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Calcium signalling in mammalian cell lines expressing wild type and mutant human α1-Antitrypsin
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Calcium signalling in mammalian cell lines expressing wild type and mutant human α1-Antitrypsin
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Journal Article
Calcium signalling in mammalian cell lines expressing wild type and mutant human α1-Antitrypsin
2019
Overview
A possible role for calcium signalling in the autosomal dominant form of dementia, familial encephalopathy with neuroserpin inclusion bodies (FENIB), has been proposed, which may point towards a mechanism by which cells could sense and respond to the accumulation of mutant serpin polymers in the endoplasmic reticulum (ER). We therefore explored possible defects in Ca
2+
-signalling, which may contribute to the pathology associated with another serpinopathy, α
1
-antitrypsin (AAT) deficiency. Using CHO K1 cell lines stably expressing a wild type human AAT (MAAT) and a disease-causing polymer-forming variant (ZAAT) and the truncated variant (NHK AAT), we measured basal intracellular free Ca
2+
, its responses to thapsigargin (TG), an ER Ca
2+
-ATPase blocker, and store-operated Ca
2+
-entry (SOCE). Our fura2 based Ca
2+
measurements detected no differences between these 3 parameters in cell lines expressing MAAT and cell lines expressing ZAAT and NHK AAT mutants. Thus, in our cell-based models of α1-antitrypsin (AAT) deficiency, unlike the case for FENIB, we were unable to detect defects in calcium signalling.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/106
/ 14
/ 14/1
/ 14/19
/ 631/1647
/ 692/308
/ alpha 1-Antitrypsin - genetics
/ alpha 1-Antitrypsin - metabolism
/ Animals
/ Calcium
/ Calcium Signaling - genetics
/ Chronic obstructive pulmonary disease
/ Dementia
/ Disease
/ Epilepsies, Myoclonic - genetics
/ Epilepsies, Myoclonic - pathology
/ Heredodegenerative Disorders, Nervous System - genetics
/ Heredodegenerative Disorders, Nervous System - pathology
/ Humanities and Social Sciences
/ Humans
/ Mutation
/ Polymers
/ Proteins
/ Science
