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Pflügers Archiv: European Journal of Physiology

Jin Han, Darrell Neufer, Henriette Pilegaard
No abstract text is available yet for this article.
February 19, 2019: Pflügers Archiv: European Journal of Physiology
James A Spudich
Several lines of evidence suggest that the primary effect of hypertrophic cardiomyopathy mutations in human β-cardiac myosin is hypercontractility of the heart, which leads to subsequent hypertrophy, fibrosis, and myofilament disarray. Here, I describe three perspectives on the molecular basis of this hypercontractility. The first is that hypercontractility results from changes in the fundamental parameters of the actin-activated β-cardiac myosin chemo-mechanical ATPase cycle. The second considers that hypercontractility results from an increase in the number of functionally accessible heads in the sarcomere for interaction with actin...
February 15, 2019: Pflügers Archiv: European Journal of Physiology
Israa Mohammad Al-Amily, Pontus Dunér, Leif Groop, Albert Salehi
We have recently shown that the G protein-coupled receptor 142 (GPR142) is expressed in both rodent and human pancreatic β-cells. Herein, we investigated the cellular distribution of GPR142 within islets and the effects of selective agonists of GPR142 on glucose-stimulated insulin secretion (GSIS) in the mouse islets and INS-1832/13 cells. Double-immunostaining revealed that GPR142 immunoreactivity in islets mainly occurs in insulin-positive cells. Potentiation of GSIS by GPR142 activation was accompanied by increased cAMP content in INS-1832/13 cells...
February 15, 2019: Pflügers Archiv: European Journal of Physiology
Theresia Kraft, Judith Montag
Hypertrophic cardiomyopathy (HCM) is mainly caused by mutations in sarcomeric proteins. Thirty to forty percent of identified mutations are found in the ventricular myosin heavy chain (β-MyHC). A common mechanism explaining how numerous mutations in several different proteins induce a similar HCM-phenotype is unclear. It was proposed that HCM-mutations cause hypercontractility, which for some mutations is thought to result from mutation-induced unlocking of myosin heads from a so-called super-relaxed state (SRX)...
February 11, 2019: Pflügers Archiv: European Journal of Physiology
Manuel Meurer, Klaus Höcherl
Magnesium (Mg2+ ) abnormalities during sepsis have been reported, but the underlying mechanisms during acute inflammation are poorly understood. We hypothesized that a decrease in GFR and/or changes in transporters or channels for Mg2+ could be responsible for the observed Mg2+ abnormalities. Therefore, we studied the metabolism of Mg2+ in a murine model of endotoxemia. LPS-induced hypermagnesemia was paralleled by a decrease in creatinine clearance and an increase in the fractional excretion of Mg2+ . In agreement with an altered renal Mg2+ handling, endotoxemia decreased the renal expression of claudin (Cldn) 10b, Cldn16, Cldn19, parvalbumin, and of the solute carrier family (Slc) 41a3...
February 6, 2019: Pflügers Archiv: European Journal of Physiology
Tomohiro Tanaka, Akiyuki Nishimura, Kazuhiro Nishiyama, Takumi Goto, Takuro Numaga-Tomita, Motohiro Nishida
A growing body of evidence suggests that exercise shows pleiotropic effects on the maintenance of systemic homeostasis through mitochondria. Dysregulation of mitochondrial dynamism is associated with metabolic inflexibility, resulting in many of the metabolic diseases and aging. Studies have suggested that exercise prevents and delays the progression of mitochondrial dysfunction by improving mitochondrial metabolism, biogenesis, and quality control. Exercise modulates functions of mitochondrial dynamics-regulating proteins through post-translational modification mechanisms...
February 1, 2019: Pflügers Archiv: European Journal of Physiology
Sunil Yadav, Yoel H Sitbon, Katarzyna Kazmierczak, Danuta Szczesna-Cordary
Genetic cardiomyopathies, a group of cardiovascular disorders based on ventricular morphology and function, are among the leading causes of morbidity and mortality worldwide. Such genetically driven forms of hypertrophic (HCM), dilated (DCM), and restrictive (RCM) cardiomyopathies are chronic, debilitating diseases that result from biomechanical defects in cardiac muscle contraction and frequently progress to heart failure (HF). Locus and allelic heterogeneity, as well as clinical variability combined with genetic and phenotypic overlap between different cardiomyopathies, have challenged proper clinical prognosis and provided an incentive for identification of pathogenic variants...
