1,25(OH)2-vitamin D3 induces translocation of the vitamin D receptor (VDR) to the plasma membrane in skeletal muscle cells

2002 ◽  
Vol 86 (1) ◽  
pp. 128-135 ◽  
Author(s):  
Daniela Capiati ◽  
Silvia Benassati ◽  
Ricardo L. Boland
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Plasma Membrane ◽  
Vitamin D Receptor ◽  
Vitamin D3 ◽  
Muscle Cells ◽  
Skeletal Muscle Cells

scholarly journals Vitamin D Receptor Agonists: Suitable Candidates as Novel Therapeutic Options in Autoimmune Inflammatory Myopathy

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Clara Crescioli
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Inflammatory Myopathy ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Mediators Of Inflammation

The primary aim in the treatment of autoimmune inflammatory myopathies (IMs) is to recover muscle function. The presence of immune/inflammatory cell infiltrates within muscle tissues represents the common feature of different IM subtypes, albeit a correlation between muscular damage extent and inflammation degree is often lacking. Treatments for IMs are based on life-long immunosuppressive therapy, with the well known adverse effects; recovery is incomplete for many patients. More effective therapies, with reduced side-effects, are highly desirable. Vitamin D receptor (VDR) agonists emerge to retain pleiotropic anti-inflammatory properties, since they regulate innate and adaptive immunity by switching the immune response from proinflammatory T helper 1 (Th1) type to tolerogenic T helper 2 (Th2) type dominance. In skeletal muscle cells less hypercalcemic VDR ligands target powerful mediators of inflammation, such as TNFαand TNFαdriven paths, without affecting immune or muscle cells viability, retaining the potentiality to counteract Th1 driven overreactivity established by the self-enhancing inflammatory loop between immune and skeletal muscle cells. This review summarizes those features of VDR agonists as candidates in future treatment of IM.

scholarly journals The exocyst complex regulates insulin-stimulated glucose uptake of skeletal muscle cells

2019 ◽  
Vol 317 (6) ◽  
pp. E957-E972
Author(s):  
Brent A. Fujimoto ◽  
Madison Young ◽  
Lamar Carter ◽  
Alina P. S. Pang ◽  
Michael J. Corley ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Cell Surface ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Cell Surface Receptor ◽  
Exocyst Complex

Skeletal muscle handles ~80–90% of the insulin-induced glucose uptake. In skeletal muscle, insulin binding to its cell surface receptor triggers redistribution of intracellular glucose transporter GLUT4 protein to the cell surface, enabling facilitated glucose uptake. In adipocytes, the eight-protein exocyst complex is an indispensable constituent in insulin-induced glucose uptake, as it is responsible for the targeted trafficking and plasma membrane-delivery of GLUT4. However, the role of the exocyst in skeletal muscle glucose uptake has never been investigated. Here we demonstrate that the exocyst is a necessary factor in insulin-induced glucose uptake in skeletal muscle cells as well. The exocyst complex colocalizes with GLUT4 storage vesicles in L6-GLUT4myc myoblasts at a basal state and associates with these vesicles during their translocation to the plasma membrane after insulin signaling. Moreover, we show that the exocyst inhibitor endosidin-2 and a heterozygous knockout of Exoc5 in skeletal myoblast cells both lead to impaired GLUT4 trafficking to the plasma membrane and hinder glucose uptake in response to an insulin stimulus. Our research is the first to establish that the exocyst complex regulates insulin-induced GLUT4 exocytosis and glucose metabolism in muscle cells. A deeper knowledge of the role of the exocyst complex in skeletal muscle tissue may help our understanding of insulin resistance in type 2 diabetes.

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