Sensing Intra‐ and Extra‐Cellular Ca 2+ in the Islet of Langerhans

2021 ◽  
pp. 2106020
Author(s):  
Weikun Huang ◽  
Tongzhi Wu ◽  
Cong Xie ◽  
Christopher K. Rayner ◽  
Craig Priest ◽  
...  
Keyword(s):  
Islet Of Langerhans ◽  
Cellular Ca

scholarly journals Activation of Xenopus Eggs by Cynops Sperm Extract is Dependent upon Both Extra-and Intra-Cellular Ca Activities

1995 ◽  
Vol 12 (5) ◽  
pp. 573-581 ◽  
Author(s):  
Yasuhiro Iwao ◽  
Michiko Kobayashi ◽  
Akiko Miki ◽  
Hiroshi Y. Kubota ◽  
Yasuaki Yoshimoto
Keyword(s):  
Sperm Extract ◽  
Cellular Ca

scholarly journals Ca 2+ toxicity and mitochondrial damage in acute pancreatitis: translational overview

2016 ◽  
Vol 371 (1700) ◽  
pp. 20150425 ◽  
Author(s):  
József Maléth ◽  
Péter Hegyi
Keyword(s):  
Acute Pancreatitis ◽  
Mitochondrial Permeability Transition ◽  
Clinical Investigation ◽  
Cell Damage ◽  
Specific Treatment ◽  
Experimental Models ◽  
Mitochondrial Damage ◽  
Cell Functions ◽  
Cellular Ca

Acute pancreatitis (AP) is a leading cause of hospitalization among non-malignant gastrointestinal disorders. The mortality of severe AP can reach 30–50%, which is most probably owing to the lack of specific treatment. Therefore, AP is a major healthcare problem, which urges researchers to identify novel drug targets. Studies from the last decades highlighted that the toxic cellular Ca 2+ overload and mitochondrial damage are key pathogenic steps in the disease development affecting both acinar and ductal cell functions. Moreover, recent observations showed that modifying the cellular Ca 2+ signalling might be beneficial in AP. The inhibition of Ca 2+ release from the endoplasmic reticulum or the activity of plasma membrane Ca 2+ influx channels decreased the severity of AP in experimental models. Similarly, inhibition of mitochondrial permeability transition pore (MPTP) opening also seems to improve the outcome of AP in in vivo animal models. At the moment MPTP blockers are under detailed clinical investigation to test whether interventions in MPTP openings and/or Ca 2+ homeostasis of the cells can be specific targets in prevention or treatment of cell damage in AP. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.

scholarly journals Important Role of Reverse Na+-Ca2+Exchange in Spinal Cord White Matter Injury at Physiological Temperature

2000 ◽  
Vol 84 (2) ◽  
pp. 1116-1119 ◽  
Author(s):  
Shuxin Li ◽  
Qiubo Jiang ◽  
Peter K. Stys
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Traumatic Injury ◽  
White Matter Injury ◽  
Mechanical Trauma ◽  
White Matter Tracts ◽  
Physiological Temperature ◽  
Cord Injury ◽  
Cellular Ca

Spinal cord injury is a devastating condition in which most of the clinical disability results from dysfunction of white matter tracts. Excessive cellular Ca2+ accumulation is a common phenomenon after anoxia/ischemia or mechanical trauma to white matter, leading to irreversible injury because of overactivation of multiple Ca2+-dependent biochemical pathways. In the present study, we examined the role of Na+-Ca2+ exchange, a ubiquitous Ca2+ transport mechanism, in anoxic and traumatic injury to rat spinal dorsal columns in vitro. Excised tissue was maintained in a recording chamber at 37°C and injured by exposure to an anoxic atmosphere for 60 min or locally compressed with a force of 2 g for 15 s. Mean compound action potential amplitude recovered to ≈25% of control after anoxia and to ≈30% after trauma. Inhibitors of Na+-Ca2+ exchange (50 μM bepridil or 10 μM KB-R7943) improved functional recovery to ≈60% after anoxia and ≈70% after traumatic compression. These inhibitors also prevented the increase in calpain-mediated spectrin breakdown products induced by anoxia. We conclude that, at physiological temperature, reverse Na+-Ca2+exchange plays an important role in cellular Ca2+ overload and irreversible damage after anoxic and traumatic injury to dorsal column white matter tracts.