January 31, 2019: Pflügers Archiv: European Journal of Physiology
Nadeshda Schelski, Trang T D Luong, Florian Lang, Burkert Pieske, Jakob Voelkl, Ioana Alesutan
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is a key regulator of osteo-/chondrogenic transdifferentiation and subsequent calcification of vascular smooth muscle cells (VSMCs). The phenotypical transdifferentiation of VSMCs is associated with increased interleukin-18 (IL-18) levels and generalized inflammation. Therefore, the present study investigated the possible involvement of SGK1 in IL-18-induced vascular calcification. Experiments were performed in primary human aortic smooth muscle cells (HAoSMCs) treated with recombinant human IL-18 protein in control or high phosphate conditions and following SGK1 knockdown by siRNA or pharmacological inhibition of SGK1, PI3K, and PDK1...
January 31, 2019: Pflügers Archiv: European Journal of Physiology
Manuel Meurer, Klaus Höcherl
Fibroblast growth factor 23 (FGF23) levels are elevated in patients with acute kidney injury (AKI). The consequences on renal Ca2+ , Mg2+ , and Pi regulatory mechanisms are unknown. We hypothesized that renal ischemia-reperfusion (I/R) injury alters the expression of important renal Ca2+ , Mg2+ , and Pi transport proteins. I/R injury was induced in male C57BL/6 mice by clamping both renal arteries for 27 min. Mice were investigated 18 h later. The mRNA and protein levels of renal Ca2+ , Mg2+ , and Pi transport proteins were measured by RT-qPCR and western blot analysis...
January 26, 2019: Pflügers Archiv: European Journal of Physiology
Nayoung Ahn, Hye Soon Kim, Kijin Kim
This study analyzed the differences in effects of a 12-week combination of exercise training program with resistance training and aerobic exercises on the risk factors of metabolic syndrome, carotid wall thickness, and thyroid function, between subclinical hypothyroidism patients and obese groups, in middle-aged women. Subjects consisted of either 20 middle-aged women in the subclinical hypothyroidism (SCH) group or 20 obese (body mass indices [BMI], ≥ 25 kg/m2 ) women without hypothyroidism in the obese (OB) group...
January 18, 2019: Pflügers Archiv: European Journal of Physiology
Keiichiro Uchida, Masatoshi Nomura, Tadashi Yamamoto, Yoshihiro Ogawa, Noriyoshi Teramoto
Although ATP-sensitive K+ (KATP ) channels play an important role in the secretion of insulin by pancreatic beta cells, the mechanisms that regulate the intracellular transport of KATP channel subunit proteins (i.e., Kir6.2 and sulfonylurea receptor 1 (SUR1)) to the plasma membrane remain uncharacterized. We investigated the possibility that an interaction between KATP channel subunit proteins and Rab8a protein, a member of the RAS superfamily, may be involved in the membrane trafficking of KATP channels. Co-immunoprecipitation and immunostaining experiments using co-expression systems with fluorescent protein-tagged Kir6...
January 10, 2019: Pflügers Archiv: European Journal of Physiology
Sujin Kim, Ji-Young Choi, Sohee Moon, Dong-Ho Park, Hyo-Bum Kwak, Ju-Hee Kang
Exercise is a well-known non-pharmacological intervention to improve brain functions, including cognition, memory, and motor coordination. Contraction of skeletal muscles during exercise releases humoral factors that regulate the whole-body metabolism via interaction with other non-muscle organs. Myokines are muscle-derived effectors that regulate body metabolism by autocrine, paracrine, or endocrine action and were reportedly suggested as "exercise factors" that can improve the brain function. However, several aspects remain to be elucidated, namely the specific activities of myokines related to the whole-body metabolism or brain function, the mechanisms of regulation of other organs or cells, the sources of "exercise factors" that regulate brain function, and their mechanisms of interaction with non-muscle organs...
January 9, 2019: Pflügers Archiv: European Journal of Physiology
Ana C Najenson, Mariana Bianchi, Ana P Courreges, Myrian R Rodriguez, Víctor H Casco, Marcelo S Vatta, Liliana G Bianciotti
Previous studies have shown that atrial natriuretic peptide (ANP) regulates exocrine pancreatic function in health and disease. As extracardiac sources of ANP have been identified and ANP-like immunoreactivity has been reported in the exocrine pancreas, in the present work we sought to establish whether ANP was produced in the rat exocrine pancreas and if conditions like fasting/feeding or acute pancreatitis were reflected on ANP expression. By using RT-PCR, immunoblotting, and immunofluorescence microscopy assays, it was found that both mRNA and protein ANP were present in the acinar cells of the exocrine pancreas...
