol Med Rep

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lipopolysaccharide-induced (lPS) neuroinflammation serves an important role in the development of depression. Monocyte chemotactic protein-1-induced protein 1 (McPiP1, also known as Zc3H12a and regnase-1) possesses endoribonuclease and deubiquitinase activities. in the present study, the effects of McPiP1 on lPS-induced depression were assessed. a mouse model of hippocampal neuroinflammation was established by intraperitoneal injection of lPS. Microglia were treated with lPS, McPiP1 overexpression vector, McPiP1 knockdown vector or Tlr4 inhibitor. McPiP1 alleviated lPS-induced depressive-like behaviors. McPiP1 facilitated M2 polarization of microglia. MCPIP1 attenuated the inflammatory response in microglia via inhibition of the Tlr4/TnF receptor associated factor 6 (TraF6)/nF-κB signaling pathway. The results indicated that McPiP1 accelerated M2-polarization of microglia and alleviated depressive-like behaviors of mice via the inhibition of the Tlr4/TraF6/nF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

MCPIP1 alleviates depressive‑like behaviors in mice by inhibiting the TLR4/TRAF6/NF‑κB pathway to suppress neuroinflammation

An,

Xia,

et al. 2023

Mol Med Rep

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“…The major proinflammatory cytokines involved in beta-cell failure during T1DM development are IL-1β, TNFα and IFNγ [1,4,32,36], which stimulate pleiotropic effects by receptor-mediated mechanisms [37][38][39][40][41][42]. Multiple molecular mechanisms have been associated with beta-cell death in T1DM including mitochondrial and endoplasmic reticulum (ER) stress responses, ROS generation and induction of NO production (only in rodent beta-cells), impaired calcium homeostasis and disturbed autophagy [30,32,40,41,[43][44][45][46][47][48][49][50][51][52][53][54][55][56]. IL-1β and TNFα stimulate ROS production particularly in mitochondria, which are in beta-cells characterized by a very low detoxification capacity of hydrogen peroxide toxicity [46,52,53,57].…”

Section: Overview Of Mechanisms Of Beta-cell Destruction In T1dmmentioning

confidence: 99%

“…Overexpression of hydrogen-peroxide detoxifying enzyme catalase has been shown to protect beta-cells against cytokine toxicity [46,52] with no detrimental effects on glucose-stimulated insulin secretion (GSIS) [58]. Proinflammatory cytokines also affect the expression of genes involved in inflammatory pathways and induce proinflammatory signaling [2,4,35,38,43,56,[59][60][61][62][63][64][65][66][67][68][69][70]. Finally, cytokines dysregulate insulin biosynthesis and glucose-stimulated insulin secretion (GSIS) [30,49,[54][55][56]71,72].…”

Section: Overview Of Mechanisms Of Beta-cell Destruction In T1dmmentioning

confidence: 99%

“…Proinflammatory cytokines also affect the expression of genes involved in inflammatory pathways and induce proinflammatory signaling [2,4,35,38,43,56,[59][60][61][62][63][64][65][66][67][68][69][70]. Finally, cytokines dysregulate insulin biosynthesis and glucose-stimulated insulin secretion (GSIS) [30,49,[54][55][56]71,72].…”

Section: Overview Of Mechanisms Of Beta-cell Destruction In T1dmmentioning

confidence: 99%

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To Be or Not to Be: The Divergent Action and Metabolism of Sphingosine-1 Phosphate in Pancreatic Beta-Cells in Response to Cytokines and Fatty Acids

Gurgul-Convey

2022

IJMS

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Sphingosine-1 phosphate (S1P) is a bioactive sphingolipid with multiple functions conveyed by the activation of cell surface receptors and/or intracellular mediators. A growing body of evidence indicates its important role in pancreatic insulin-secreting beta-cells that are necessary for maintenance of glucose homeostasis. The dysfunction and/or death of beta-cells lead to diabetes development. Diabetes is a serious public health burden with incidence growing rapidly in recent decades. The two major types of diabetes are the autoimmune-mediated type 1 diabetes (T1DM) and the metabolic stress-related type 2 diabetes (T2DM). Despite many differences in the development, both types of diabetes are characterized by chronic hyperglycemia and inflammation. The inflammatory component of diabetes remains under-characterized. Recent years have brought new insights into the possible mechanism involved in the increased inflammatory response, suggesting that environmental factors such as a westernized diet may participate in this process. Dietary lipids, particularly palmitate, are substrates for the biosynthesis of bioactive sphingolipids. Disturbed serum sphingolipid profiles were observed in both T1DM and T2DM patients. Many polymorphisms were identified in genes encoding enzymes of the sphingolipid pathway, including sphingosine kinase 2 (SK2), the S1P generating enzyme which is highly expressed in beta-cells. Proinflammatory cytokines and free fatty acids have been shown to modulate the expression and activity of S1P-generating and S1P-catabolizing enzymes. In this review, the similarities and differences in the action of extracellular and intracellular S1P in beta-cells exposed to cytokines or free fatty acids will be identified and the outlook for future research will be discussed.

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Investigation of the shared gene signatures and molecular mechanisms between obstructive sleep apnea syndrome and asthma

Que,

Meng,

Ding

et al. 2024

Gene

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MCPIP1 is a novel link between diabetogenic conditions and impaired insulin secretory capacity

Cited by 4 publications

References 46 publications

MCPIP1 alleviates depressive‑like behaviors in mice by inhibiting the TLR4/TRAF6/NF‑κB pathway to suppress neuroinflammation

MCPIP1 alleviates depressive‑like behaviors in mice by inhibiting the TLR4/TRAF6/NF‑κB pathway to suppress neuroinflammation

To Be or Not to Be: The Divergent Action and Metabolism of Sphingosine-1 Phosphate in Pancreatic Beta-Cells in Response to Cytokines and Fatty Acids

Investigation of the shared gene signatures and molecular mechanisms between obstructive sleep apnea syndrome and asthma

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