scholarly journals Intercellular communication in the rat anterior pituitary gland: an in vivo and in vitro study

1975 ◽  
Vol 67 (2) ◽  
pp. 469-476 ◽  
Author(s):  
WH Fletcher ◽  
NC Anderson ◽  
JW Everett
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
In Vitro Study ◽  
Anterior Pituitary Gland ◽  
Stimulus Secretion Coupling ◽  
Unpublished Observation ◽  
Cellular Ca

The concept of "stimulus-secretion coupling" suggested by Douglas and co-workers to explain the events related to monamine discharge by the adrenal medulla (5, 7) may be applied to other endocrine tissues, such as adrenal cortex (36), pancreatic islets (4), and magnocellular hypothalamic neurons (6), which exhibit a similar ion-dependent process of hormone elaboration. In addition, they share another feature, that of joining neighbor cells via membrane junctions (12, 26, and Fletcher, unpublished observation). Given this, and the reports that hormone secretion by the pars distalis also involves a secretagogue-induced decrease in membrane bioelectric potential accompanied by a rise in cellular [Ca++] (27, 34, 41), it was appropriate to test the possibility that cells of the anterior pituitary gland are united by junctions.

scholarly journals The hypothalamic satiety peptide CART is expressed in anorectic and non-anorectic pancreatic islet tumors and in the normal islet of Langerhans

FEBS Letters ◽  
1999 ◽  
Vol 447 (2-3) ◽  
pp. 139-143 ◽  
Author(s):  
Per B Jensen ◽  
Peter Kristensen ◽  
Jes T Clausen ◽  
Martin E Judge ◽  
Sven Hastrup ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Islet Of Langerhans

Effects of lipotoxicity on a novel insulin-secreting human pancreatic β-cell line, 1.1B4

2013 ◽  
Vol 394 (7) ◽  
pp. 909-918 ◽  
Author(s):  
Srividya Vasu ◽  
Neville H. McClenaghan ◽  
Jane T. McCluskey ◽  
Peter R. Flatt
Keyword(s):  
Mrna Expression ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Endoplasmic Reticulum Stress Response ◽  
Future Research ◽  
The Novel ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Expression Of Genes ◽  
Cellular Ca

Abstract The novel insulin-secreting human pancreatic β-cell line, 1.1B4, demonstrates stability in culture and many of the secretory functional attributes of human pancreatic β-cells. This study investigated the cellular responses of 1.1B4 cells to lipotoxicity. Chronic 18-h exposure of 1.1B4 cells to 0.5 mm palmitate resulted in decreased cell viability and insulin content. Secretory responses to classical insulinotropic agents and cellular Ca2+ handling were also impaired. Palmitate decreased glucokinase activity and mRNA expression of genes involved in secretory function but up-regulated mRNA expression of HSPA5, EIF2A, and EIF2AK3, implicating activation of the endoplasmic reticulum stress response. Palmitate also induced DNA damage and apoptosis of 1.1B4 cells. These responses were accompanied by increased gene expression of the antioxidant enzymes SOD1, SOD2, CAT and GPX1. This study details molecular mechanisms underlying lipotoxicity in 1.1B4 cells and indicates the potential value of the novel β-cell line for future research.

Expression of glucose transporter 4 in the human pancreatic islet of Langerhans

2004 ◽  
Vol 314 (4) ◽  
pp. 1121-1125 ◽  
Author(s):  
Honami Kobayashi ◽  
Takashi Mitsui ◽  
Seiji Nomura ◽  
Yasumasa Ohno ◽  
Kenji Kadomatsu ◽  
...  
Keyword(s):  
Pancreatic Islet ◽  
Glucose Transporter ◽  
Islet Of Langerhans ◽  
Glucose Transporter 4 ◽  
Human Pancreatic Islet
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