January 8, 2019: Pflügers Archiv: European Journal of Physiology
Su-Kyung Shin, Hyun-Woo Cho, Seung-Eun Song, Jae-Hoon Bae, Seung-Soon Im, Inha Hwang, Hunjoo Ha, Dae-Kyu Song
Hydrogen peroxide (H2 O2 ) produced endogenously can cause mitochondrial dysfunction and metabolic complications in various cell types by inducing oxidative stress. In the liver, oxidative and endoplasmic reticulum (ER) stress affects the development of non-alcoholic fatty liver disease (NAFLD). Although a link between both stresses and fatty liver diseases has been suggested, few studies have investigated the involvement of catalase in fatty liver pathogenesis. We examined whether catalase is associated with NAFLD, using catalase knockout (CKO) mice and the catalase-deficient human hepatoma cell line HepG2...
January 7, 2019: Pflügers Archiv: European Journal of Physiology
Moshe Levi, Enrico Gratton
The cloning of the renal NaPi-2a (SLC34A1) and NaPi-2c (SLC34A3) phosphate transporters has made it possible to characterize the molecular and biophysical regulation of renal proximal tubular reabsorption of inorganic phosphate (Pi). Dietary factors, such as Pi and K, and several hormones and phosphatonins, including parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and glucocorticoids, regulate the transporters through various transcriptional, translational, and post-translational mechanisms that involve acute trafficking via endocytosis or exocytosis, interactions with PDZ domain proteins, lipid microdomains, and diffusion and clustering in the apical brush border membrane...
January 6, 2019: Pflügers Archiv: European Journal of Physiology
Oleg Pisarenko, Irina Studneva, Alexander Timoshin, Oksana Veselova
Disturbed homeostasis of nitric oxide (NO) is one of the causes of myocardial ischemia/reperfusion (I/R) injury during open-heart surgery. This study was designed to explore mechanisms of action of dinitrosyl iron complexes with reduced glutathione ({(GS- )2 Fe+ (NO+ )2 }+ , DNIC-GS) added to crystalloid cardioplegia or reperfusion solution in isolated working rat hearts. Hearts of male Wistar rats were subjected to cardioplegic arrest by St. Thomas' Hospital cardioplegic solution (STH) and normothermic global ischemia followed by reperfusion...
January 6, 2019: Pflügers Archiv: European Journal of Physiology
Robert Mallmann, Katarina Ondacova, Lucia Moravcikova, Bohumila Jurkovicova-Tarabova, Michaela Pavlovicova, Lucia Lichvarova, Viera Kominkova, Norbert Klugbauer, Lubica Lacinova
Voltage-gated Ca2+ channels are embedded in a network of protein interactions that are fundamental for channel function and modulation. Different strategies such as high-resolution quantitative MS analyses and yeast-two hybrid screens have been used to uncover these Ca2+ channel nanodomains. We applied the yeast split-ubiquitin system with its specific advantages to search for interaction partners of the CaV 2.2 Ca2+ channel and identified four proteins: reticulon 1 (RTN1), member 1 of solute carrier family 38 (SLC38), prostaglandin D2 synthase (PTGDS) and transmembrane protein 223 (TMEM223)...
January 5, 2019: Pflügers Archiv: European Journal of Physiology
A Choukèr, Jürgen Bereiter-Hahn, D Singer, G Heldmaier
For long-duration manned space missions to Mars and beyond, reduction of astronaut metabolism by torpor, the metabolic state during hibernation of animals, would be a game changer: Water and food intake could be reduced by up to 75% and thus reducing payload of the spacecraft. Metabolic rate reduction in natural torpor is linked to profound changes in biochemical processes, i.e., shift from glycolysis to lipolysis and ketone utilization, intensive but reversible alterations in organs like the brain and kidney, and in heart rate control via Ca2+ ...
December 19, 2018: Pflügers Archiv: European Journal of Physiology
Heini Murer, Jürg Biber, Ian C Forster, Andreas Werner
No abstract text is available yet for this article.
December 19, 2018: Pflügers Archiv: European Journal of Physiology
Juan V Sanchez-Andres, Willy J Malaisse, Itaru Kojima
Over recent years, the presence of the sweet taste receptor TIR3 in rodent and human insulin-producing pancreatic islet β-cells was documented. The activation of this receptor by sweet-tasting sucralose mimics several biochemical and functional effects of D-glucose in the β-cells. The present study extends this analogy to the bioelectrical response of β-cells. In this respect, sucralose was inefficient in the absence of D-glucose, but induced on occasion electrical activity in mouse β-cells exposed to low non-stimulatory concentrations of the hexose and potentiated, in a concentration-related manner, the response to stimulatory concentrations of D-glucose...
December 14, 2018: Pflügers Archiv: European Journal of Physiology
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