TY  - JOUR
A1  - Münch, Miriam
A1  - Hsin, Chih-Hsuan
A1  - Ferber, Elena
A1  - Berger, Susanne
A1  - Müller, Martin J.
T1  - Reactive electrophilic oxylipins trigger a heat stress-like response through HSFA1 transcription factors
JF  - Journal of Experimental Botany
N2  - Electrophilic oxylipins trigger a heat-shock-like response in the absence of heat through the canonical heat-shock transcription factor A1, thereby helping to cope with stresses associated with protein damage.Abiotic and biotic stresses are often characterized by an induction of reactive electrophile species (RES) such as the jasmonate 12-oxo-phytodienoic acid (OPDA) or the structurally related phytoprostanes. Previously, RES oxylipins have been shown massively to induce heat-shock-response (HSR) genes including HSP101 chaperones. Moreover, jasmonates have been reported to play a role in basal thermotolerance. We show that representative HSR marker genes are strongly induced by RES oxylipins through the four master regulator transcription factors HSFA1a, b, d, and e essential for short-term adaptation to heat stress in Arabidopsis. When compared with Arabidopsis seedlings treated at the optimal acclimation temperature of 37 A degrees C, the exogenous application of RES oxylipins at 20 A degrees C induced a much weaker induction of HSP101 at both the gene and protein expression levels which, however, was not sufficient to confer short-term acquired thermotolerance. Moreover, jasmonate-deficient mutant lines displayed a wild-type-like HSR and were not compromised in acquiring thermotolerance. Hence, the OPDA- and RES oxylipin-induced HSR is not sufficient to protect seedlings from severe heat stress but may help plants to cope better with stresses associated with protein unfolding by inducing a battery of chaperones in the absence of heat.
KW  - arabidopsis-thaliana
KW  - shock response
KW  - gene-expression
KW  - model
KW  - acquired thermotolerance
KW  - 12-oxo-phytodienoic acid
KW  - thermotolerance
KW  - plants
KW  - detoxification
KW  - acquisition
KW  - activation
KW  - heat stress
KW  - jasmonates
KW  - phytoprostanes
KW  - reactive electrophilic species
KW  - unfolded protein response
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-186766
VL  - 67
IS  - 21
ER  - 
TY  - JOUR
A1  - Wang, Hongjie
A1  - Karnati, Srikanth
A1  - Madhusudhan, Thati
T1  - Regulation of the homeostatic unfolded protein response in diabetic nephropathy
JF  - Pharmaceuticals
N2  - A growing body of scientific evidence indicates that protein homeostasis, also designated as proteostasis, is causatively linked to chronic diabetic nephropathy (DN). Experimental studies have demonstrated that the insulin signaling in podocytes maintain the homeostatic unfolded protein response (UPR). Insulin signaling via the insulin receptor non-canonically activates the spliced X-box binding protein-1 (sXBP1), a highly conserved endoplasmic reticulum (ER) transcription factor, which regulates the expression of genes that control proteostasis. Defective insulin signaling in mouse models of diabetes or the genetic disruption of the insulin signaling pathway in podocytes propagates hyperglycemia induced maladaptive UPR and DN. Insulin resistance in podocytes specifically promotes activating transcription factor 6 (ATF6) dependent pathogenic UPR. Akin to insulin, recent studies have identified that the cytoprotective effect of anticoagulant serine protease-activated protein C (aPC) in DN is mediated by sXBP1. In mouse models of DN, treatment with chemical chaperones that improve protein folding provides an additional benefit on top of currently used ACE inhibitors. Understanding the molecular mechanisms that transmute renal cell specific adaptive responses and that deteriorate renal function in diabetes will enable researchers to develop new therapeutic regimens for DN. Within this review, we focus on the current understanding of homeostatic mechanisms by which UPR is regulated in DN.
KW  - unfolded protein response
KW  - ER stress
KW  - diabetic nephropathy
KW  - insulin signaling
KW  - aPC
KW  - podocytes
KW  - XBP1
KW  - ATF6
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-267143
SN  - 1424-8247
VL  - 15
IS  - 4
ER  -